Scholarly Literature
This is an aggregation of scholarly literature from peer-reviewed journals, bioRxiv , medRxiv and arXiv preprint servers focused on natural and engineered selfish genetic elements and genetic biocontrol. New citations are added as they appear. This content is intended for anyone interested in the scholarly literature on gene drive and genetic biocontrol.
Sperm competition and the dynamics of X chromosome drive: Stability and extinction
4326Taylor, JEJ, J., Genetics, 160:1721-1731. 2002-01-04 00:00:00.
Several empirical studies of sperm competition in populations polymorphic for a driving X chromosome have revealed that Sex-ratio males (those carrying a driving X) are at a disadvantage relative to Standard males. Because the frequency of the driving X chromosome determines the population-level sex ratio and thus alters male and female mating rates, the evolutionary consequences of sperm competition for sex chromosome meiotic drive are subtle. As the SR allele increases in frequency, the ratio of females to males also increases, causing an increase in the male mating rate and a decrease in the female mating rate. While the former change may exacerbate the disadvantage of Sex-ratio males during sperm competition, the latter change decreases the incidence of sperm competition within the population. We analyze a model of the effects of sperm competition on a driving X chromosome and show that these opposing trends in male and female mating rates call result in two coexisting locally stable equlibria, one corresponding to a balanced polymorphism of the SR and ST alleles and the second to fixation of the ST allele. Stochastic fluctuations of either the Population sex ratio or the SR frequency call then drive the population away from the balanced polymorphism and into the basin of attraction for the second equilibrium, resulting in fixation of the SR allele and extinction of the population.
Sex-ratio drive in Drosophila simulans: Variation in segregation ratio of X chromosomes from a natural population
4325Montchamp-Moreau, CC, M., Genetics, 162:1221-1231. 2002-01-03 00:00:00.
The sex-ratio trait that exists in a dozen Drosophila species is a case of naturally occurring X chromosome drive that causes males to produce female-biased progeny. Autosomal and Y polymorphism for suppressors are known to cause variation in drive expression, but the X chromosome polymorphism has never been thoroughly investigated. We characterized 41 X chromosomes from a natural population of Drosophila simulans that had been transferred to a suppressor-free genetic background. We found two clear-cut groups of chromosomes, sex-ratio and standard. The sex-ratio X chromosomes differed in their segregation ratio (81-96% females in the progeny), the less powerful drivers being less stable in their expression. A sib analysis, using a moderate driver, indicated that within-X variation in drive expression depended on genetic (autosomal) or epigenetic factors and that the age of the males also affected the trait. The other X chromosomes produced equal or roughly equal sex ratios, but again with significant variation. The continuous pattern of variation observed within both groups suggested that, in addition to a major sex-ratio gene, many X-linked loci of small effect modify the segregation ratio of this chromosome and are maintained in a polymorphic state. This was also supported by the frequency distribution of sex ratios produced by recombinant X chromosomes.
Segregation distortion induced by wild-type RanGAP in Drosophila
4324Kusano, AS, C.; Ganetzky, B., Proceedings of the National Academy of Sciences of the United States of America, 99:6866-6870. 2002-01-02 00:00:00.
Segregation Distorter (SD) is a meiotic drive system in Drosophila that causes preferential transmission of the SD chromosome from SD/SD+ males owing to the induced dysfunction of SD+ spermatids. The key distorter locus, Sid, is a dominant neomorphic allele encoding a truncated, but enzymatically active, RanGAP (RanGTPase-activating protein) whose nuclear mislocalization underlies distortion by disrupting the Ran signaling pathway. Here, we show that even wild-type RanGAP can cause segregation distortion when it is overexpressed in the male germ line or when the gene dosage of a particular modifier locus is increased. Both manipulations result in substantial nuclear accumulation of RanGAP. Distortion can be suppressed by overexpression of Ran or Ran guanine nucleotide exchange factor (RanGEF) in the male germ line, indicating that the primary consequence of nuclear mislocalization of RanGAP is reduction of intranuclear RanGTP levels. These results prove that segregation distortion does not depend on any unique properties of the mutant RanGAP encoded by Sid and provide a unifying explanation for the occurrence of distortion in a variety of experimental situations.
Sperm development, age and sex chromosome meiotic drive in the stalk-eyed fly, Cyrtodiopsis whitei
4337Wilkinson, GSS, M. I., Heredity, 87:17-24. 2001-01-15 00:00:00.
The cytological basis of X chromosome meiotic drive or sex ratio (SR) has been reported for several species of Drosophila but not for other species. Here we describe how sperm development in the stalk-eyed fly, Cyrtodiopsis whitei, influences progeny sex proportion, in order to determine if a common developmental mechanism could cause meiotic drive in these distantly related taxa. Because age has been found to affect the degree of segregation distortion in some Drosophila, we tested flies from six to 26 weeks of age. We find that spermatocyst bundles in SR males frequently contain incompletely elongated spermatid nuclei independently of male age. Older males have, however, more spermatocyst bundles in their testes than younger males. Abnormal spermatid elongation affects male fertility since SR males produce 74% as many progeny per week as ST males. The proportion of spermatocyst bundles with improperly elongated spermatid nuclei explains 71% of the variation in progeny sex proportion. After reviewing the literature on sperm development and meiotic drive, we conclude that the cytological basis of meiotic drive in diopsids closely resembles Drosophila. Across species in both groups, the production of fertile males is associated with less than half of all spermatids not elongating normally in a spermatocyst bundle. We discuss the possibility that frequency-dependent selection on male fertility could stabilize the drive polymorphism in these unusual flies.
Meiotic drive alters sperm competitive ability in stalk-eyed flies
4336Wilkinson, GSF, C. L., Proceedings of the Royal Society B-Biological Sciences, 268:2559-2564. 2001-01-14 00:00:00.
Meiotic drive results when sperm carrying a driving chromosome preferentially survive development. Meiotic drive should therefore influence sperm competition because drive males produce fewer sperm than non-drive males. Whether meiotic drive also influences the competitive ability of sperm after ejaculation is unknown. Here we report the results from reciprocal crosses that are designed for estimating the sperm precedence of male stalk-eyed flies (Cyrtodiopsis whitei) with or without X-linked meiotic drive. We find that nearly half of all sex-ratio males, as compared with 14 % of non-sex-ratio males, fail to produce young in a reciprocal cross. Furthermore, the proportion of progeny sired by a sex-ratio male in a female jointly inseminated by a non-sex-ratio male was less than expected from the number of sperm transferred. These effects are not due to differential sperm storage by females because, after a single mating with a sex-ratio male, all females stored sperm and because two sex-ratio males share paternity after jointly mating with a female. In addition to demonstrating a new mechanism of sperm competition, these results provide insight into the maintenance of sex-ratio polymorphisms. Sex-ratio males have less than one-half the fertility of non-sex-ratio males, as is required in order for frequency-dependent selection on males to produce a stable sex-ratio polymorphism.
Selection and segregation distortion in a sex-differentiated population
4335Weissing, FJvB, M., Theoretical Population Biology, 60:327-341. 2001-01-13 00:00:00.
We extend the classical model for selection at an autosomal locus in a sex-differentiated population to include segregation distortion. The equations remain the same, but the fitness parameters are interpreted differently and refer to alleles instead of genotypes. We derive conditions for internal and external stability of the equilibria, i.e., stability with respect to perturbations of alleles that are already present at equilibrium and stability with respect to invasion attempts by newly arising alleles. We show that, in a sex-differentiated population, external stability of an equilibrium can be judged on the basis of Shaw-Mohler criteria. Throughout, we compare the situation in populations with and without sex differentiation. Interestingly, internal stability is more difficult to achieve in a population without sex differentiation than in a population in which selection and segregation distortion are restricted to one sex. In a companion paper we show how the general results of the present paper can lead to new insights into specific systems such as the t complex of the house mouse. (C) 2001 Elsevier Science.
Competition at the Mouse t Complex: Rare Alleles Are Inherently Favored
4334van Boven, MW, Franz J., Theoretical Population Biology, 60:343-358. 2001-01-12 00:00:00.
We investigate the competition between alleles at a segregation distorter locus. The focus is on the invasion prospects of rare mutant distorter alleles in a population in which a wildtype and a resident distorter allele are present. The parameters are chosen to reflect the situation at the t complex of the house mouse, one of the best-studied examples of segregation distortion. By analyzing the invasion chances of rare alleles, we provide an analytical justification of earlier simulation results. We show that a new distorter allele can successfully invade even if it is inferior both at the gamete and at the individual level. In fact, newly arising distorter alleles have an inherent rareness advantage if their negative fitness consequences are restricted to homozygous condition. Likewise, rare mutant wildtype alleles may often invade even if their viability or fertility is reduced. As a consequence, the competition between alleles at a segregation distorter locus should lead to a high degree of polymorphism. We discuss the implications of this conclusion for the t complex of the house mouse and for the evolutionary stability of “honest” Mendelian segregation.
Sex-ratio segregation distortion associated with reproductive isolation in Drosophila
4333Tao, YH, D. L.; Laurie, C. C., Proceedings of the National Academy of Sciences of the United States of America, 98:13183-13188. 2001-01-11 00:00:00.
Sex-ratio distortion is the most common form of non-Mendelian segregation observed in natural populations. It may occur even more frequently than direct observations suggest, because the dysgenic population consequences of a biased sex ratio are expected to result in the rapid evolution of suppressors, resulting in suppressed or "cryptic" segregation distortion. Here we report evidence for cryptic sex-ratio distortion that was discovered by introgressing segments of the genome of Drosophila mauritiana into the genome of Drosophila simulans. The autosomal suppressor of sex-ratio distortion, which is also associated with a reduction in hybrid male fertility, has been genetically localized to a region smaller than 80-kb pairs in chromosome 3.
Sex chromosome meiotic drive
4332Jaenike, J, Annual Review of Ecology and Systematics, 32:25-49. 2001-01-10 00:00:00.
Sex chromosome drive refers to the unequal transmission of X and Y chromosomes from individuals of the heterogametic sex, resulting in biased sex ratios among progeny and within populations, The presence of driving sex chromosomes can reduce mean fitness within a population, bring about intragenomic conflict between the X chromosome, the Y, and the autosomes, and alter the intensity or mode of sexual selection within species. Sex chromosome drive, or its genetic equivalent, is known in plants, mammals. and flies. Many species harboring driving X chromosomes have evolved Y-linked and autosomal suppressors of drive. If a drive polymorphism is not stable, then driving chromosomes may spread to fixation and cause the extinction of a species. Certain characteristics of species, such as population density and female mating rate, may affect the probability of fixation of driving chromosomes. Thus, sex chromosome drive could be an agent of species-level selection.
The role of selfish genetic elements in eukaryotic evolution
4331Hurst, GDDW, J. H., Nature Reviews Genetics, 2:597-606. 2001-01-09 00:00:00.
'Selfish genetic elements', such as transposons, homing endonucleases, meiotic drive chromosomes and heritable microorganisms, are common features of eukaryotes. However, their importance in the evolution of eukaryotic genomes is still controversial. In this review, we discuss these diverse elements and their potential importance in the evolution of genetic systems, adaptation, and the extinction and birth of species.
An unusual sex-determination system in South American field mice (genus Akodon): The role of mutation, selection, and meiotic drive in maintaining XY females
4330Hoekstra, HEH, J. M., Evolution, 55:190-197. 2001-01-08 00:00:00.
The mechanism of sex determination in mammals appears highly conserved: the presence of a Y chromosome triggers the male developmental pathway, whereas the absence of a Y chromosome results in a default female phenotype. However, if the Y chromosome fails to initiate the male pathway (referred to as Y*), XY* females can result, as is the case in several species of South American field mice (genus Akodon). The breeding genetics in this system inherently select against the Y* chromosome such that the frequency of XY* females should decrease rapidly to very low frequencies. However, in natural populations of Akodon, XY* females persist at substantial frequencies; for example, 10% of females are XY* in A. azarae and 30% in A. boliviensis. We develop a mathematical model that considers the potential roles of three evolutionary forces in maintaining XY* females: Y-to-Y* chromosome transitions (mu ration), chromosome segregation distortion (meiotic drive), and differential fecundity (selection). We then test the predictions of our model using data from breeding colonies of A. azarae. We conclude that any single force is inadequate to maintain XY* females. However, a combination of segregation bias of the male and female Y chromosomes during spermatogenesis/oogenesis and increased fecundity in XY* females could account for the observed frequencies of XY* females.
Outcrossed sex allows a selfish gene to invade yeast populations
4329Goddard, MRG, D.; Burt, A., Proceedings of the Royal Society B-Biological Sciences, 268:2537-2542. 2001-01-07 00:00:00.
Homing endonuclease genes (HEGs) in eukaryotes are optional genes that have no obvious effect on host phenotype except for causing chromosomes not containing a cop), of the gene to be cut, thus causing them to be inherited at a greater than Mendelian rate via gene conversion. These genes are therefore expected to increase in frequency in outcrossed populations, but not in obligately selfed populations. In order to test this idea, we compared the dynamics of the VDE HEG in six replicate outcrossed and inbred populations of yeast (Saccharomyces cerevisiae). VDE increased in frequency from 0.21 to 0.55 in four outcrossed generations, but showed no change in frequency in the inbred populations. The absence of change in the inbred populations indicates that any effect of VDE on mitotic replication rates is less than 1%. The data from the outcrossed populations best fit a model in which 82% of individuals are derived from outcrossing and VDE is inherited by 74% of the meiotic products from heterozygotes (as compared with 50% for Mendelian genes), These results empirically demonstrate how a host mating system plays a key role in determining the population dynamics of a selfish gene.
Nonrandom segregation during meiosis: the unfairness of females
4328de Villena, FPMS, C., Mammalian Genome, 12:331-339. 2001-01-06 00:00:00.
Most geneticists assume that chromosome segregation during meiosis is Mendelian (i.e., each allele at each locus is represented equally in the gametes). The great majority of reports that discuss non-Mendelian transmission have focused on systems of gametic selection, such as the mouse t-haplotype and Segregation distorter in Drosophila, or on systems in which post-fertilization selection takes place, Because the segregation of chromosomes in such systems is Mendelian and unequal representation of alleles among offspring is achieved through gamete dysfunction or embryonic death, there is a common perception that true disturbances in the randomness of chromosome segregation are rare and of limited biological significance. In this review we summarize data on nonrandom segregation in a wide variety of genetic systems. Despite apparent differences between some systems, the basic requirements for nonrandom segregation can be deduced from their shared characteristics: i) asymmetrical meiotic division(s); ii) functional asymmetry of the meiotic spindle poles: and iii) functional heterozygosity at a locus that mediates attachment of a chromosome to the spindle. The frequency with which all three of these requirements al e fulfilled in natural populations is an known, but our analyses indicate that nonrandom segregation occurs with sufficient frequency during female meiosis, and in exceptional cases of male meiosis, that it has important biological, clinical, and evolutionary consequences.
Transmission ratio distortion due to the bl gene in table beet
4327Austin, DG, I. L., Journal of the American Society for Horticultural Science, 126:340-343. 2001-01-05 00:00:00.
The bl gene conditions a blotchy phenotype (irregular sectors of red and white root color) in table beet (Beta vulgaris ssp, vulgaris). Segregation of the bl gene was found to be consistent with a single recessive gene, however, some evidence for a departure from a single gene model was observed when blbl plants were used as females. Tn this report, segregation of the bl gene was examined in greater detail in 10 F-2 populations derived from crosses of red blotchy-rooted females (genotype blbl, denoted blotchy) with red-rooted males (BlBl, denoted red,), and 10 Fz populations derived from the reciprocal cross. Tn blbl x BlBl crosses, the proportion of red-rooted progeny was greater than 0.75 in seven of the crosses, and was significantly greater (P = 0.005) in three crosses. A test for heterogeneity was significant, indicating that the proportion of red-rooted progeny differed significantly in these 10 crosses. In BlBl x blbl crosses, the proportion of red-rooted progeny was <0.75 in seven of the crosses and there were no significant departures from the expected 3:1 ratio in any of the individual crosses. However, a pooled estimate of the segregation ratio showed a significant (P < 0.01) departure from the 3:1 ratio (pooled estimate = 0.71.), These data demonstrate transmission ratio distortion at the bl locus when blbl plants are used as both females and males in matings with wild type plants, but the degree of distortion is greater when blbl plants are used as females. Ratio distortion in such crosses may be due to a variety of factors, including increased transmission of the bl gene through female or male gametes depending on the direction of the cross, reduced fitness of maternally derived blbl progeny, epigenetic phenomena, increased fitness of paternally derived blbl progeny, or linkage of the bl gene to viability genes.
Success in Zanzibar: Eradication of tsetse
27123A. R. Msangi, N. Kiwia, I. I. Malele, F. Mramba, K. M. Saleh, W. A. Mussa, K. G. Juma, V. A. Dyck, M. J. B. Vreysen, A. G. Parker, U. Feldmann, Z. R. Zhu and H. Pan, Area-Wide Control of Fruit Flies and Other Insect Pests, 2000-06-06 13:17:29.
There are about 22 species of tsetse flies found nowhere else in the world except in 36 countries of sub-Saharan Africa Tsetse flies transmit a debilitating and often fatal disease, trypanosomosis, which causes tremendous losses of livestock, and severely limits agricultural production (it reduces output of milk and meat, causes mortality, infertility and abortion in livestock, deprives the rural population of draught power and manure to improve and increase crop production) Tsetse flies also transmit human trypanosomosis, commonly known as 'sleeping sickness' It is estimated that over 55 million people living in rural sub-Saharan Africa are at risk from this fatal disease Tanzania's Zanzibar Island is situated 35 km off the eastern coast and comprises two main islands, Unguja and Pemba Previous surveys revealed that out of the seven tsetse species found on mainland Tanzania, only Glossina austeni Newstead infested Unguja Island No tsetse fly was found on the island of Pemba The fly is responsible for the cyclical transmission of trypanosomosis in livestock, the causative agents being mainly Trypanosoma congolense and, to a lesser extent, T vivax It is estimated that in Zanzibar, the disease causes annual losses of US$2 million Since fly suppression by conventional techniques has often resulted in short-term success, Tanzania has always appreciated that the long-term solution to the trypanosomosis problem is the eradication of tsetse flies in the country In 1994, the International Atomic Energy Agency (IAEA) and the United Republic of Tanzania embarked on a project with the objective of eradicating tsetse flies from Zanzibar Island by applying the sterile insect technique (SIT) (Dyck et al 1995, in press) Previous tsetse eradication efforts in Tanzania using SIT, enabled the establishment of a modest capacity on tsetse mass rearing in Tanga (Williamson et al 1983) The Zanzibar tsetse project was successfully completed in 1997 The estimated cost was US$7,941,000 but only US$5,788,097 was actually spent Financial assistance came from international donors such as the governments of Belgium, Canada, China, Sweden, the UK and the USA The results and achievements of the Zanzibar tsetse fly eradication project are presented in this paper
Glossina austeni (Diptera: Glossinidae) Eradicated on the Island of Unguja, Zanzibar, Using the Sterile Insect Technique
27121M. J. B. Vreysen, K. M. Saleh, M. Y. Ali, A. M. Abdulla, Z.-R. Zhu, K. G. Juma, V. A. Dyck, A. R. Msangi, P. A. Mkonyi and H. U. Feldmann, Journal of Economic Entomology, 123-135. 2000-02-01 12:59:17.
An area-wide integrated tsetse eradication project was initiated in Zanzibar in 1994 by the International Atomic Energy Agency and the governments of Tanzania and Zanzibar, to eradicate Glossina austeni Newstead from Unguja Island (Zanzibar) using the sterile insect technique. Suppression of the tsetse population on Unguja was initiated in 1988 by applying residual pyrethroids as a pour-on formulation to livestock and by the deployment of insecticide impregnated screens in some of the forested areas. This was followed by sequential releases of gamma-sterilized male flies by light aircraft. The flies, packaged in carton release containers, were dispersed twice a week along specific flight lines separated by a distance of 1–2 km. More than 8.5 million sterile male flies were released by air from August 1994 to December 1997. A sterile to indigenous male ratio of >50:1 was obtained in mid-1995 and it increased to >100:1 by the end of 1995. As a consequence the proportion of sampled young females (1–2 ovulations), with an egg in utero in embryonic arrest or an uterus empty as a result of expulsion of a dead embryo, increased from <25% in the 1st quarter to >70% in the last quarter of 1995. In addition, the age structure of the female population became significantly distorted in favor of old flies (≥4 ovulations) by the end of 1995. The apparent density of the indigenous fly population declined rapidly in the last quarter of 1995, followed by a population crash in the beginning of 1996. The last trapped indigenous male and female flies were found in weeks 32 and 36, 1996, respectively. Time for 6 fly generations elapsed between the last catch of an indigenous fly and the end of the sterile male releases in December 1997.
Co-existence of hosts and sex ratio distorters in structured populations
4343Hatcher, MJD, A. M.; Tofts, C., Evolutionary Ecology Research, 2:185-205. 2000-01-21 00:00:00.
Vertically transmitted parasites occur in several invertebrate species, and alter host reproduction by a variety of mechanisms, including sex ratio distortion via feminization. Efficient feminizers are predicted to drive homogenous host populations extinct due to the absence of males. However, group (interdemic) selection may enable host-parasite co-existence through extinction-colonization turnover of local subpopulations. Here we analyse the effects of feminizers on host metapopulations, in relation to the underlying mechanism of host sex determination. We examine host metapopulations with (a) fixed probabilistic sex ratio control, (b) female heterogamety (WZ/ZZ) and (c) male heterogamety (XX/XY) with and without YY viability. Under some circumstances, host and parasite can co-exist in metapopulations despite deterministic instability of local populations, in which case the parasite persists at lower frequency than predicted for homogenous populations. However, co-existence is sensitive to host sex determining mechanism. Long-term co-existence is unlikely in chromosomal systems, where sex ratio selection and novel mating type combinations result in the loss of female-determining alleles from infected host subpopulations. The consequent loss of uninfected females precludes stochastic parasite exclusion and thus prevents local population recovery. Hence, host-feminizer co-existence via interdemic selection requires intrinsic patch recovery in addition to recolonization from neighbouring subpopulations. We conclude that metapopulation structure can only buffer host populations against parasite-mediated extinction if female-determining alleles are retained in the host population.
Persistence of selfish genetic elements: population structure and conflict
4342Hatcher, MJ, Trends in Ecology & Evolution, 15:271-277. 2000-01-20 00:00:00.
Selfish genetic elements are vertically transmitted factors that spread by obtaining a transmission advantage relative to the rest of the genome of their host organism, often with a cost to overall host fitness. In many cases, conventional population genetics theory predicts them spreading through populations, reaching fixation and becoming undetectable or sometimes driving the population extinct. However, in several well studied systems, these genetic elements are known to persist at relatively low, stable frequencies. Recent research suggests that several processes might explain these observations, including population structure, intragenomic conflict and coevolution.
Non-Mendelian segregation of sex chromosomes in heterospecific Drosophila males
4341Dermitzakis, ETM, J. P.; Waldrip, H. M.; Clark, A. G., Genetics, 154:687-694. 2000-01-19 00:00:00.
Interspecific hybrids and backcrossed organisms generally suffer from reduced viability and/or fertility. To identify and genetically map these defects, we introgressed regions of the Drosophila sechellia genome into the D. simulans genome. A female-biased sex ratio was observed in 24 of the 221 recombinant inbred lines, and subsequent tests attributed the skew to failure of Y-bearing sperm to fertilize the eggs. Apparently these introgressed lines fail to suppl ess a normally silent meiotic drive system. Using molecular markers we mapped two regions of the Drosophila genome that appear to exhibit differences between D. simulans and D. sechellia in their regulation of sex chromosome segregation distortion. The data indicate that the sex ratio phenotype results from an epistatic interaction between at least two factors. We discuss whether this observation is relevant to the meiotic drive theory of hybrid male sterility.
A genetic test to determine the origin of maternal transmission ratio distortion: Meiotic drive at the mouse Om locus
4340de Villena, FPMdlC-E, E.; Briscoe, T. L.; Sapienza, C., Genetics, 154:333-342. 2000-01-18 00:00:00.
We have shown previously that the progeny of crosses between heterozygous females and C57BL/G males show transmission ratio distortion at the Om locus on mouse chromosome 11. This result has been replicated in several independent experiments. Here we show that the distortion maps to a single locus on chromosome 11, closely linked to Om, and that gene conversion is not implicated in the origin of this phenomenon. To further investigate the origin of the transmission ratio distortion we generated a test using the well-known effect of recombination on maternal meiotic drive. The genetic test presented here discriminates between unequal segregation of alleles during meiosis and lethality, based on the analysis of genotype at both the distorted locus and the centromere of the same chromosome. We used this test to determine the cause of the transmission ratio distortion observed at the Om locus. Our results indicate that transmission ratio distortion at Om is due to unequal segregation of alleles to the polar body at the second meiotic division. Because die presence of segregation distortion at Om also depends on rile genotype of the sire, our results confirm that the sperm can influence segregation of maternal chromosomes to the second polar body.
Heritability of the maternal meiotic drive system linked to Om and high-resolution mapping of the Responder locus in mouse
4339de Villena, FPMdlC-E, E.; Williams, J. W.; Malette, J. M.; Rosa, M.; Sapienza, C., Genetics, 155:283-289. 2000-01-17 00:00:00.
Matings between (C57BL/6 X DDK)F-1 females and C57BL/6 males result in a significant excess of offspring inheriting maternal DDK alleles in the central region of mouse chromosome 11 due to meiotic drive at the second meiotic division. We have shown previously that the locus subject to selection is in the vicinity of D11Mit66, a marker closely linked to the Om locus that controls the preimplantation embryolethal phenotype known as the "DDK syndrome." We have also shown that observation of meiotic drive in this system depends upon tl-le genotype of the sire. Here we show that females that are heterozygous at Om retain the meiotic drive phenotype and define a 0.32-cM candidate interval for the Responder locus in this drive system. In addition, analysis of the inheritance of alleles at Om among the offspring of F-1 intercrosses indicates that the effect of the sire is determined by the sperm genotype at Om or a locus linked to Om.
Sex-ratio meiotic drive in Drosophila simulans is related to equational nondisjunction of the Y chromosome
4338Cazemajor, MJ, D.; Montchamp-Moreau, C., Genetics, 154:229-236. 2000-01-16 00:00:00.
The sex-ratio trait, an example of naturally occurring X-linked meiotic drive, has been reported in a dozen Drosophila species. Males carrying a sex-ratio X chromosome produce an excess of female offspring caused by a deficiency of Y-bearing sperm. In Drosophila simulans, such males produce similar to 70-90% female offspring, and 15-30% of the male offspring are sterile. Here, we investigate the cytological basis of the drive in this species. We show that the sex-ratio trait is associated with nondisjunction of Y chromatids in meiosis II. Fluorescence in situ hybridization (FISH) using sex-chromosome-specific probes provides dir-ect evidence that the drive is caused by the failure of the resulting spermatids to develop into functional sperm. XYY progeny were not observed, indicating that few or no YY spermatids escape failure. The recovery of XO males among the progeny of sex-ratio males shows that some nullo-XY spermatids become functional sperm and likely explains the male sterility. A review of the cytological data. in other species shows that aberrant behavior of the Y chromosome may be a common basis of sex-ratio meiotic drive in Drosophila and the signal that triggers differential spermiogenesis failure.
Spore-killing meiotic drive factors in a natural population of the fungus Podospora anserina
4348van der Gaag, MD, A. J. M.; Oosterhof, J.; Slakhorst, M.; Thijssen, Jagm; Hoekstra, R. F., Genetics, 156:593-605. 2000-01-06 00:00:00.
In fungi, meiotic drive is observed as spore killing. In the secondarily homothallic ascomycete Podospora anserina it is characterized by the abortion of two of the four spores in the ascus. We have identified seven different types of meiotic drive elements (Spore killers). Among 99 isolates from nature, six of these meiotic drive elements occurred in a local population. Spore killers comprise 23% of the natural population of P. anserina in Wageningen, The Netherlands, sampled from 1991 to 1997. One Spore-killer type was also found in a French strain dating from 1937. All other isolates found so far are sensitive to spore killing. All seven Spore killer types differ in the percentage of asci that show killing and in their mutual interactions. Interactions among Spore killer types showed either mutual resistance or dominant epistasis. Most killer elements could be assigned to linkage group III but are not tightly linked to the centromere.
Chromosomally-induced meiotic drive in Drosophila males: Checkpoint or fallout?
4347Tomkiel, JE, Genetica, 109:95-103. 2000-01-05 00:00:00.
In male Drosophila melanogaster, anomalies in sex chromosome pairing at meiosis often lead to complete or partial sperm dysfunction. This observation has led to the suggestion that defects in either the efficiency or configuration of chromosome pairing at metaphase trigger a checkpoint mechanism that leads to the elimination of meiotic products. Here, we discuss this model in consideration of recent observations on the conservation of metaphase checkpoint components in male meiosis, and on the phenotype of new alleles of the male-specific meiotic mutant teflon. Based on these observations, we propose an alternative hypothesis for the cause of sperm dysfunction in cases of chromosomal sterility and drive. We suggest that disruption of the prophase compartmentalization of sex chromatin, rather than abnormal pairing at metaphase, may be the causative defect. Such disruption may occur as a result of perturbations in sex chromosome pairing, or by translocations involving autosomal and sex chromatin. We discuss how this hypothesis may account for previously described examples chromosomal causes of meiotic drive and sterility in Drosophila.
Segregation distortion of mouse t-haplotypes: The molecular basis emerges
4346Schimenti, J, Trends in Genetics, 16:240-243. 2000-01-04 00:00:00.
The t haplotype is an ancestral version of proximal mouse chromosome 17 that has evolved mechanisms to persist as an intact genomic variant in mouse populations. t haplotypes contain mutations that affect embryonic development, male fertility and male transmission ratio distortion (TRD), Collectively, these mutations drive the evolutionary success of t haplotypes, a phenomenon that remains one of the longstanding mysteries of mouse genetics. Molecular genetic analysis of TRD has been confounded by inversions that arose to lock together the various elements of this complex trait. Our first molecular glimpse of the TRD mechanism has finally been revealed with the cloning of the t complex responder (Tcr) locus, a chimeric kinase with a genetically cis active effect. Whereas + sperm in a +/t male have impaired flagellar function caused by the deleterious action of trans-active, t-haplotype-encoded 'distorters,' the mutant activity of Tcr counterbalances the distorter effects, maintaining the motility and fertilizing ability of t sperm.
Physical mapping of male fertility and meiotic drive quantitative trait loci in the mouse t complex using chromosome deficiencies
4345Planchart, AY, Y.; Schimenti, J. C., Genetics, 155:803-812. 2000-01-03 00:00:00.
The t complex spans 20 cM of the proximal region of mouse chromosome 17. A variant form, the t haplotype (t), exists at significant frequencies in wild mouse populations and is characterized by the presence of inversions that suppress recombination with Mild-type (+) chromosomes. Transmission ratio distortion and sterility are associated with t and affect males only. It is hypothesized that these phenomena are caused by trans-acting distorter/sterility factors that interact with a responder locus (Tcr(t)) and that the distorter and sterility factors are the same because homozygosity of the distorters causes male sterility. One factor, Tcd1, was previously shown to be amorphic using a chromosome deletion. To overcome limitations imposed by recombination suppression, we used a series of deletions within the t complex in trans to t chromosomes to characterize the Tcd1 region. The find that the distorter activity of Tcd1 is distinct from a linked sterility factor, originally called tcs1. YACs mapped with respect to deletion breakpoints localize tcs1 to a 1.1-Mb interval flanked by D17Aus9 and Tctex1. We present evidence for the existence of multiple proximal t complex regions that exhibit distorter activity. These studies demonstrate the utility of chromosome deletions for complex trait analysis.
Nonrandom segregation of the mouse univalent X chromosome: Evidence of spindle-mediated meiotic drive
4344LeMaire-Adkins, RH, P. A., Genetics, 156:775-783. 2000-01-02 00:00:00.
A fundamental principle of Mendelian inheritance is random segregation of alleles to progeny; however, examples of distorted transmission either of specific alleles or of whole chromosomes have been described in a variety of species. In humans and mice, a distortion in chromosome transmission is often associated with a chromosome abnormality. One such example is the fertile XO female mouse. A transmission distortion effect that results in an excess of XX over XO daughters among the progeny of XO females has been recognized for nearly four decades. Utilizing contemporary methodology that combines immuno-fluorescence, FISH, and three-dimensional confocal microscopy, we have readdressed the meiotic segregation behavior of the single X chromosome in oocytes from XO females produced on two different inbred backgrounds. Our studies demonstrate that segregation of the univalent X chromosome at the first meiotic division is nonrandom, with preferential retention of the X chromosome in the oocyte in similar to 60% of cells. We propose that this deviation from Mendelian expectations is facilitated by a spindle-mediated mechanism. This mechanism, which appears to be a general feature of the female meiotic process, has implications the frequency of nondisjunction in our species.
A male-biased primary sex ratio and larval mortality in Eucheira socialis (Lepidoptera : Pieridae)
4363Underwood, DLAS, A. M., Evolutionary Ecology Research, 1:703-717. 1999-01-21 00:00:00.
We investigated the sex ratio and sex-biased mortality in the Mexican pierid butterfly, Eucheira socialis westwoodi. We studied two populations between 1990 and 1997 along Mexico Highway 40, which runs from Mazatlan, Sinaloa to Durango, Durango, Populations occurring between km 64 and 101 and between km 163 and 213 were designated 'eastern' and 'western', respectively We determined the primary sex ratio of egg masses from these populations in 1992, 1995, 1996 and 1997, The primary sex ratio varied from 68.0 to 75.5% male and from 63.7 to 79.3% male in the eastern and western populations, respectively. The frequency of significantly male-biased full sib groups was between 55 and 100% in the east and between 67 and 94% in the west. For all years, in both populations, the primary sex ratio was significantly different from 1:1. Lf the probability of a given zygote being male is the same across sibships, the distribution of the primary sex ratio should be binomial. For years where at least 10 egg masses were collected, the distribution of primary sex ratio was significantly different from a binomial in all years in the east and two of three years in the west. We studied larval and pupal mortality in these populations in 1990, 1991 and 1997. Larval mortality was consistently disproportionately male, varying from 83 to 100% male. Pupal mortality tended to be female-biased. The operational sex ratio varied from 65 to 71% male in the east and from 70 to 76% male in the west.
Genetic and molecular characterization of sting, a gene involved in crystal formation and meiotic drive in the male germ line of Drosophila melanogaster
4362Schmidt, AP, G.; Bozzetti, M. P.; Tritto, P.; Pimpinelli, S.; Schafer, U., Genetics, 151:749-760. 1999-01-20 00:00:00.
The sting mutation, caused by a P element inserted into polytene region 32D, was isolated by a screen for male sterile insertions in Drosophila melanogaster. This sterility is correlated with the presence of crystals in spermatocytes and spermatids that are structurally indistinguishable from those produced in males carrying a deficiency of the Y-linked crystal (cry) locus. In addition, their morphology is needle-like in Ste(+) flies and star-shaped in Ste flies, once again as observed in cry(-) males. The sti mutation leads to meiotic drive of the sex chromosomes, and the strength of the phenomenon is correlated with the copy number of the repetitive Ste locus. The same correlation is also true for the penetrance of the male sterile mutation. A presumptive sti null allele results in male sterility and lethal maternal effect. The gene was cloned and shown to code for a putative protein that is 866 amino acids long. A C-terminal domain of 52 amino acids is identified that is well conserved in proteins from different organisms. The gene is expressed only in the germline of both sexes. The interaction of sting with the Ste locus can also be demonstrated at the molecular level. While an unprocessed 8-kb Ste primary transcript is expressed in wild-type males, in X/Y-homoozygous sti males, as in X/Y cry(-) males, a 0.7-kb mRNA is produced.
Meiotic drive and evolution of female choice
4361Reinhold, KE, L.; Misof, B.; Kurtz, J., Proceedings of the Royal Society B-Biological Sciences, 266:1341-1345. 1999-01-19 00:00:00.
As a special version of the good-genes hypothesis, it was recently proposed that females could benefit from choosing drive-resistant males in a meiotic drive system. Here, we examine with a three-locus, six-allele population genetic model whether female choice for drive resistance can evolve. An allele leading to female preference for drive-resistant males was introduced at low frequency into a population polymorphic for meiotic drive and drive resistance. Our simulations show that female choice of drive-resistant males is disadvantageous when resistance is Y-linked. This disadvantage occurs because, at equilibrium, drive-resistant males have lower reproductive success than drive-susceptible males. Thus, female choice of drive-susceptible males can evolve when resistance is Y-linked. When resistance is autosomal, selection on female choice for drive resistance is less strong and depends on the frequency of choice: female preference of resistant males is favoured when choice is rare and disadvantageous when choice is frequent, leading to a stable equilibrium at a low frequency of the choice allele. Independent of the location of drive resistance alleles, males with the non-driving allele always have above average reproductive success. Female choice is therefore beneficial when choosy females prefer males with the non-driving allele.
Transmission ratio distortion in females on chromosome 10p11-p15
4360Paterson, ADP, A., American Journal of Medical Genetics, 88:657-661. 1999-01-18 00:00:00.
A number of recent reports of linkage of markers on chromosome 10p to schizophrenia, and evidence for linkage in one study to bipolar affective disorder, provide encouragement for psychiatric genetics, after nonreplication of linkage findings at other chromosomal regions, The same region on chromosome 10 also demonstrates evidence for linkage to obesity, female alcoholism, and female type 1 diabetes. However, evidence for linkage can be confounded by the biological phenomenon of transmission ratio distortion. Transmission ratio distortion (also termed segregation distortion or meiotic drive) results in non-Mendelian segregation of alleles to live born offspring, and has not been investigated at the majority of loci for complex traits. We examined evidence for transmission ratio distortion using 40 Centre d'Etude du Polymorphisme Humain (CEPH) pedigrees across chromosome 10 using CEPH genotype data. Evidence for linkage of females to D10S211 was found (multipoint non-parametric linkage Z score [NPL] = 1.84, P = 0.040), while there was no linkage of this marker to male sex, The observation of possible transmission ratio distortion in females on chromosome 10p requires additional study, and may impact on the interpretation of positive linkage findings in this region. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:657-661, 1999. (C) 1999 Wiley-Liss, Inc.
Truncated RanGAP encoded by the Segregation Distorter locus of Drosophila
4359Merrill, CB, L.; Kusano, A.; Ganetzky, B., Science, 283:1742-1745. 1999-01-17 00:00:00.
Segregation Distorter (SD) in Drosophila melanogaster is a naturally occurring meiotic drive system in which the SD chromosome is transmitted from SD/SD+ males in vast: excess over its homolog owing to the induced dysfunction of SD+-bearing spermatids. The Sd Locus is the key distorting gene responsible for this phenotype. A genomic fragment from the Sd region conferred full distorting activity when introduced into the appropriate genetic background by germline transformation. The only functional product encoded by this fragment is a truncated version of the RanGAP nuclear transport protein. These results demonstrate that this mutant RanGAP is the functional Sd product.
Models of sex-ratio meiotic drive and sexual selection in stalk-eyed flies
4358Lande, RW, G. S., Genetics Research, 74:245-253. 1999-01-16 00:00:00.
Hypertrophied sexually dimorphic eye stalks have evolved independently in several families of Diptera, with the eyespan of males exceeding their total body length in some species. These structures function in intermale contests for territories and in mate attraction, the classical mechanisms of sexual selection. In the family Diopsidae, species with extremely exaggerated eye stalks and marked sexual dimorphism in relative eyespan also usually have strongly female-biased sex ratios in nature caused by X-linked meiotic drive, whereas species with relatively small eye stalks have little or no sexual dimorphism, often lack meiotic drive and have even sex ratios. We investigate the possible connection between sexual selection and sex-ratio meiotic drive by analysing a three-locus model for the evolution of female choice for a male character associated with meiotic drive. Both meiotic drive and the male character are X-linked and the female preference is autosomal. Our model shows that suppressed recombination between meiotic drive and the male character, e.g. by inversion of the X chromosome, is necessary for sex-ratio selection to promote the origin of female mating preferences and exaggerated secondary sexual characters. With complete suppression of recombination, sexual selection reduces the frequency of meiotic drive, and may eliminate it. Very rare recombination, gene conversion or mutation, at rates characteristic of chromosome inversions in Drosophila, restores the meiotic drive polymorphism to its original equilibrium. Sex-ratio meiotic drive may thus act as a catalyst accelerating the origin of female mating preference and exaggerated male traits.
How common are meiotically driving sex chromosomes in insects?
4357Jiggins, FMH, G. D. D.; Majerus, M. E. N., American Naturalist, 154:481-483. 1999-01-15 00:00:00.
In summary, we argue that the hypothesis that sex chromosome; meiotic drive is common within the insects is in; fact not proved. We feel that, although it is unlikely that; it will be found exclusively in the Diptera, there is a case; to be made that the Diptera are a hot spot for the occurrence; of sex chromosome meiotic drive. Further research; is clearly necessary to clarify this point. If the Diptera; are found to be different, then we must ask why this; is so. Meiotic drive often involves the destruction of gametes; that do not bear the drive allele causing a reduction; in the number of functional gametes. This may mean that; meiotically driving sex chromosomes are unlikely to spread; in female heterogametic taxa such as the Lepidoptera because; a reduction in the number of eggs is more costly; than a reduction in the number of sperm. Among male; heterogametic taxa, it is unclear what could make Dipteran; meiosis special.
Suppression of sex-ratio meiotic drive and the maintenance of Y-chromosome polymorphism in Drosophila
4356Jaenike, J, Evolution, 53:164-174. 1999-01-14 00:00:00.
Like several other species of Drosophila, D. quinaria is polymorphic for X-chromosome meiotic drive; matings involving males that carry a "sex-ratio" X chromosome (X(SR)) result in the production of strongly female-biased offspring sex ratios (Jaenike 1996). A survey of isofemale lines of D, quinaria from several populations reveals that there is genetic variation for partial suppression of this meiotic drive. Crossing experiments show that there is Y-linked. and probably autosomal, variation for suppression of drive. Y-linked suppressors of X-chromosome drive have now been described in several species of Diptera. I develop a simple model for the maintenance of Y-chromosome polymorphism in species polymorphic for X-linked meiotic drive. One interesting feature of this model is that, if there is a stable Y-chromosome polymorphism, then the equilibrium frequency of the standard and sex-ratio X chromosomes is determined solely by Y-chromosome parameters, not by the fitness effects of the different X chromosomes on their carriers. This model suggests that Y-chromosome polymorphism may be easier to maintain than previously thought, and I hypothesize that karyotypic variation in Y chromosomes will be found to be associated with suppression of sex-ratio meiotic drive in other species of Drosophila.
Invasion of one insect species, Adalia bipunctata, by two different male-killing bacteria
4355Hurst, GDDvdS, J. H. G.; Majerus, T. M. O.; Bertrand, D.; Zakharov, I. A.; Baungaard, J.; Volkl, W.; Stouthamer, R.; Majerus, M. E. N., Insect Molecular Biology, 8:133-139. 1999-01-13 00:00:00.
Male-killing bacteria, which are inherited through the female line and kill male progeny only, are known from five different orders of insect. Our knowledge of the incidence of these elements has stemmed from discovery of their phenotype in different species, Our estimate of the frequency with which insects have been invaded by these elements therefore depends on each observation of the male-killing phenotype within a species being associated with a single microorganism. We here record an example of a single insect species being infected with two taxonomically distinct male-killing bacteria. Western European populations of the two-spot ladybird, Adalia bipunctata, have previously been shown to bear a male-killing Rickettsia, However, we here show that the majority of the male-killing lines tested from Central and Eastern Europe do not bear this bacterium. Rather, 16S rDNA sequence analysis suggests male-killing is associated with st member of the genus Spiroplasma. We discuss this conclusion in relation to the evolutionary genetics of male-killing bacteria, and the evolution of male-killing behaviour in the eubacteria.
Population dynamics under parasitic sex ratio distortion
4354Hatcher, MJT, D. E.; Dunn, A. M.; Tofts, C., Theoretical Population Biology, 56:11-28. 1999-01-12 00:00:00.
We analyse the population dynamic effects of sex ratio distortion by vertically transmitted, feminizing parasites, We show that, for diploid hosts, sex ratio distortion may lead to extinction as males become too rare to maintain the host population through reproduction. Feminizers can magnify Allee effects, broadening the range of conditions leading to extinction of small populations, Depending on male mating constraints and strength of density dependence, feminizers may either increase or decrease the equilibrium host density. Under conditions leading to deterministic host extinction, stochastic elimination of the parasite may allow the host population to recover. Hence, infection by parasitic sex ratio distorters may be transient in finite populations. We consider the implications of this process for parasite prevalence, host population regulation, and sex ratio evolution. (C) 1999 Academic Press.
Recurrent invasion and extinction of a selfish gene
4353Goddard, MRB, A., Proceedings of the National Academy of Sciences of the United States of America, 96:13880-13885. 1999-01-11 00:00:00.
Homing endonuclease genes show super-Mendelian inheritance, which allows them to spread in populations even when they are of no benefit to the host organism. To test the idea that regular horizontal transmission is necessary for the long-term persistence of these genes, we surveyed 20 species of yeasts for the omega-homing endonuclease gene and associated group I intron. The status of omega could be categorized into three states (functional, nonfunctional, or absent), and status was not clustered on the host phylogeny. Moreover, the phylogeny of w differed significantly from that of the host, strong evidence of horizontal transmission. Further analyses indicate that horizontal transmission is more common than transposition, and that it occurs preferentially between closely related species. Parsimony analysis and coalescent theory suggest that there have been 15 horizontal transmission events in the ancestry of our yeast species, through simulations indicate that this value is probably an underestimate. Overall, the data support a cyclical model of invasion, degeneration, and loss, followed by reinvasion, and each of these transitions is estimated to occur about once every 2 million years. The data are thus consistent with the idea that frequent horizontal transmission is necessary for the long-term persistence of homing endonuclease genes, and further, that this requirement limits these genes to organisms with easily accessible germ lines. The data also show that mitochondrial DNA sequences are transferred intact between yeast species; if other genes do not show such high levels of horizontal transmission, it would be due to lack of selection, rather than lack of opportunity.
Transmission ratio distortion at the INS-IGF2 VNTR
4352Eaves, IAB, S. T.; Forster, P.; Ferber, K. M.; Ehrmann, D.; Wilson, A. J.; Bhattacharyya, S.; Ziegler, A. G.; Brinkmann, B.; Todd, J. A., Nature Genetics, 22:324-325. 1999-01-10 00:00:00.
Transmission ratio distortion (TRD) is defined as a statistically significant departure from mendelian transmission. So far, evidence of this in humans has been limited or controversial1,2,3,4, and the few established examples involve chromosome rearrangements in lower organisms5.; ; The variable number of tandem repeat (VNTR) polymorphism 596 bp 5´ of the insulin gene (INS) regulates expression of both INS and the gene encoding insulin-like growth factor 2 (IGF2). The VNTR can be subdivided into two main allele sizes, class I and class III, in Europeans. Class III alleles are associated with reduced expression of INS and IGF2 in the pancreas and placenta6. As lower expression of VNTR class III-associated INS/IGF2 alleles early in fetal development may reduce the chances of survival in utero, the locus is considered a candidate for exhibiting TRD.
Are Drosophila SR drive chromosomes always balanced?
4351Carvalho, ABV, S. C., Heredity, 83:221-228. 1999-01-09 00:00:00.
SR chromosomes are the best-known case of sex chromosome meiotic drive. These X chromosomes cause the production of female-biased progenies in several Drosophila species; Due to their meiotic drive advantage, they are expected to spread and become fixed, resulting in population extinction due to the lack of males. However, this apparently does not occur: SR chromosomes are maintained in balanced polymorphisms, resulting from the equilibrium between their meiotic drive advantage and deleterious fitness effects. In this paper we review the current explanations for their deleterious effects and we argue that it is highly improbable that all newly emerged SR are sufficiently deleterious to avoid fixation. Unbalanced SR almost certainly arise and go unnoticed because of three possible outcomes: (i) fixation followed by extinction of the population or species; (ii) fixation followed by the emergence and fixation of drive suppressors, restoring the normal 1:1 sexual proportion; or (iii) transformation into balanced SR due to partial suppression. If these outcomes really occur, then extant cases of sex-chromosome meiotic drive such as SR, causing small deviations on the population sexual proportion are only the tip of the iceberg and strong sexual proportion shifts (possibly followed by extinction) are a more common feature of species evolution than is usually assumed.
Evolution of driving X chromosomes and resistance factors in experimental populations of Drosophila simulans
4350Capillon, CA, A., Evolution, 53:506-517. 1999-01-08 00:00:00.
Sex-ratio drive is a particular case of meiotic drive, described in several Drosophila species, that causes males bearing driving X chromosome to produce a large excess of females in their progeny. In Drosophila simulans, driving X chromosomes and resistance factors located on the Y chromosome and on the autosomes have been previously reported. In this paper, we report the study of the dynamics of sex-ratio factors in experimental populations. We followed the evolution in frequency of driving X chromosomes in the absence of resistance factors and the evolution of resistance factors in the presence of driving X chromosomes. The driving X chromosome was lost, contrarily to theoretical expectations that predict its rapid invasion. Autosomal resistances increased in frequency, and resistant Y chromosomes invaded the population very quickly, as predicted by theoretical models. Fitness measurements showed that the loss of the driving X chromosome was due to a strong deleterious effect that was expressed only when distorting males were in competition with standard males. However, the spread of autosomal resistances reduced this deleterious effect. Implications for the maintenance of polymorphism in natural populations are discussed.
Meiotic drive of chromosomal knobs reshaped the maize genome
4349Buckler, ESP-D, T. L.; Buckler, C. S. K.; Dawe, R. K.; Doebley, J. F.; Holtsford, T. P., Genetics, 153:415-426. 1999-01-07 00:00:00.
Meiotic drive is the subversion of meiosis so that particular genes are preferentially transmitted to the progeny. Meiotic drive generally causes the preferential segregation of small regions of the genome; however, in maize we propose that meiotic drive is responsible for the evolution of large repetitive DNA arrays on all chromosomes. A maize meiotic drive locus found on an uncommon form of chromosome 10 [abnormal 10 (Ab10)] may be largely responsible for the evolution of heterochromatic chromosomal knobs, which can confer meiotic drive potential to every maize chromosome. Simulations were used to illustrate the dynamics of this meiotic drive model and suggest knobs might be deleterious in the absence of Ab10. Chromosomal knob data from maize's wild relatives (Zea mays ssp. parviglumis and mexicana) and phylogenetic comparisons demonstrated that the evolution of knob size, frequency, and chromosomal position agreed with the meiotic drive hypothesis. Knob chromosomal position was incompatible with the hypothesis that knob repetitive DNA is neutral or slightly deleterious to the genome. We also show iv that environmental factors and transposition may play a role in the evolution of knobs. Because knobs occur at multiple locations on all maize chromosomes, the combined effects of meiotic drive and genetic linkage may have reshaped genetic diversity throughout the maize genome in response to the presence of Ab10. Meiotic drive may be a major force of genome evolution, allowing revolutionary changes in genome structure and diversity over short evolutionary periods.
Segregation distortion in a deme structured population: opposing demands of gene, individual and group selection
4364van Boven, MW, F. J., Journal of Evolutionary Biology, 12:80-93. 1999-01-02 00:00:00.
The evolution of segregation distortion is governed by the interplay of selection at different levels. Despite their systematic advantage at the gamete level, none of the well-known segregation distorters spreads to fixation since they induce severe negative fitness effects at the individual level. In a deme-structured population, selection at the population level also plays a role. By means of a population genetical model, we analyse the various factors that determine the success of a segregation distorter in a metapopulation, Our focus is on the question of how the success of a distorter allele is affected by its segregation ratio and its fitness effects at the individual level. The analysis reveals that distorter alleles with high segregation ratios are the best invaders and reach the highest frequencies within single demes. However, the productivity of a deme harbouring a distorter with a high segregation ratio may be significantly reduced. As a consequence, an efficient distorter will be underrepresented in the migrant pool and, moreover, it may increase the probability of deme extinction. In other words, efficient distorters with high segregation ratios may well succumb to their own success. Therefore, distorters with intermediate segregation ratios may reach the highest frequency in the metapopulation as a result of the opposing forces of gamete, individual and group selection. We discuss the implications of this conclusion for the t complex of the house mouse.
Mariner transposition and transformation of the yellow fever mosquito, Aedes aegypti
6256C. J. Coates, N. Jasinskiene, L. Miyashiro and A. A. James, Proceedings of the National Academy of Sciences of the United States of America, 95:3748-3751. 1998-03-07 19:31:51.
The mariner transposable element is capable of interplasmid transposition in the embryonic soma of the yellow fever mosquito, Aedes aegypti. To determine if this demonstrated mobility could be utilized to genetically transform the mosquito, a modified mariner element marked with a wild type allele of the Drosophila melanogaster cinnabar gene was microinjected into embryos of a kynurenine hydroxylase-deficient, white-eyed recipient strain. Three of 69 fertile male founders resulting from the microinjected embryos produced families with colored-eyed progeny individuals, a transformation rate of 4%. The transgene-mediated complementation of eve color was observed to segregate in a Mendelian manner, although one insertion segregates with the recessive allele (female-determining) of the sex-determining locus, and a separate insertion is homozygous lethal. Molecular analysis of selected transformed families demonstrated that a single complete copy of the construct had integrated independently in each case acid that it had done so in a transposase-mediated manner. The availability of a mariner transformation system greatly enhances our ability to study and manipulate this important vector species.
Stable transformation of the yellow fever mosquito, Aedes aegypti, with the Hermes element from the housefly
6254N. Jasinskiene, C. J. Coates, M. Q. Benedict, A. J. Cornel, C. S. Rafferty, A. A. James and F. H. Collins, Proceedings of the National Academy of Sciences of the United States of America, 95:3743-3747. 1998-03-07 19:28:29.
The mosquito Aedes aegypti is the world's most important vector of yellow fever and dengue viruses, Work is currently in progress to control the transmission of these viruses by genetically altering the capacity of wild Ae, aegypti populations to support virus replication. The germ-line transformation system reported here constitutes a major advance toward the implementation of this control strategy, A modified Hermes transposon carrying a 4.7-kb fragment of genomic DNA that includes a wild-type allele of the Drosophila melanogaster cinnabar (cn) gene was used to transform a white-eyed recipient strain of Ae, aegypti. Microinfection of preblastoderm mosquito embryos with this construct resulted in 50% of the emergent G(0) adults showing some color in their eyes, Three transformed families were recovered, each resulting from an independent insertion event of the cn(+)-carrying transposon, The cn(+) gene functioned as a semidominant transgene and segregated in Mendelian ratios, Hermes shows great promise as a vector for efficient, heritable, and stable transformation of this important mosquito vector species.
Meiotic drive favors Robertsonian metacentric chromosomes in the common shrew (Sorex araneus, Insectivora, Mammalia)
4380Wyttenbach, AB, P.; Hausser, J., Cytogenetics and Cell Genetics, 83:199-206. 1998-01-18 00:00:00.
Meiotic drive has attracted much interest because it concerns the robustness of Mendelian segregation and its genetic and evolutionary stability. We studied chromosomal meiotic drive in the common shrew (Sorex araneus, Insectivora, Mammalia), which exhibits one of the most remarkable chromosomal polymorphisms within mammalian species. The open question of the evolutionary success of metacentric chromosomes (Robertsonian fusions) versus acrocentrics in the common shrew prompted us to test whether a segregation distortion in favor of metacentrics is present in female and/or male meiosis. Performing crosses under controlled laboratory conditions with animals from natural populations, we found a clear trend toward a segregation distortion in favor of metacentrics during male meiosis, two chromosome combinations (gm and ji) being significantly preferred over their acrocentric homologs. Apart for one Robertsonian fusion (hi), this trend was absent in female meiosis. We propose a model based on recombination events between twin acrocentrics to explain the difference in transmission ratios of the same metacentric in different sexes and unequal drive of particular metacentrics in the same sex. Pooled data for female and male meiosis revealed a trend toward stronger segregation distortion for larger metacentrics. This is partially in agreement with the frequency of metacentrics occurring in natural populations of a chromosome race showing a high degree of chromosomal polymorphism.
Male eye span in stalk-eyed flies indicates genetic quality by meiotic drive suppression
4379Wilkinson, GSP, D. C.; Crymes, L., Nature, 391:276-279. 1998-01-17 00:00:00.
In some species, females choose mates possessing ornaments that predict offspring survival(1-5). However, sexual selection by female preference for male genetic quality(6-8) remains controversial because conventional genetic mechanisms maintain insufficient variation in male quality to account for costly preference and ornament evolution(9,10). Here we show that females prefer ornaments that indicate genetic quality generated by transmission conflict between the sex chromosomes, By comparing sex-ratio distributions in stalk-eyed fly (Cyrtodiopsis) progeny we found that female-biased sex ratios occur in species exhibiting eye-stalk sexual dimorphism(11,12) and female preferences for long eye span(13,14). Female-biased sex ratios result from meiotic drive(15), the preferential transmission of a 'selfish' X-chromosome. Artificial selection for 22 generations on male eye-stalk length in sexually dimorphic C. dalmanni produced longer eye-stalks and male-biased progeny sex ratios in replicate lines. Because male-biased progeny sex ratios occur when a drive-resistant Y chromosome pairs with a driving X chromosome(15), long eye span is genetically linked to meiotic drive: suppression. Male eye span therefore signals genetic quality by influencing the reproductive value of offspring(16).
Sex determination, sex ratios, and genetic conflict
4378Werren, JHB, L. W., Annual Review of Ecology and Systematics, 29:233-261. 1998-01-16 00:00:00.
Genetic mechanisms of sex determination are unexpectedly diverse and change rapidly during evolution. We review the role of genetic conflict as the driving force behind this diversity and turnover. Genetic conflict occurs when different components of a genetic system are subject to selection in opposite directions. Conflict may occur between genomes (including paternal-maternal and parental-zygotic conflicts) or within genomes (between cytoplasmic and nuclear genes or sex chromosomes and autosomes). The sex-determining system consists of parental sex-ratio genes, parental-effect sex determiners, and zygotic sex determiners, which are subject to different selection pressures because of differences in their modes of inheritance and expression. Genetic conflict theory is used to explain the evolution of several sex-determining mechanisms, including sex chromosome drive, cytoplasmic sex-ratio distortion, and cytoplasmic male sterility in plants. Although still limited, there is growing evidence that genetic conflict could be important in the evolution of sex-determining mechanisms.
Evolution of segregation distortion: Potential for a high degree of polymorphism
4377van Boven, MW, F. J., Journal of Theoretical Biology, 192:131-142. 1998-01-15 00:00:00.
By means of a population genetical model, we study the evolution of segregation distortion. Most models of segregation distortion focus on a single distorter allele. In contrast, we consider the competition between a large number of distorters. Motivated by systems as the t complex of the house mouse or the Sd complex of Drosophila melanogaster, we assume that there is some "complementation" between distorter alleles, i.e. that the fitness of individuals heterozygous for two distorter alleles is higher than the fitness of homozygous individuals. In the presence of complementation, the most efficient distorter allele with the highest segregation ratio often does not outcompete less efficient distorters. In fact, our results show that coexistence of a large number of distorter alleles is more typical than the competitive exclusion of less efficient distorters by a single superior allele. We first consider the analytically tractable system where all distorters show the same amount of complementation. In this case, all distorters with a segregation ratio higher than a certain critical value will persist, resulting in a polymorphic population where the average segregation ratio is only slightly larger than 0.5. If the degree of complementation varies, there may be more than one stable equilibrium, and the outcome of competition may depend on the initial conditions. Motivated by empirical examples, we also consider the case that the distorting ability of an allele is negatively related to its effects on individual fitness. Interestingly, the outcome of competition depends crucially on details of such a trade-off. We conclude that verbal arguments are insufficient to predict the evolution of segregation distortion. (C) 1998 Academic Press Limited.
The dynamics of maternal-effect selfish genetic elements
4376Smith, NGC, Journal of Theoretical Biology, 191:173-180. 1998-01-14 00:00:00.
Maternal-effect selfish genes such as Medea or Seat act to kill progeny that do not bear a copy of the selfish gene present in the mother. Previous models of this system allowed for two types of allele, the selfish (killer) type and the sensitive (susceptible) wild-type. These models predict that the invasion conditions of the selfish allele are quite broad and that if invasion is possible a high frequency equilibrium is to be expected. The selfish element is therefore predicted to persist. Here a hypothetical third allele that neither kills nor is killed (i.e, insensitive) is considered. Such an allele could enter a population by recombination, mutation or migration. The incorporation of this third allele profoundly affects the dynamics of the system and, under some parameter values, it is possible for the spread of the insensitive allele to lead, eventually, to the fixation of the wild-type allele (reversible evolution). This is most likely if the death of progeny provides no direct benefit to the surviving sibs (i.e. in the absence of fitness compensation), as in insects without gregarious broods. Under these circumstances the selfish element cannot spread when infinitely rare, only after having risen to some finite frequency. A fitness cost to bearing the killer allele then causes its loss. However, if fitness compensation is found (e.g, in placental mammals) the invasion of the selfish element from an infinitely low level is possible for a wide range of costs and both stable coexistences of all three alleles and limit cycles of all three are then found. It is therefore to be expected that in mammals selfish maternal-effect genes are more likely both to spread and to persist than in insects, due to their different levels of fitness compensation. (C) 1998 Academic Press Limited.
