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.
Autosomal suppressors of sex-ratio in Drosophila mediopunctata
4422Decarvalho, ABK, L. B., Heredity, 71:546-551. 1993-01-20 00:00:00.
The sex-ratio trait has been described as the production of progenies with excess of females due to X-linked meiotic drive in the parental males. This trait has a variable expression in Drosophila mediopunctata. We describe here the existence and chromosomal localization of autosomal suppressors of sex-ratio in this species. There are at least four such genes (one on each major autosome) and the strongest effect.is localized on chromosome IV. These genes possibly result from the operation of 'Fisher's Principle'; a mechanism of Natural Selection leading to a 1:1 sex ratio.
Didymium iridis reproductive systems: Additions and meiotic drive
4421Clark, JL, J. C., Mycologia, 85:764-768. 1993-01-19 00:00:00.
Three heterothallic Mexican isolates (Mex 1, Mex 2, and Mex 3) of Didymium iridis belong to the reproductively isolated A5 mating series of this morphospecies. This was unexpected in that the sole previous A5 isolate was from Georgia and the Mexican isolates were collected in southern Mexico adjacent to the Central American Al series region. The Mexican isolates were also unusual in that mating alleles did not generally segregate in a normal 1:1 ratio. The A5(3) or A5(4) mating types, when present in a plasmodium, caused the partial or total elimination of the other mating allele during growth or sporulation. Isolates from Guatemala (Gua 2) and Panama (Pan 8) were found to belong to the Central American Al mating series. Each of these isolates was collected as a haploid selfed plasmodium which contained a single mating type respectively designated A1(13) and A1(14). Four nonheterothallic isolates from California (Ca 8), Guatemala (Gua 1), Japan (jap 1) and South Africa (SA 2) were also investigated.
Deletion analysis of the selfish B-chromosome, Paternal Sex-Ratio (PSR), in the parasitic wasp Nasonia vitripennis
4420Beukeboom, LWW, J. H., Genetics, 133:637-648. 1993-01-18 00:00:00.
Paternal Sex Ratio (PSR) is a ''selfish'' B chromosome in the parasitoid wasp Nasonia vitripennis. It is transmitted via sperm, but causes supercondensation and destruction of the paternal chromosomes in early fertilized eggs. Because this wasp has haplodiploid sex determination, the effect of PSR is to convert diploid (female) eggs into haploid (male) eggs that carry PSR. Characterizing its genetic structure is a first step toward understanding mechanisms of PSR action. The chromosome is largely heterochromatic and contains several tandemly repeated DNA sequences that are not present on the autosomes. A deletion analysis of PSR was performed to investigate organization of repeats and location of functional domains causing paternal chromosome destruction. Deletion profiles using probes to PSR-specific repetitive DNA indicate that most repeats are organized in blocks on the chromosome. This study shows that the functional domains of PSR can be deleted, resulting in nonfunctional PSR chromosomes that are transmitted to daughters. A functional domain may be linked with the psr22 repeat, but function may also depend on abundance of PSR-specific repeats on the chromosome. It is hypothesized that the repeats act as a ''sink'' for a product required for proper paternal chromosome processing. Almost all deletion chromosomes remained either functional of nonfunctional in subsequent generations following their creation. One chromosome was exceptional in that it reverted from nonfunctionality to functionality in one lineage. Transmission rates of nonfunctional deletion chromosomes were high through haploid males, but low through diploid females.
Transmission and expression of the parasitic Paternal Sex-Ratio (PSR) chromosome
4419Beukeboom, LWW, J. H., Heredity, 70:437-443. 1993-01-17 00:00:00.
B-chromosomes are often considered genomic parasites. They are extra to the normal chromosomal complement, are unnecessary for survival of an individual, and are often inherited at higher than Mendelian rates. Paternal Sex Ratio (PSR) is an extreme example of a parasitic B-chromosome in the wasp Nasonia vitripennis. It is transmitted via sperm but then destroys the other paternal chromosomes in the early fertilized egg. PSR disrupts the normal haplodiploid sex determination system of this wasp by converting diploid (female) eggs into haploid eggs that develop into PSR-bearing males. Transmission and expression of PSR was measured in single pair crosses between carrier males and standard females. Presence of the chromosome was detected by probing offspring with PSR-specific repetitive DNA. Most (equal to or more than 90 per cent) PSR males produced all-male offspring. Overall transmission rates of PSR to fertilized eggs varied beween 0.94 and 1.0. Some males (up to 10 per cent) produced daughters at varying frequencies. Of 226 daughters tested, only one carried PSR (and this may have been a laboratory error) indicating that daughters result from failure of transmission rather than loss of expression. Transmission of PSR to males in families that included female offspring varied from 0 to 94 per cent. Incomplete transmission is most likely the result of loss of PSR in some spermatogonial cell lineages and indicates some mitotic instability. Implications of the results to the aetiology and population genetics of PSR are discussed.
Meiotic drive on aberrant Chromosome-1 in the mouse is determined by a linked distorter
4418Agulnik, SIS, I. D.; Orlova, G. V.; Ruvinsky, A. O., Genetical Research, 61:91-96. 1993-01-16 00:00:00.
An aberrant chromosome 1 carrying an inverted fragment with two amplified DNA regions was isolated from wild populations of Mus musculus. Meiotic drive favouring the aberrant chromosome was demonstrated for heterozygous females. Its cause was preferential passage of aberrant chromosome 1 to the oocyte. Genetic analysis allowed us to identify a two-component system conditioning deviation from equal segregation of the homologues. The system consists of a postulated distorter and responder. The distorter is located on chromosome 1 distally to the responder, between the ln and Pep-3 genes, and it acts on the responder when in trans position. Polymorphism of the distorters was manifested as variation in their effect on meiotic drive level in the laboratory strain and mice from wild populations.
The peculiar journey of a selfish chromosome: Mouse t-haplotypes and meiotic drive
4428Silver, LM, Trends in Genetics, 9:250-254. 1993-01-06 00:00:00.
Mouse t haplotypes are descendents of a variant form of chromosome 17 that evolved the ability to propagate itself at the expense of the wild-type homolog from heterozygous +/t males. Although once enigmatic, these widespread selfish chromosomes have revealed many of their secrets in response to a combined assault with molecular, genetic and phylogenetic techniques. This review summarizes the current understanding of t haplotypes and their raison d'etre.
Meiotic behavior of B- chromosomes in the grasshopper Omocestus burri: A case of drive in females
4427Santos, JLD, A. L.; Fernandez, A.; Diez, M., Hereditas, 118:139-143. 1993-01-05 00:00:00.
The meiotic behaviour of an iso-B chromosome of the grasshopper Omocestus burri has been studied in a natural population located at Villar del Cobo (Teruel, Spain) by means of cytological observations of male and female meiosis. Whereas B chromosomes do not accumulate in the male germ line, they are included in the secondary oocyte at an increased frequency over mendelian expectations. Therefore, an accumulation mechanism of the accessory chromosome based on meiotic drive takes place in the females of this species.
Evolutionary dynamics of spore killers
4426Nauta, MJH, R. F., Genetics, 135:923-930. 1993-01-04 00:00:00.
Spore killing in ascomycetes is a special form of segregation distortion. When a strain with the Killer genotype is crossed to a Sensitive type, spore killing is expressed by asci with only half the number of ascospores as usual, all surviving ascospores being of the Killer type. Using population genetic modeling, this paper explores conditions for invasion of Spore killers and for polymorphism of Killers, Sensitives and Resistants (which neither kill, nor get killed), as found in natural populations. The models show that a population with only Killers and Sensitives can never be stable. The invasion of Killers and stable polymorphism only occur if Killers have some additional advantage during the process of spore killing. This may be due to the effects of local sib competition or some kind of ''heterozygous'' advantage in the stage of ascospore formation or in the short diploid stage of the life cycle. This form of segregation distortion appears to be essentially different from other, well-investigated forms, and more field data are needed for a better understanding of spore killing.
Cheaters sometimes prosper: Distortion of Mendelian segregation by meiotic drive
4425Lyttle, TW, Trends in Genetics, 9:205-210. 1993-01-03 00:00:00.
Two of Mendel's three laws were quickly discarded as information on the organization and transmission of genes accumulated at the beginning of this century, but bis law of segregation has shown remarkable staying power. In fact, within most of population genetic theory for sexual diploids is buried the tacit assumption that heterozygous alleles are represented in gametes in a 1:1 ratio. Nevertheless, there is a small, but important, group of genetic systems that subvert the law of segregation, and show 'meiotic drive.'
The evolution of unusual chromosomal systems in coccoids: Extraordinary sex-ratios revisited
4424Haig, D, Journal of Evolutionary Biology, 6:69-77. 1993-01-02 00:00:00.
Coccoids (scale insects) exhibit a wide variety of chromosomal systems. In many species, paternal chromosomes are eliminated from the male germline such that all of a male's sperm transmit an identical set of maternal chromosomes. In such species, an offspring's sex is determined by whether or not paternal chromosomes are inactivated in the egg's cytoplasm after fertilization. This paper presents a model of the evolution of paternal genome loss in coccoids from an ancestral system of XX-XO sex determination. The model is based on Hamilton's (1967) theory that different genetic elements within the genome have different unbeatable sex ratios. In this model (1) meiotic drive by the X chromosome in XO males causes female-biased sex ratios; (2) the maternal set of autosomes in males evolves effective sex linkage to exploit X-drive; and (3) genes expressed in mothers are selected to convert some of their XX daughters into sons. A similar model may explain the evolution of haplodiploidy.
Selfish genes in mosquitos
6274C. F. Curtis, Nature, 357:450. 1992-06-11 16:47:56.
Hurst and coUeagues1.2 state that "within any population of [the mosquito] Culex pipiens there are two sorts of individual, those that bear/harbour Wolbachia [bacteria] and those that do not". But, according to Yen and Barr3, all wild-type C. pipiens appropriately examined before 1973 were found to carry Wolbachia, It was only when Yen and Barr produced uninfected individuals artificially by tetracycline treatment that it was found that matings of uninfected females x infected males were sterile, whereas all matings by uninfected males were fertile.
The New World Screwworm Eradication Programme. North Africa 1988-1992
25556Food and Agriculture Organization, FAO, 1992-06-01 08:59:36.
This book documents a programme which was unusual in several respects. The campaign to eradicate the New World screwworm from North Africa was unusually large in financial terms. At the same time it was unusually short. Era dica tion itself took about six months, although it was preceded by one year of preparation and followed by one year of continued surveillance and preventive actions. It involved an unusually large array of partners: 22 donors, eight countries at immediate risk, four UN agencies and several contractors from the private sector. What have been the main factors contributing to the success of the programme?
Evolution of the mouse t-haplotype – Recent and worldwide introgression to Mus musculus
4433Morita, TK, H.; Murata, K.; Nozaki, M.; Delarbre, C.; Willison, K.; Satta, Y.; Sakaizumi, M.; Takahata, N.; Gachelin, G.; Matsushiro, A., Proceedings of the National Academy of Sciences of the United States of America, 89:6851-6855. 1992-01-11 00:00:00.
Mouse t haplotypes are variants of chromosome 17, consisting of four inversions. Despite the homozygous lethality and pleiotropic effect on embryonic development, sperm production, and recombination, they have widely spread in natural populations of the house mouse (10-40% in frequency) because of the meiotic drive advantage. We sequenced 14 Tcp-1 (t-complex polypeptide 1) genes from four t haplotypes, nine wild mice, and a rat as a reference. From a comparison of intron sequences of 610 base pairs, we dated the origin of t haplotypes to 2.9 +/- 0.7 million years ago, which predates the splitting of Mus musculus subspecies (almost-equal-to 1 million years ago). However, the Tcp-1 intron sequences of t haplotypes from different M. musculus subspecies from various parts of the world show no divergence, indicating the recent introgression (no earlier than 0.8 million years ago) of a single ancestral type. Nucleotide changes in coding regions are also consistent with this conclusion. Hence, polymorphisms among t haplotypes including lethality factors have accumulated during this short time period independently in each M. musculus subspecies.
Male and female segregation distortion for heterochromatic supernumerary segments on the s(8) chromosome of the grasshopper Chorthippus jacobsi
4432Lopezleon, MDC, J.; Camacho, J. P. M., Chromosoma, 101:511-516. 1992-01-10 00:00:00.
The mode of inheritance of supernumerary segments located on three different chromosome pairs was investigated in controlled crosses with specimens of the grasshopper Chorthippus jacobsi. While extra segments located on chromosomes M5 and M6 showed Mendelian inheritance, that on S8 did not. Thus, the two supernumerary heterochromatic chromosome segments located distally on the S8 chromosome accumulated through non-Mendelian transmission through both sexes. The observed transmission patterns may be explained by gametic selection for spermatozoa carrying segmented S8 chromosomes, in addition to meiotic drive for segmented S8 chromosomes in heterozygous females. The significance of these findings for the maintenance of these polymorphisms in natural populations is discussed.
Population genetics of a parasitic chromosome – Experimental analysis of PSR in subdivided populaltions
4431Beukeboom, LWW, J. H., Evolution, 46:1257-1268. 1992-01-09 00:00:00.
Nasonia vitripennis is a parasitoid wasp that harbors several non-Mendelian sex-ratio distorters. These include MSR (Maternal Sex Ratio), a cytoplasmic element that causes nearly all-female families, and PSR (Paternal Sex Ratio), a supernumerary chromosome that causes all-male families. As in other hymenoptera, N. vitripennis has haplodiploid sex determination. Normally, unfertilized (haploid) eggs develop into males and fertilized (diploid) eggs develop into females. The PSR chromosome violates this normal pattern; it is inherited through sperm, but then causes destruction of the paternal chromosomes (except itself, thus converting diploid fertilized eggs (normally females) into haploid eggs that develop into PSR-bearing males. PSR is an extreme example of "parasitic" or "selfish" DNA. Because N. vitripennis has a highly subdivided population structure in nature, population-level selection may be important in determining the dynamics of PSR in natural populations. A theoretical analysis shows that subdivided population structure reduces PSR frequency, whereas high fertilization proportion (such as produced by the MSR element) increases PSR frequency. Population experiments using two deme sizes (3- and 12-foundress groups) and strains producing two fertilization proportions [wild-type (LabII)-57-67% female, and MSR (MI)-90-93% female] confirm these predictions. PSR achieved frequencies over 0.90 in 12-foundress group MSR populations in contrast to 0.20-0.40 in wild-type 12-foundress populations. PSR was selected against in wild-type populations composed of three-foundress groups. In MSR populations with three-foundress groups, presence of PSR selected against the MSR cytoplasmic element, eventually leading to low frequencies of both PSR and MSR. Complicated dynamics may occur when these two sex-ratio distorters are both present in highly subdivided populations. The existence of PSR in natural populations may depend on the presence of MSR. Results indicate that population subdivision could be important in determining the frequency of sex ratio distorters in N. vitripennis.
Can transposable elements be used to drive disease refractoriness genes into vector populations?
6271M. G. Kidwell and J. M. C. Ribeiro, Parasitology Today, 8:325-329. 1992-01-08 16:40:55.
A number of biological procedures are currently being considered as alternatives to insecticide-based methods for the control of insect vectors of disease. Among these are the adaptation of various genetic mechanisms to drive genes of interest, such as refractoriness to malaria in mosquitoes, into natural populations, for vector control purposes. Here, Margaret Kidwell and Jose Ribeiro develop a rationale for the possible use of transposable genetic elements, one of these potential drive mechanisms, and some of the problems being faced in seeking to determine the feasibility of such a strategy are described.
Effects of deletions on mitotic stability of the Paternal Sex-Ratio (PSR) chromosome from Nasonia
4430Beukeboom, LWR, K. M.; Werren, J. H., Chromosoma, 102:20-26. 1992-01-08 00:00:00.
Paternal-Sex-Ratio (PSR) is a B chromosome that causes all-male offspring in the parasitoid wasp Nasonia vitripennis. It is only transmitted via sperm of carrier males and destroys the other paternal chromosomes during the first mitotic division of the fertilized egg. Because of haplodiploidy, the effect of PSR is to convert diploid (female) eggs into haploid eggs that develop into PSR-bearing males. The PSR chromosome was previously found to contain several families of repetitive DNA, which appear to be present in local blocks. PSR chromosomes with irradiation-induced deletions have decreased rates of transmission and increased variation in transmission. This study investigates whether these differences in transmission of deletion chromosomes are due to mitotic instability. Two deletion chromosomes (E306 and F316) and the wild-type PSR chromosome were examined. A cytogenetic assay of testes revealed that wild-type PSR males contained the chromosome in 98%-100% of their spermatocytes. Similar counts from carriers of two deletion chromosomes were lower and varied between individuals from 50%-100%. One F316 male did not contain the chromosome in any of its spermatocytes although the chromosome was present in somatic tissues based on hybridization to PSR-specific repetitive DNA. A molecular analysis of males found the wild-type PSR chromosome to be present in all somatic tissues. Tissue specific differences in the presence or PSR were found in several males from the two deletion lines. The results show that deletions can result in mosaicism due to increased mitotic instability of PSR. Such individuals sometimes partially or completely fail to transmit the chromosome. Patterns of mosaicism of 13 chromosomes in other organisms are discussed.
Meiotic drive for the aberrant Chromosome-1 in mice is determined by a linked distorter
4429Agulnik, SIS, I. D.; Orlova, G. V.; Ruvinsky, A. O., Genetika, 28:47-57. 1992-01-07 00:00:00.
AN aberrant chromosome 1 carrying an inverted fragment with two amplified DNA regions was isolated from natural populations of Mus musculus. A meiotic drive favouring the aberrant chromosome was previously demonstrated for heterozygous females. The cause for this was the preferential passage of the chromosome 1 to the oocyte. Genetic analysis made it possible to identify a two-component system conditioning the deviation from equal segregation of the homologues. The system consists of the postulated distorter and a responder. The distorter is located on the chromosome 1 distally to the responder, between the ln and Pep 3 genes, the former acting on the responder when in the trans position. Polymorphism of the distorters was manifested as variation in their effect on the meiotic drive level in the laboratory strain and mice from natural populations.
Genetic scrambling as a defense against meiotic drive
4443Haig, DG, A., Journal of Theoretical Biology, 153:531-558. 1991-01-21 00:00:00.
Genetic recombination has important consequences, including the familiar rules of Mendelian genetics. Here we present a new argument for the evolutionary function of recombination based on the hypothesis that meiotic drive systems continually arise to threaten the fairness of meiosis. These drive systems act at the expense of the fitness of the organism as a whole for the benefit of the genes involved. We show that genes increasing crossing over are favoured, in the process of breaking up drive systems and reducing the fitness loss to organisms.
Divergence of meiotic drive-suppression systems as an explanation for sex-biased hybrid sterility and inviability
4442Frank, SA, Evolution, 45:262-267. 1991-01-20 00:00:00.
Two empirical generalizations about speciation remain unexplained: the tendency of the heterogametic sex to be sterile or inviable in F1 hybrids (Haldane's rule), and the tendency of the X chromosome to harbor the genetic elements that cause this sex bias in hybrid fitness. I suggest that divergence of meiotic drive systems on the sex chromosomes can explain these observations. The theory follows from two simple facts. First, sex chromosomes are particularly susceptible to the forces of meiotic drive. Second, divergence of meiotic drive systems can cause hybrid sterility and inviability. The main objection to the theory is that meiotic drive is apparently rare, whereas the observed pattern of hybrid fitness is widespread. I answer this objection by showing that divergence of meiotic drive systems can explain the two generalizations even if large departures from Mendelian segregation are rarely observed.
Meiotic drive in Lucilia cuprina and chromosomal evolution
4441Foster, GGW, M. J., American Naturalist, 137:403-415. 1991-01-19 00:00:00.
In females heterozygous for pericentric inversions that alter the relative lengths of the long and short arms of a chromosome, crossing-over within the inversion can lead to unequal segregation at anaphase II, favoring the homologue with the more centrally located centromere. It is suggested that this phenomenon may have played a role in the evolution of centromere position in certain species groups.
A comparative approach to the population genetics theory of segregation distortion
4440Feldman, MWO, Sarah P., American Naturalist, 137:443-456. 1991-01-18 00:00:00.
Mathematical models of four well-known naturally occurring systems of segregation distortion are compared. These include the sex-ratio chromosome of Drosophila pseudoobscura, the Segregation Distorter (SD) complex of D. melanogaster, the t locus in Mus musculus, and the sex-ratio system in Aedes aegypti. Dynamics of these models are compared with the classical one-locus multiple-allele viability system. For the SD complex and the sex-ratio model of A. aegypti, the role of recombination is reviewed. Departures from Mendelian segregation cause fascinating irregularities in the relationship between linkage and linkage disequilibrium, as well as in predictions for the evolution of recombination itself.
X-chromosome segregation distortion in Drosophila
4439Curtsinger, JW, American Naturalist, 137:344-348. 1991-01-17 00:00:00.
The sex-ratio trait exhibits both discrete and continuous variation in Drosophila pseudoobscura. The discrete variation is caused by X-chromosome meiotic drive. The evolutionary forces maintaining the meiotic-drive polymorphism include strong viability selection against homozygous females and virility selection in males. The relative importance of the two factors is unresolved. The evidence for a genetic component in the continuous sex-ratio variation comes from artificial-selection experiments, large-scale estimation of segregation ratios corrected for viability effects, and an examination of the rates of spermatid loss. Segregation ratio can be treated as a typical quantitative character subject to major and minor genetic modifiers.
Sex-ratio distortion caused by meiotic drive in mosquitos
4458Wood, RJN, M. E., American Naturalist, 137:379-391. 1991-01-16 00:00:00.
Meiotic-drive genes have been described in two species of mosquito, Aedes aegypti and Culex quinquefasciatus. In both species, a Y (M)-linked gene causes a change in sex ratio in favor of males. More is known about the Distorter gene (D) in A. aegypti, but the gene in C. quinquefasciatus appears to be similar. D is located on the right arm of the sex chromosome, is marked with the intercalary Giemsa C-band when present, and is linked closely to the sex locus or region. D undergoes meiotic drive only when in coupling with M, the male-determining gene, which does not recombine with the centromere. Sensitivity to the MD haplotype is controlled at m, the female-determining gene. Therefore, m is considered to be the responder. The m haplotype is polymorphic for sensitivity to MD (m(r1), m(r2), m(s1)-m(s6)). Sensitivity is influenced, in some strains, by a second sex-linked gene t (tolerance to Distorter). Another sex-linked gene, A, enhances the effect of D. Meiotic drive is associated with breaks on the sex chromosomes. First seen at diplotene, mainly at four discrete positions, 90% of these breaks occur on the X (m) chromosome. They usually appear on a chiasmic arm of the bivalent, with the result that most acentric fragments remain attached to the unbroken homologue by a chiasma. Examination of developing spermatozoa in Distorter males reveals extreme sperm depletion, a high degree of abnormality (e.g., multiple axonemes), and an increased DNA content up to the 4C level. Surprisingly, however, the effective fertility of these males is hardly reduced. Evidently, spermatozoa are produced in nondistorter males in vast excess. The Distorter gene has been found in populations from Africa, America, Australia, and Sri Lanka. Resistance to it is much more widespread. The presence of natural resistance argues against the use of D for population control, but its effect has been shown to be enhanced in the presence of certain translocations and the A gene, causing it to become effective in field cage trials, even in the presence of some resistance. There is also experimental support for using D to bring about changes in populations ("population replacement").
Why is Mendelian segregation so exact
4438Crow, JF, Bioessays, 13:305-312. 1991-01-16 00:00:00.
The precise 1:1 segregation of Mendelian heredity is ordinarily taken for granted, yet there are numerous examples of 'cheating' genes that perpetuate themselves in the population by biasing the Mendelian process in their favor. One example is the Segregation Distortion system of Drosophila melanogaster, in which the distorting gene causes its homologous chromosome to produce a nonfunctional sperm. This system depends on three closely linked components, whose molecular basis is beginning to be understood. The system is characterized by numerous modifiers changing the degree of distortion. Mathematical theory shows that unlinked modifiers that change the degree of distortion in the direction of Mendelism always increase in the population. This provides a mechanism for removing cheaters and preserving the honesty of the Mendelian gene-shuffle.
Male sex-ratio trait in Drosophila pseudoobscura: Frequency of autosomal aneuploid sperm
4437Cobbs, GJ, L.; Gordon, L., Genetics, 127:381-390. 1991-01-15 00:00:00.
Males with the SR X chromosome show the "sex-ratio" (sr) phenotype in which they produce almost entirely daughters. The few sons (about 1%) are invariably sterile X/O males and result entirely from nullo-XY sperm. The "male-sex-ratio" (msr) phenotype is a modified form of sr in which SR/Y males produce a higher frequency of sterile X/O sons. The msr trait is due to the presence of the SR X-chromosome in males which are also homozygous for one or more autosomes from the L116 strain. Here the frequency of nullo-3 and diplo-3 sperm from msr males was measured by crossing to a compound-3 strain and found to be 13.8% and 3.2%, respectively, of the total viable sperm. The sr males produced very low levels of nullo-3 sperm at a frequency not different from control X/Y males and a slightly elevated frequency of diplo-3 sperm over X/Y males. The msr males were found to have only 12% the fecundity of sr males and in matings to cause a high frequency of brown inviable eggs. These results indicate that high rates of autosomal aneuploidy are not restricted to chromosome 3 but also occur for chromosomes 2, 4 and 5. The overall frequency of autosomal aneuploid sperm is estimated to be approximately 50%. Microscopic studies of meiosis in testes from msr males indicates meiotic nondisjunction and meiotic chromosome loss are responsible for the msr phenotype. Last, microscopic studies of sperm cysts from msr males reveal high levels of spermiogenic failure.
The paternal-sex-ratio chromosome of Nasonia
4457Werren, JH, American Naturalist, 137:392-402. 1991-01-15 00:00:00.
Paternal sex ratio (PSR) is a supernumerary chromosome that is transmitted through sperm to fertilized eggs and then gains a transmission advantage by causing supercondensation of the paternal chromosomes (except itself). Because of haplodiploidy, this converts diploid females into haploid (PSR) males. PSR gains a transmission advantage because the unpaired chromosome has a higher frequency of transmission through male (mitotic) gametngenesis than through female (meiotic) gametogenesis. PSR increases in panmictic populations that produce more than 50% fertilized eggs. PSR frequency is typically reduced by population subdivision because of increased local competition among PSR males and reduced availability of females resulting from PSR action. Genetic and molecular studies of PSR have recently begun. PSR is highly heterochromatic and contains large tandem arrays of repetitive DNA unique to it. PSR apparently acts by "imprinting" the set of paternal chromosomes, resulting in their supercondensation during mitosis. Deletion studies are under way to characterize the genetic basis of PSR action and "protection" from its own action.
Meiotic drive in Neurospora and other fungi
Turner, BCP, D. D., American Naturalist, 137:416-429. 1991-01-14 00:00:00.When a gene complex called Spore killer is heterozygous, ascospores representing two of the four products of each meiosis are killed. Only those that receive the killer complex survive. This article reviews what is known of the mode of action of the Neurospora Spore killers, their chromosomal basis, and their occurrance in nature. Similar genes or gene complexes have been found in other fungi. An example from Podospora anserina is analyzed.
Sex ratio polymorphism in Drosophila pseudoobscura
4436Beckenbach, AT, American Naturalist, 137:340-343. 1991-01-14 00:00:00.
I studied "sex-ratio" (SR) genotype frequencies in two populations of Drosophila pseudoobscura from southeastern Arizona: Bear Creek Canyon and Tucson. Wild-inseminated females were collected, their fecundities measured in the laboratory, and their SR genotypes inferred by cytological analysis of their progenies. A statistically significant fecundity deficiency was observed among SR/SR females from Bear Creek Canyon. The SR frequency in the Tucson population increased at a rate consistent with the operation of meiotic drive unopposed by selection.
Meiotic drive of t-haplotypes – chromosome segregation in mice with tertiary trisomy
4435Agulnik, AIA, S. I.; Ruvinsky, A. O., Genetical Research, 57:51-54. 1991-01-13 00:00:00.
The properties of the t haplotypes, specific mutant states of the proximal region of chromosomes 17 in the house mouse, are of continuing interest. One such property is increased transmission of the t haplotype by heterozygous t/+ males to offspring. Using the reciprocal translocation T(16; 17)43H we have constructed males with tertiary trisomy of chromosome 17 (+ T43/ + +/Rb7 +) carrying the Robertsonian translocation Rb(16.17)7Bnr. Only the progeny of these males which had inherited either T43/ + or Rb7 from their male parent were viable. The segregation patterns in the offspring of t-bearing trisomics were analysed on days 16-18 of embryonic development. It was found that, when the t12 haplotype is in the normal acrocentric (males + + T43/ + t12 + /Rb7 + +), its presence in the gamete + t12 + / + + T43 does not produce meiotic drive. However, when t6 is in Rb7, meiotic drive was observed: 80% of offspring carried the t haplotype. It is concluded that the meiotic drive is probably inhibited by the presence of a normal homologue of chromosome 17 in the same sperm. Possible mechanisms for the t haplotype effect are discussed.
Segregation distortion in Drosophila melanogaster: Genetic and molecular analysis
4455Temin, RGG, B.; Powers, P. A.; Lyttle, T. W.; Pimpinelli, S.; Dimitri, P.; Wu, C. I.; Hiraizumi, Y., American Naturalist, 137:287-331. 1991-01-13 00:00:00.
The Segregation Distorter (SD) complex in the centromeric region of chromosome 2 in Drosophila melanogaster is responsible for a naturally occurring and strong system of male meiotic drive. Earlier recombinational dissection and deletional analysis showed that the SD complex resolves into three major loci: the euchromatic Sd, or Segregation distorter gene at the base of the left arm of the chromosome (2L), and two heterochromatic genes: E(SD), the Enhancer of SD, and Rsp, the Responder, in the center of the left arm and the right arm (2R), respectively. Rsp exists in the major allelic forms, Rsp(s), for sensitive, and Rsp(i), for insensitive. Males that are heterozygous for an SD chromosome (SdE(SD)Rsp(i)) and a sensitive SD+ homologue (Sd+ E(SD)+ Rsp(s)) transmit predominantly or even exclusively the SD-bearing chromosome to the progeny. The distortion of the segregation ratio is traceable to failure in chromatin condensation and maturation of those spermatids that receive the Rsp(s) homologue during meiosis. Characterization of the properties of null alleles of Sd, E(SD), and Rsp that were generated by delection determined the precise cytological locations of the components and established the functional relationship of each to its wild-type counterpart, suggesting a model whereby a deleterious action of Sd, along with E(SD), on the Rsp(s) target sets in motion the events culminating in sperm dysfunction. Further genetic analysis of E(SD), a gene required for full expression of drive, showed that E(SD) in two doses can cause significant distortion even in the absence of Sd. This distortion is suppressible by a suppressor of SD action. Thus, E(SD) is more than a simple modifier of Sd; rather, it is an effector locus that, like Sd, can act at the Rsp(s) target. Cloning and molecular analysis of the Sd locus reveal that the alteration uniquely associated with Sd is a 5-kb tandem duplication within the polytene band 37D5, which is where Sd is known to map. The Sd-associated duplication appears to be part of a large gene about 100 kb in size. A 4.2-kb SD-specific transcript has been identified, and analyses of the cDNAs indicate a complex transcription pattern. Since Responder plays such a key role in segregation distortion, recent progress in analyzing this locus has been exciting. Studies of Rsp at the genetic, cytogenetic, and molecular levels have been mutually reinforcing and consistent in demonstrating that Rsp is an extended locus that is (1) subdivisible and (2) associated with a 120-bp repeated sequence of DNA that is rich in adenine-thymine pairs and whose copy number is correlated with the degree of sensitivity. In an exceptional situation, there are certain Sd Rsp(i)/Sd+ Rsp(s) males carrying particular modifiers in which the Rsp(i) chromosome can be transmitted at frequencies of less than 0.50 relative to the Rsp(s) chromosome, suggesting that the genetics of segregation ratios may involve even further complexities, which need to be unraveled.
Expression of meiotic drive elements Spore Killer-2 and Spore Killer-3 in asci of Neurospora tetrasperma
4454Raju, NBP, D. D., Genetics, 129:25-37. 1991-01-12 00:00:00.
It was shown previously that when a chromosomal Spore killer factor is heterozygous in Neurospora species with eight-spored asci, the four sensitive ascospores in each ascus die and the four survivors are all killers. Sk-2K and Sk-3K are nonrecombining haplotypes that segregate with the centromere of linkage group III. No killing occurs when either one of these killers is homozygous, but each is sensitive to killing by the other in crosses of Sk-2K x Sk-3K. In the present study, Sk-2K and Sk-3K were transferred by recurrent backcrosses from the eight-spored species Neurospora crassa into Neurospora tetrasperma, a pseudohomothallic species which normally makes asci with four large spores, each heterokaryotic for mating type and for any other centromere-linked genes that are heterozygous in the cross. The action of Sk-2K and Sk-3K in N. tetrasperma is that predicted from their behavior in eight-spored species. A sensitive nucleus is protected from killing if it is enclosed in the same ascospore with a killer nucleus. Crosses of Sk-2K x Sk-2S, Sk-3K x Sk-3S, and Sk-2K X Sk-3K all produce four-spored asci that are wild type in appearance, with the ascospores heterokaryotic and viable. The Eight-spore gene E, which shows variable penetrance, was used to obtain N. tetrasperma asci in which two to eight spores are small and homokaryotic. When killer and sensitive alleles are segregating in the presence of E, only those ascospores that contain a killer allele survive. Half of the small ascospores are killed. In crosses of Sk-2K x Sk-3K (with E heterozygous), effectively all small ascospores are killed. The ability of N. tetrasperma to carry killer elements in cryptic condition suggests a possible role for Spore killers in the origin of pseudohomothallism, with adoption of the four-spored mode restoring ascospore viability of crosses in which killing would otherwise occur.
Meiotic drive of t haplotypes: chromosome segregation in mice with tertiary trisomy
4434Agulnik, AIA, Sergei I.; Ruvinsky, Anatoly O., Genetics Research, 57:51. 1991-01-12 00:00:00.
The properties of the / haplotypes, specific mutant states of the proximal region of chromosomes17 in the house mouse, are of continuing interest. One such property is increased transmission ofthe / haplotype by heterozygous // + males to offspring. Using the reciprocal translocationT(16; 17)43H we have constructed males with tertiary trisomy of chromosome 17( + T43/+ +/Rb7 + ) carrying the Robertsonian translocation Rb(16.17)7Bnr. Only the progeny ofthese males which had inherited either T43/ + or Rb7 from their male parent were viable. Thesegregation patterns in the offspring of /-bearing trisomics were analysed on days 16-18 ofembryonic development. It was found that, when the tn haplotype is in the normal acrocentric(c?c?+ + T43/ + //2+/Rb7 + +), its presence in the gamete +/" + /+ + T43 does not producemeiotic drive. However, when t6 is in Rb7, meiotic drive was observed: 80 % of offspring carriedthe / haplotype. It is concluded that the meiotic drive is probably inhibited by the presence of anormal homologue of chromosome 17 in the same sperm. Possible mechanisms for the t haplotypeeffect are discussed
On the components of Segregation Distortion in Drosophila melanogaster 5: Molecular analysis of the SD locus
4453Powers, PAG, B., Genetics, 129:133-144. 1991-01-11 00:00:00.
Segregation Distorter (SD) is a naturally occurring meiotic drive system comprising at least three distinct loci: Sd, Rsp and E(SD). Heterozygous SD/SD+ males transmit the SD chromosome in vast excess over the normal homolog. The distorted transmission involves the induced dysfunction of the spermatids that receive the SD+ chromosome. In the 220-kb region of DNA that contains the Sd gene, we identified a 5-kb tandem duplication that is uniquely associated with all SD chromosomes, absent in SD+ chromosomes, and detectably altered in Sd revertants. On northern blots, genomic probes from the tandem duplication detect an SD-specific 4-kb transcript in addition to several smaller transcripts present in both SD and SD+. Seven classes of cDNAs derived from these transcripts have been isolated. All of these cDNAs share extensive sequence identity at their 3' ends but differ at their 5' ends. Sequence analysis indicates that these cDNAs potentially encode four distinct, but related, polypeptides. Introduction of the tandem duplication into SD+ flies by germline transformation did not confer the dominant gain-of-function Sd phenotype. This result, taken together with our analysis of the Sd cDNAs, suggests that the duplication is part of a much larger gene that encodes several different polypeptides.
X-Y pairing, meiotic drive and ribosomal DNA in Drosophila melanogaster males
4452McKee, BD, American Naturalist, 137:332-339. 1991-01-10 00:00:00.
One of the genotypic features responsible for sex-chromosome meiotic drive and sterility in Drosophila melanogaster males has now been defined clearly. Separation of a significant fraction of X euchromatin from the X pairing site causes either meiotic drive or sterility, depending on whether the separation occurs alone or in combination with rearrangements involving the Y chromosome. The relationship between X-chromosome integrity and the late-spermatid developmental breakdowns responsible for meiotic drive and sterility is still not understood. X-Y pairing is important for some aspect of spermatogenesis in addition to its role in X-Y disjunction. Transcriptional inactivation and meiotic timing are two possibilities that are worth exploring, and there are likely to be others. With molecular probes for genes active in spermatogenesis becoming available, ideas such as the pairing dependence of transcriptional inactivation should become amenable to direct tests. It is hoped that an increased use of molecular methods will shed new light on this fascinating genetic problem.
Segregation distorters
4451Lyttle, TW, Annual Review of Genetics, 25:511-557. 1991-01-09 00:00:00.
Segregation distorters are genetic elements that exhibit the phenomenon of meiotic drive; that is, the mechanics of the meiotic divisions cause one member of a pair of heterozygous alleles or heteromorphic chromosomes to be transmitted to progeny in excess of the expected Mendelian proportion of 50% ( 1 34 , 1 36). In this review, we refer to these as genic or chromosomal drive, respectively. Genic meiotic drive is initially limited in its impact to the population dynamics of the drive locus itself and those loci fortuitiously in close linkage. Alleles at these latter loci may enjoy indirect drive through genetic hitchhiking, leading eventually to the establishment of drive haplotypes (64). The haplotype may be extended by incorporating chromosome rearrangements that reduce recombination and promote further linkage disequilibrium between the drive locus and more distant modifier loci ( 1 04 , 1 28, 1 64). In the extreme , the haplotype becomes coextensive with the chromosome, leading to a form of chromosomal meiotic drive. For a parent heterozygous for either type of drive system, the statistic k is used to denote the proportion of progeny (and by inference, successful gametes) that carry the allele or chromosome exhibiting segregation distortion. Thus , k can vary from 0 . 5 (Mendelian segregation segregation) to 1 .0 (complete segregation distortion with only one gamete class recovered in the progeny) .
The genetics and evolutionary biology of meiotic drive: Preface
Lyttle, TW, American Naturalist, 137:281-282. 1991-01-08 00:00:00.More than 30 years have passed since the concept and the term meiotic drive were introduced by Sandler and Novitski. Many years have also passed since the preceding conference, which embraced both segregation distortion in Drosophial and transmission-distortion in the mouse, and since meiotic drive in these and other organisms were reviewed comprehensively. During this perio, notable advances have been made, new exampes of meiotic drive have been reported in many organisms, including fungi and plants, and the powerful tools of molecular genetics have been applied to understanding its chromosomal basis.
The Genetic Basis of Transmission-Ratio Distortion and Male Sterility Due to the t Complex
4449Lyon, MF, American Naturalist, 137:349-358. 1991-01-07 00:00:00.
The abnormal transmission ratios observed in male mice heterozygous for a complete t haplotype have been shown by breeding studies to be due to three or more distorter genes acting on a responder gene. The action of the t form of the responder is relatively resistant to this harmful action. When the distorters are homozygous, their harmful action is more severe. The t form of the responder is then affected, and the males are sterile. The distorter and responder genes are distributed over a region occupying the proximal third of mouse chromosome 17. Crossover suppression between t and wild-type bapiotypes in this region is due to the presence of inversions and is thought to be selectively advantageous in locking the genetic factors together. The recessive lethals carried by many t haplotypes are also thought to be advantageous in removing the sterile males from the population. Transmission ratio is also affected by genetic background, and there is evidence of differences among t haplotypes either in the responder or in cis-acting effects of distorters.
Meiotic drive against an autosomal supernumerary segment promoted by the presence of a B-chromosome in females of the grasshopper Eyprepocnemis plorans
4448Lopezleon, MDC, J.; Camacho, J. P. M., Chromosoma, 100:282-287. 1991-01-06 00:00:00.
Twenty-seven out of 50 progeny analyses performed with specimens of the grasshopper Eyprepocnemis plorans were informative about the transmission of a supernumerary heterochromatic chromosome segment. The simultaneous presence of a B chromosome in some of the parents involved in the crosses permitted us to test the relationship between both types of supernumerary heterochromatin with respect to their transmission. The results demonstrated that the supernumerary segment is partly eliminated through females possessing B chromosomes. The implications of this in relation to the occurrence of the extra segment in natural populations are discussed.
Sander,Larry – The father of meiotic drive
4447Lindsley, DL, American Naturalist, 137:283-286. 1991-01-05 00:00:00.
The symposium at which the following papers were presented was deprived of what surely would have been a major intellectual contribution by the sudden death of its co-organizer, Larry Sandler, in February 1987. Larry was a leading contributor to the study of segregation distortion and meiotic drive, beginning with his seminal research as a graduate student with Ed Novitski at the University of Missouri and continuing, in collaboration with Yuichiro Hiraizumi, as a post- doctoral fellow with Jim Crow and as a fledgling faculty member at the University of Wisconsin. Many of us at the conference worked with him personally and benefited from his insights and his enthusiasm for genetic analysis of meiotic problems. We all felt a great sense of loss and missed his lively contributions at the symposium.
Behavioral reduction in the transmission of deleterious t-haplotypes by wild house mice
4446Lenington, SH, I. L., The American Naturalist, 137:366-378. 1991-01-04 00:00:00.
About 25% of wild house mice are heterozygous (+/t) for a variable recessive haplotype of the T locus. Although t haplotypes are highly deleterious when homozygous, they are maintained in wild mouse populations because they are associated with transmission-ratio distortion in heterozygous males, which may transmit their t haplotype to 90%-100% of their progeny. In a study of factors affecting variation in male transmission ratio in matings between wild-caught +/t males and +/+ females, we found (1) that male transmission ratio is considerably lower in litters produced as a result of postpartum-estrus matings than in litters produced as a result of cycling-estrus matings, (2) that the frequency of postpartum-estrus litters is much higher when +/t males mate with females caught from the same location as themselves than when they mate with females caught elsewhere, and (3) that, as a result of findings I and 2, the male transmission ratio is considerably lower in within-population matings than in betweenpopulation matings. These data suggest that the frequency of t haplotypes within populations may be correlated with the migration rate and that t haplotypes may be found in high frequencies only in populations for which the migration rate is high.
B-chromosome drive
4445Jones, RN, American Naturalist, 137:430-442. 1991-01-03 00:00:00.
The view of B-chromosome polymorphisms that is coming into favor resembles the so-called "parasitic" model, which was first advanced 45 yr ago. Since that time, repeated and ongoing efforts have been made to ascribe an adaptive role to B's (e.g., in terms of phenotypic advantage, effects of variability, etc.), but success in this direction has been singularly lacking. Consistently and repeatedly, the data indicate that harmful effects, or at best neutral or undetectable effects, are associated with B's and provide evidence of the potency of accumulation mechanisms based on drive. Modeling exercises have proved useful in examining these polymorphisms, and of the ones that have been published to date, all have favored drive as the main force generating B-chromosome polymorphisms.
Molecular and chromosomal studies on the origin of t-haplotypes in mice
4444Hammer, MF, American Naturalist, 137:359-365. 1991-01-02 00:00:00.
Mouse t haplotypes are variant forms of the proximal third of chromosome 17 that enhance their representation in the gene pool by means of a male-specific transmission-ratio distortion. As with other systems of meiotic drive, they are maintained as independent genetic entities by inversions that suppress recombination with their wild-type homologues. This article reviews some of the evidence for the origin of this complex system based on DNA and chromosomal comparisons. Such comparisons suggest a stepwise evolution of t haplotypes, whereby the proximal and distal inversion occurred on separate chromosomal lineages and at different times. The initial event leading to the spread of t haplotypes may have been an inversion occurring on the wild-type chromosome (nondriving) 2-4 million yr ago. An additional implication of the data is that meiotic drive gives t haplotypes the ability to traverse species boundaries and spread rapidly around the world.
Tsetse fly eradication in Burkina Faso and evaluation of traps and targets
26174M. Clair, D. Cuisance, H. Politzar, P. Merot and B. Bauer, STERILE INSECT TECHNIQUE FOR TSETSE CONTROL AND ERADICATION, 1990-05-01 14:50:02.
Control operations against tsetse flies with the sterile insect technique (SIT) were conducted by the Centre de recherches sur les trypanosomoses animales (CRTA) (Institut d’élevage et de médecine vétérinaire des pays tropicaux/Gesellschaft fur Technische Zusammenarbeit (IEMVT/GTZ) Project), Bobo-Dioulasso (Burkina Faso). The project ended in 1984 with the eradication in the Sideradougou pastoral zone ofthe three tsetse species present there (Glossina palpalis gambiensis, G. tachinoides and G. morsitans submorsitans). Since 1985, besides monitoring of this area, the CRTA oriented its activities towards improving trapping by carrying out research on the form and colour of targets as well as the use of olfactory attractants.
Sex-ratio meiotic drive in Drosophila testacea
4462James, ACJ, J., Genetics, 126:651-656. 1990-01-20 00:00:00.
We document the occurrence of "sex ratio" meiotic drive in natural populations of Drosophila testacea. "Sex ratio" males sire greater than 95% female offspring. Genetic analysis reveals that this effect is due to a meiotically driven X chromosome, as in other species of Drosophila in which "sex ratio" has been found. In contrast to other drosophilids, the "sex ratio" and standard chromosomes of D. testacea do not differ in gene arrangement, implying that the effect may be due to a single genetic factor in this species. In all likelihood, the "sex ratio" condition has evolved independently in D. testacea and in the Drosophila obscura species group, as the loci responsible for the effect occur on different chromosomal elements. An important ecological consequence of "sex ratio" is that natural populations of D. testacea exhibit a strong female bias. Because D. testacea mates, oviposits, and feeds as adults and larvae on mushrooms, this species provides an excellent opportunity to study the selective factors in nature that prevent "sex ratio" chromosomes from increasing to fixation and causing the extinction of the species.
Evolution of the segregation ratio – Modification of gene conversion and meiotic drive
4461Bengtsson, BOU, M. K., Theoretical Population Biology, 38:192-218. 1990-01-19 00:00:00.
We compare the evolutionary pressures that direct the modification of gene conversion and meiotic drive at loci subject to purifying and overdominant viability selection. Gene conversion differs from meiotic drive in that modifers do not affect their own segregation ratios, even when linked to the viability locus. Segregation distortion generates gametic level disequilibria between alleles at the viability locus and modifiers of gene conversion and meiotic drive: enhancers of segregation distortion become positively associated with driven alleles. Suppression of gene conversion evolves if the driven allele is marginally disadvantageous (overdominant viability selection), and higher rates evolve if the driven alleles are relatively advantageous (purifying viability selection). Gametic disequilibria permit enhancers of meiotic drive that are linked to the driven locus to promote their own segregation. We attribute the failure of genetic modifiers of gene conversion and meiotic drive to maximinize mean fitness to the generation of such associations.
Meiotic drive in female mice heterozygous for the HSR inserts on Chromosome-1
4460Agulnik, SIA, A. I.; Ruvinsky, A. O., Genetical Research, 55:97-100. 1990-01-18 00:00:00.
Chromosome 1 with one or two long insertions has been previously found in natural mouse populations. The inheritance of chromosome 1 with two insertions from the Yakutsk population is analysed in this paper. It was demonstrated that heterozygous females transmit this chromosome to 80–85% of offspring. The observations made at M II, in conjunction with the recombination data, allowed us to conclude that preferential passage of the chromosome 1 with insertions to the oocyte and egg, rather than to the first and second polar bodies at meiosis, is the causative factor of the distorted segregation. A meiotic drive of such potency has not been previously reported for female mammals. The possible mechanism of the drive is discussed.
Meiotic drive of the aberrant Chromosome-1 in the house mouse
4459Agulnik, SIA, A. I.; Ruvinsky, A. O., Genetika, 26:664-669. 1990-01-17 00:00:00.
Animals with aberrant chromosome 1 carrying one or two large insertions were earlier described in natural populations of Mus musculus. In the present work, inheritance of the aberrant chromosome 1 from the Yakutsk population was investigated. It was shown that 80-85% of the progeny from heterozygous females received chromosome 1 with insertions. From chromosomal analysis of blastocytes and oocytes at the MII stage, it was concluded that the preferential distribution of the aberrant chromosome into oocytes during the first and especially, the second meiotic divisions is relevant to the segregation distortion observed. The mechanism of this powerful meiotic drive is discussed.
Rapid spread of transposable P elements in experimental populations of Drosophila melanogaster.
6265A. G. Good, G. A. Meister, H. W. Brock, T. A. Grigliatti and D. A. Hickey, Genetics, 1223:387-396. 1989-05-08 16:20:58.
The invasion of P elements in natural populations of Drosophila melanogaster was modeled by establishing laboratory populations with 1 %, 5% and 10% P genomes and monitoring the populations for 20 generations. In one experiment, the ability of flies to either induce or suppress gonadal sterility in different generations was correlated with the amount of P element DNA. In a second experiment, the percentage of genomes that contained P elements, and the distribution of P elements among individual flies was monitored. The ability to induce gonadal dysgenesis increased rapidly each generation. However, the increase in P cytotype lagged behind by five to ten generations. The total amount of P element DNA and the frequency of flies containing P elements increased each generation. The number of P elements within individual genomes decreased initially, but then increased. Finally, the distribution of P elements within the genomes of individuals from later generations varied considerably, and this pattern differed from the parental P strain. These results suggest that the interaction between the assortment and recombination of chromosomal segments, and multiplicative transposition could result in the rapid spread of P elements in natural populations
Genetics-driving genes and chromosomes
4463Charlesworth, B, Nature, 332:394-395. 1988-01-21 00:00:00.
Thereare several genetic and chromosomal systems in which Mendel's first law - the equal probability of transmission of maternal and paternal alternative alleles or homologues - is violated. This phenomenon was named 'meiotic drive' in 1957 by Sandler and Novitski, who drew attention to the fact that it operates as an evolutionary force which can cause an increase in the population frequency of the allele or chromosome which is favoured in transmission, even if it confers a disadvantage on its carriers in terms of fitness at the level of the individual
