Scholarly Literature

This is a database of scholarly literature that concentrates currently on natural and engineered selfish genetic elements (gene drives).  The latest are shown here.
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Heritability of the maternal meiotic drive system linked to Om and high-resolution mapping of the Responder locus in mouse

4339
de 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

4338
Cazemajor, 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

4348
van 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?

4347
Tomkiel, 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

4346
Schimenti, 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

4345
Planchart, 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

4344
LeMaire-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)

4363
Underwood, 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

4362
Schmidt, 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

4361
Reinhold, 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

4360
Paterson, 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

4359
Merrill, 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

4358
Lande, 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?

4357
Jiggins, 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

4356
Jaenike, 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

4355
Hurst, 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

4354
Hatcher, 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

4353
Goddard, 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

4352
Eaves, 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?

4351
Carvalho, 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.

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