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.
Male sterility and meiotic drive associated with sex chromosome rearrangements in Drosophila: Role of X-Y pairing
4375McKee, BDW, K.; Merrill, C.; Ren, X. J., Genetics, 149:143-155. 1998-01-13 00:00:00.
In Drosophila melanogaster, deletions of the pericentromeric X heterochromatin cause X-Y nondisjunction, reduced male fertility and distorted sperm recovery ratios (meiotic drive) in combination with a normal Y chromosome and interact with Y-autosome translocations (T(Y;A)) to cause complete male sterility. The pericentromeric heterochromatin has been shown to contain the male-specific X-Y meiotic pairing sites, which consist mostly of a 240-bp repeated sequence in the intergenic spacers (IGS) of the rDNA repeats. The experiments in this paper address the relationship between X-Y pairing failure and the meiotic drive and sterility effects of Xh deletions. X-linked insertions either of complete rDNA repeats or of rDNA fragments that contain the IGS were found to suppress X-Y nondisjunction and meiotic drive in Xh(-)/Y males, and to restore fertility to Xh(-)/T(Y;A) males for eight of nine tested Y-autosome translocations. rDNA fragments devoid of IGS repeats proved incapable of suppressing either meiotic drive or chromosomal sterility. These results indicate that the various spermatogenic disruptions associated with X heterochromatic deletions are all consequences of X-Y pairing failure. We interpret these findings in terms of a novel model in which misalignment of chromosomes triggers a checkpoint that acts by disabling the spermatids that derive from affected spermatocytes.
Segregation distortion in myotonic dystrophy
4374Magee, ACH, A. E., Journal of Medical Genetics, 35:1045-1046. 1998-01-12 00:00:00.
Myotonic dystrophy (DM) is an autosomal dominant disease which, in the typical pedigree, shows a three generation anticipation cascade. This results in infertility and congenital myotonic dystrophy (CDM) with the disappearance of DM in that pedigree. The concept of segregation distortion, where there is preferential transmission of the larger allele at the DM locus, has been put forward to explain partially the maintenance of DIM in the population. In a survey of DM in Northern Ireland, 59 pedigrees were ascertained. Sibships where the status of all the members had been identified were examined to determine the transmission of the DM expansion from affected parents to their offspring. Where the transmitting parent was male, 58.3% of the offspring were affected, and in the case of a female transmitting parent, 68.7% were affected. Studies on meiotic drive in DIM have shown increased transmission of the larger allele at the DM locus in non-DIM heterozygotes for CTGn. This study provides further evidence that the DM expansion tends to be transmitted preferentially.
Sex ratio distortion in Acraea encedon (Lepidoptera : Nymphalidae) is caused by a male-killing bacterium
4373Jiggins, FMH, G. D. D.; Majerus, M. E. N., Heredity, 81:87-91. 1998-01-11 00:00:00.
Females of the butterfly Acraea encedon produce either entirely female offspring or males and females in an almost 1:1 sex ratio. The sex ratio produced is maternally inherited and was previously attributed to sex chromosome meiotic drive. We report that all-female lineages are associated with low egg-hatching rates and that the trait is cured by antibiotic treatment. We thus reject the hypothesis that this sex ratio bias is caused by a meiotically driven sex chromosome and, instead, propose that it is associated with a maternally inherited bacterium that kills males.
Selfish genes and meiotic drive
4372Hurst, LD, Nature, 391:223-223. 1998-01-10 00:00:00.
Work by Gerald Wilkinson and colleagues3 on stalk-eyed flies (Diopsidae), described on page 276, provides the strongest evidence to date about the nature of some of the genes females prefer. As their name suggests, stalk-eyed flies have their eyes perched on the end of side-projecting stalks (see the cover of this issue). These can reach ridiculous proportions. In two of the species studied, males have considerably greater eye span than females, and male eye span even exceeds body length. In both of these species females show a strong preference for males with a large eye span. In a third species, male eye span was much shorter (indeed no different to female eye span) and there was no female choice.
Selfish genetic elements and speciation
4371Hurst, GDDS, M., Heredity, 80:2-8. 1998-01-09 00:00:00.
This review concerns the importance of selfish genetic elements (SGEs) in speciation. We assess the importance of medea genes, meiotic drive elements, transposable elements and the bacterium Wolbachia in the creation of postzygotic isolation. Although all of these elements can contribute to postzygotic isolation, their contribution will often disappear if there is gene flow between the populations. Further, there is the possibility that incompatibilities produced by SGEs may lessen over time. We conclude that although some of the case studies are tantalizing, particularly those associated with Wolbachia, the role of selfish genetic elements in speciation remains unproven.
Identification of the t complex-encoded cytoplasmic dynein light chain Tctex1 in inner arm I1 supports the involvement of flagellar dyneins in meiotic drive
4370Harrison, AO-C, P.; King, S. M., Journal of Cell Biology, 140:1137-1147. 1998-01-08 00:00:00.
The cytoplasmic dynein light chain Tctex1 is a candidate for one of the distorter products involved in the non-Mendelian transmission of mouse t haplotypes. It has been unclear, however, how the t-specific mutations in this protein, which is found associated with cytoplasmic dynein in many tissues, could result in a male germ cell-specific phenotype. Here, we demonstrate that Tctex1 is not only a cytoplasmic dynein component, but is also present both in mouse sperm and Chlamydomonas flagella. Genetic and biochemical dissection of the Chlamydomonas flagellum reveal that Tctex1 is a previously undescribed component of inner dynein arm Il. Combined with the recent identification of another putative t complex distorter, Tctex2, within the outer dynein arm, these results support the hypothesis that transmission ratio distortion (meiotic drive) of mouse t haplotypes involves dysfunction of both flagellar inner and outer dynein arms but does not require the cytoplasmic isozyme.
Malaria: existing methods of vector control and molecular entomology
4369Curtis, CFT, H., British Medical Bulletin, 54:311-325. 1998-01-07 00:00:00.
In general, the most effective means of malaria vector control is the killing of adult mosquitoes with a residual insecticide applied to bednets or sprayed on house walls and ceilings. Major reductions in all-cause child mortality have been achieved in Africa by these means. In some circumstances, personal protection and larval control may also make a contribution. We discuss the prospects of genetic control by release of sterile male mosquitoes or driving genes for refractoriness to malaria into wild populations. Many major malaria vectors belong to complexes of sibling species which differ in vectorial and biological characteristics. Distinguishing the species by cytogenetic or molecular methods is important for epidemiological studies and could improve the targeting of control.
Wolbachia as a possible means of driving genes into populations
4368Curtis, CFS, S. P., Parasitology, 116:S111-S115. 1998-01-06 00:00:00.
Cytoplasmic incompatibility consists of sterility in cross matings, the crossing type being maternally inherited. It can be explained by the action of Wolbachia symbionts which are transmitted through the egg cytoplasm and leave an imprint on the sperm which prevents it fertilizing unless it is 'rescued' by the action of the same type of Wolbachia in the egg. Thus matings between infected males and uninfected females are sterile, but the reciprocal matings are fertile. Hence uninfected females are at risk of failing to transmit their uninfected cytoplasm if they cross mate, but infected females are at no such risk. Therefore natural selection favours the infected state and in two wild insect populations the infection has been observed spreading. If a gene for inability to transmit malaria could be introduced into Wolbachia and if this could be introduced into Anopheles (where these symbionts appear not to occur naturally), release of a limited number of such insects should trigger a process of displacement of malaria vectors, by the non-vector type. A simple model is used to demonstrate the limitations to this process which would be introduced by immigration.
Localization of the genes controlling B chromosome transmission rate in maize (Zea mays ssp. mays, Poaceae)
4367Chiavarino, AMR, M.; Rosi, P.; Poggio, L.; Naranjo, C. A., American Journal of Botany, 85:1581-1585. 1998-01-05 00:00:00.
In previous papers we found that the frequency of B chromosomes in native races of maize varies considerably in different populations. Moreover, we found genotypes that control high and low transmission rates (TR) of B chromosomes in the Pisingallo race. In the present work crosses were made to determine whether the genes controlling B-TR are located on the normal chromosome set (As) or on the B chromosomes (Bs). We made female f.0B X male m.2B crosses between and within high (H) and low (L) B-TR groups. The Bs were transmitted on the male side in all cases. The mean B-TR from the progeny of f.0B (H) X m.2B (H) and f.0B (H) X m.2B (L) crosses was significantly higher than that from f.0B (L) X m.2B (L) and f.0B (L) X m.2B (H) crosses. The results show that the B-TR of the crosses corresponds to the H or L B-TR of the 0B female parents irrespective of the Bs of the male parent. This indicates that B-TR is genetically controlled by the 0B female parent and that these genes are located on the A chromosomes.
Selfish DNA and breeding system in flowering plants
4366Burt, AT, R., Proceedings of the Royal Society B-Biological Sciences, 265:141-146. 1998-01-04 00:00:00.
In many species, some individuals carry one or more B chromosomes: extra, or supernumerary chromosomes not part of the normal complement. In most well-studied cases, B's lower the fitness of their carrier and persist in populations only because of accumulation mechanisms analogous to meiotic drive. It has been suggested that such genomic parasites are expected to persist only in outcrossed sexual species, in which uninfected lines of descent can be continuously reinfected; in inbred or asexual species, all selection is between lines of descent, and the genomic parasites are either lost or must evolve into commensals or mutualists. Here we present a simple population genetic model of the effect of outcrossing rate on the frequency of B chromosomes, and find that outcrossing facilitates the spread of parasitic B's, but inhibits the spread of mutualists. Data compiled from the literature on breeding system and B chromosomes of British plants indicate that B's are much more likely to be reported from obligately outcrossed species than inbred species. These results support the ideas that most B chromosomes are parasitic, and that breeding systems play a central role in the biology of selfish genes.
Putting the brake on drive: meiotic drive of t haplotypes in natural populations of mice
4365Ardlie, KG, Trends in Genetics, 14:189-193. 1998-01-03 00:00:00.
Mouse t haplotypes are a 'selfish' form of chromosome 17 that show non-mendelian transmission from heterozygous +/t males. The considerable transmission bias in favour of t haplotypes should result in very high frequencies of these chromosomes in natural populations, but they seldom occur at the high frequencies expected. Recent research on this and other meiotic drive systems has shown bow a variety of mechanisms have evolved to suppress drive, and to re-establish mendelian segregation.
Polymorphism for Y-linked suppressors of sex-ratio in two natural populations of Drosophila mediopunctata
4383Carvalho, ABV, S. C.; Klaczko, L. B., Genetics, 146:891-902. 1997-01-21 00:00:00.
In several Drosophila species there is a trait known as ''sex-ratio'': males carrying certain X chromosomes (called ''SR'') produce female biased progenies due to X-Y meiotic drive. In Drosophila mediopunctata this trait has a variable expression due to Y-linked suppressors of sex-ratio expression, among other factors. There are two types of Y chromosomes (suppressor and nonsuppressor) and two types of SR chromosomes (suppressible and unsuppressible). Sex-ratio expression is suppressed in males with the SRsuppressible/Y-suppressor genotype, whereas the remaining three genotypes produce female biased progenies. Now we have found that similar to 10-20% of the Y chromosomes from two natural populations 1500 km apart are suppressors of sex-ratio expression. Preliminary estimates indicate that Y-suppressor has a meiotic drive advantage of 6% over Y-nonsuppressor. This Y polymorphism for a nonneutral trait is unexpected under current population genetics theory. We propose that this polymorphism is stabilized by an equilibrium between meiotic drive and natural selection, resulting from interactions in the population dynamics of X and Y alleles. Numerical simulations showed that this mechanism may stabilize nonneutral Y polymorphisms such as we have found in D. mediopunctata.
Identification of a male meiosis-specific gene, Tcte2, which is differentially spliced in species that form sterile hybrids with laboratory mice and deleted in t chromosomes showing meiotic drive
4382Braidotti, GB, D. P., Developmental Biology, 186:85-99. 1997-01-20 00:00:00.
Tcte2 (t complex testes expressed 2) is a male meiosis-specific gene that maps to band 3.3 of mouse chromosome 17. Two distinct male fertility defects, hybrid sterility and transmission ratio distortion, have previously been mapped to this region. Hybrid sterility arises in crosses between different mouse species and the F1 generation males have defects in the first meiotic division and are sterile. Transmission ratio distortion is shown by males heterozygous for the t haplotype form of chromosome 17 and is a type of meiotic drive in which male gametes function unequally at fertilization. The Tcte2 gene expresses a coding mRNA and a number of putative non-ORF transcripts in meiosis I. A deletion of the 5' part of the locus abolishes Tcte2 expression on the t haplotype form of chromosome 17. Additionally, the series of putative non-ORF RNAs at the Tcte2 locus are differentially spliced in species that show hybrid sterility when crossed to laboratory mice. The identification of polymorphisms in t haplotypes and in different mouse species allows alleles of Tcte2 to be proposed as candidates for loci which contribute to both meiotic drive and hybrid sterility phenotypes. While theoretical considerations have previously been used to propose that speciation and meiotic drive involve alleles of the same genes, Tcte2 is the first cloned candidate gene to support this link at a molecular level. (C) 1997 Academic Press.
The sex-ratio trait in Drosophila simulans: Geographical distribution of distortion and resistance
4381Atlan, AM, H.; Landre, C.; Montchamp-Moreau, C., Evolution, 51:1886-1895. 1997-01-19 00:00:00.
The sex-ratio trait we describe here in Drosophila simulans results from X-linked meiotic drive. Males bearing a driving X chromosome can produce a large excess of females (about 90%) in their progeny. This is, however, rarely the case in the wild, where resistance factors, including autosomal suppressors and insensitive Y chromosomes, prevent the expression of the driver. In this study, we searched for drive and resistance factors in strains of Drosophila simulans collected all over the world. Driving X chromosomes were found in all populations whenever a good sample size was available. Their frequency may reach up to 60%. However, the presence of driving X chromosomes never results in an excess of females, due to the systematic co-occurrence of resistance factors. The highest frequencies of driving X chromosomes were observed in islands, while populations from East and Central Africa (the supposed center of origin of the species) showed the highest level of resistance. The geographical pattern of drive and resistance factors, as well as the results of crosses between strains from different geographical areas, suggest that the sex-ratio system described here has a unique and ancient origin in the species.
Non-Mendelian transmission at the Machado-Joseph disease locus in normal females: Preferential transmission of alleles with smaller CAG repeats
4389Rubinsztein, DCL, J., Journal of Medical Genetics, 34:234-236. 1997-01-07 00:00:00.
Machado-Joseph disease (MJD), also known as spinocerebellar ataxia type 3, is a neurodegenerative disorder which is associated with a CAG repeat expansion in the MJD1 gene on chromosome 14q32.1. A recent study reported an excess of transmission of disease chromosomes relative to normal chromosomes from affected fathers, while this phenomenon was not observed in female meioses. These data were compatible with meiotic drive. We investigated the transmission of alleles with larger versus smaller CAG repeat numbers in the MJD1 gene in normal heterozygotes from the 40 CEPH families. Our data suggest that there was no segregation distortion in male meioses, while the smaller CAG allele was inherited in 57% of female meioses (p<0.016). The pattern of inheritance of smaller versus larger CAG alleles at this significantly different when female meioses were compared (p=0.0139). While previous data suggest that meiotic drive may be a feature of certain human diseases, including the trinucleotide diseases MJD, myotonic dystrophy, and dentatorubral-pallidoluysian atrophy, these data are compatible with meiotic drive also occurring among non-disease associated CAG sizes.
Sex chromosome meiotic drive in stalk-eyed flies
4388Presgraves, DCS, E.; Wilkinson, G. S., Genetics, 147:1169-1180. 1997-01-06 00:00:00.
Meiotically driven sex chromosomes can quickly spread to fixation and cause population extinction unless balanced by selection or suppressed by genetic modifiers. We report results of genetic analyses that demonstrate that extreme female-biased sex ratios in two sister species of stalk-eyed flies, Cyrtodiopsis dalmanni and C. whitei, are due to a meiotic drive element on the X chromosome (X-d). Relatively high frequencies of X-d in C. dalmanni and C. whitei (13-17% and 29%, respectively) cause female-biased sex ratios in natural populations of both species. Sex ratio distortion is associated with spermatid degeneration in male carriers of X-d. Variation in sex ratios is caused by Y-linked and autosomal factors that decrease the intensity of meiotic drive. Y-linked polymorphism for resistance to drive exists in C. dalmanni in which a resistant Y chromosome reduces the intensity and reverses the direction of meiotic drive. When paired with X-d, modifying Y chromosomes (Y-m) cause the transmission of predominantly Y-bearing sperm, and on average, production of 63% male progeny. The absence of sex ratio distortion in closely related monomorphic outgroup species suggests that this meiotic drive system may predate the origin of C. whitei and C. dalmanni. We discuss factors likely to be involved in the persistence of these sex linked polymorphisms and consider the impact of X-d on the operational sex ratio and the intensity of sexual selection in these extremely sexually dimorphic flies.
Variation in Y chromosome meiotic drive in Aedes aegypti (Diptera: Culicidae): a potential genetic approach to mosquito control
4387OwusuDaaku, KOW, R. J.; Butler, R. D., Bulletin of Entomological Research, 87:617-623. 1997-01-05 00:00:00.
Reciprocal crosses between strains of Aedes aegypti (Linnaeus) from different geographical areas have revealed an unexpectedly complex pattern of holandrically inherited male biased sex ratios in F2. The variation has been interpreted in terms of a web of X-Y interactions in F1, in which the Y chromosome may or may not show meiotic drive against the X chromosome with which it is paired. The pattern of inheritance is not in agreement with a single form of Y chromosome, driving with different degrees of intensity against Xs of different sensitivity, but indicates different forms of driving Y chromosome. A rule has emerged that if F1 males from any cross give rise to a male distorted sex ratio in their progeny (F2), the males from the reciprocal cross give rise to a normal sex ratio. All eleven newly colonized strains from Ghana showed Y meiotic drive against the Xs of five strains, one of American and four of Australian origin, although one of the eleven showed a greater degree of drive than the other ten against the same sensitive strains. The variation observed is discussed in relation to previous studies on meiotic drive by the MD haplotype, and to the possible exploitation of sex ratio distortion in controlling this potentially dangerous insect.
Selected lines of Aedes aegypti with persistently distorted sex ratios
4386OwusuDaaku, KOW, R. J.; Butler, R. D., Heredity, 79:388-393. 1997-01-04 00:00:00.
A breeding scheme to isolate X chromosomes sensitive to drive by the T8 (Trinidad) Y chromosome of Aedes aegypti (the MD haplotype) is reported. Crosses with an Australian strain Th.I (Thursday Island) revealed not only sensitive and resistant X chromosomes but also some with the capacity to drive against the T8 Y chromosome. Four strains were created in which sex ratio was male-distorted (28-36 per cent female) for 10 generations, with no regression towards sexual parity. The proportion of females varied significantly between generations in each of the four strains. Further selection produced strains with normal sex ratios, capable of generating fewer than 15 per cent female on outcrossing to T8 males.
Abnormal spermiogenesis is associated with the X-linked sex-ratio trait in Drosophila simulans
4385MontchampMoreau, CJ, D., Heredity, 79:24-30. 1997-01-03 00:00:00.
The sex-ratio trait, known in several Drosophila species, results from X-linked meiotic drive that affects Y-bearing sperm and causes males to produce female-biased progeny. We describe spermiogenesis in three types of D, simulans males: wild-type, sex-ratio, and males that bear driver X chromosomes but do not express the sex-ratio trait because of autosomal and Y-linked suppression, Sex-ratio males show numerous spermatid nuclei in abnormal positions throughout their cysts, which occurs rarely, if ever, in the two other types, The degree of the spermiogenic failure in sex-ratio males is correlated with the bias towards females in their progeny. This proves that: the trait is a case of meiotic drive and strongly suggests that the abnormal spermatids are Y-bearing ones, The number of cysts per testis, hence the production of X-bearing sperm. is not increased in sex-ratio males. Implications for the spread of the sex-ratio trait in natural populations of D. simulans are discussed.
Meiotic drive at the myotonic dystrophy and the cone-rod dystrophy loci on chromosome 19q13.3
4384Inglehearn, CFG, C. Y., American Journal of Human Genetics, 60:1562-1563. 1997-01-02 00:00:00.
The apparently conflicting observations of a high new mutation rate at the myotonic dystrophy (DM) locus on chromosome 19q13.3 and of a founder effect for DM chromosomes led researchers to invoke the influence of meiotic drive at this locus. Two studies (Carey et al. 1994; Gennarelli et al. 1994) suggested such an effect in male meioses, whereas one study (Shaw et al. 1995) found evidence for segregation distortion in female meioses. In the October 1996 issue of the Journal, Leeflang et al. demonstrated convincing evidence that, if such an effect exists in male meioses, it must operate postejaculation, presumably influencing sperm motilityor sperm survival. In so doing, the authors also reviewed the literature both supporting and opposing the influence of the action of meiotic drive at the DM locus. However, they appear to have missed a report from our laboratory (Evans et al. 1994) of a similar observation for dominant cone-rod dystrophy (CORD2), a form of retinal degeneration that also maps to chromosome 19q. The data from the study of the CORD2 locus suggest segregation distortion in female meioses. The most recent locus refinement for CORD2 (Bellingham et al., in press) places it in an interval 0.8-2.4 Mb distal to the DM locus, on the metric FISH map of Gordon et al. (1995). Is it not possible that the close proximity of these two loci, both of which apparently have such an unusual pattern of inheritance, is more than a coincidence?
Segregation distortion in unstructured and structured populations: Competition between ‘sterile’ t haplotypes
4403VanBoven, MW, F. J., Netherlands Journal of Zoology, 46:216-226. 1996-01-21 00:00:00.
By means of two simple models we investigate the competition between sex-specific segregation distorters in unstructured and structured populations. The models are motivated by the t complex of the house mouse. Some variants at this gene complex, the t haplotypes, distort Mendelian segregation in their favour in heterozygous males. The selective advantage at the gamete level is counterbalanced by strong negative fitness effects at the individual level. A large number of t haplotypes with varying degrees of segregation distortion has been found. In order to address this phenomenon we explicitly model the competition between two t haplotypes which induce male sterility when homozygous. Surprisingly, a distorter which is inferior at the gamete level and equivalent in every other respect to a more efficient distorter may well persist in a population. We argue that rare distorters are inherently favoured, and that, as a result, fitness considerations alone are not sufficient to predict the outcome of competition. Since 'sterile' t haplotypes are not only influenced by gamete and individual selection, but also by selection at the level of the group, we furthermore study the relation between unstructured and structured populations. It is shown that the persistence of a seemingly inferior distorter is also possible in a structured population. In contrast, a single efficient distorter with high segregation ratio may not even be able to persist in a structured population. Hence, in a metapopulation with migration between local demes, the segregation ratio is an even worse predictor of the evolutionary success of a segregation distorter than in an unstructured population.
Competition between segregation distorters: Coexistence of ”superior” and ”inferior” haplotypes at the t complex
4402vanBoven, MW, F. J.; Heg, D.; Huisman, J., Evolution, 50:2488-2498. 1996-01-20 00:00:00.
By means of population genetical models, we investigate the competition between sex-specific segregation distorters. Although the models are quite general, they are motivated by a specific example, the t complex of the house mouse. Some variants at this gene complex, the t haplotypes. distort Mendelian segregation in heterozygous males in their favor. The selective advantage at the gamete level is counterbalanced by strong negative fitness effects at the individual level (male sterility or even lethality in both sexes). A plethora of different t haplotypes has been found, both in the field and in the lab. Up to now, however, models have focused on the equilibrium frequency of a single t haplotype. In contrast, we explicitly model the competition between several t haplotypes, A deterministic model for a large, well-mixed population predicts a surprisingly high degree of polymorphism. Haplotypes with seemingly inferior fitness characteristics may easily coexist with ''superior'' haplotypes. For instance, a lethal haplotype with a low segregation ratio may stably coexist with a sterile haplotype with a high segregation ratio, Stable coexistence is even possible for haplotypes with a segregation disadvantage. A simple stochastic model shows that the same principles apply in the context of a structured metapopulation. Although counterintuitive at first sight, all our results can be explained by the fact that segregation distorters have an inherent advantage when they are rare. We conclude that fitness comparisons are not sufficient to predict the outcome of competition when selective forces are acting at different levels.
Genetic control of B chromosome transmission rate in Zea mays ssp mays (Poaceae)
4401Rosato, MC, A. M.; Naranjo, C. A.; Puertas, M. J.; Poggio, L., American Journal of Botany, 83:1107-1112. 1996-01-19 00:00:00.
We selected genotypes of high and low B chromosome transmission rate (TR) in a native race of maize (Pisingallo) from northwest Argentina. We made 20 female 0B x male 1B and 20 f.1B x m.0B crosses. The former (G0m) showed a large variation of B TR, with a mean of TR +/- SE = 0.52 +/- 0.06, ranging from 0.17 to 0.98. In the latter (G0f) the mean was TR = 0.47 +/- 0.02 ranging from 0.31 to 0.58. Plants showing the highest and the lowest TR were selected to constitute the progenitors of the G1 generations. We made 19 f.0B x m.2B crosses, studying 24-30 plants per cross. The TR of the high (H) and low (L) lines in G1m (G1mH and G1mL) significantly differed (TRH = 0.65 +/- 0.03, TRL = 0.40 +/- 0.01), indicating that the H and L lines are different groups. The large variation in male TR suggests that preferential fertilization of gametes carrying B chromosomes does not always occur. We also selected plants showing high and low TR in the progenies of f.1B x m.0B crosses (G0f), and made 24 f.1B x m.0B crosses, studying 23-30 plants per cross. The TRs of the H and L lines in G1f (G1fH and G1fL) were significantly different (TRH = 0.48 +/- 0.025, TRL = 0.40 +/- 0.02). The TRs in G0f and G1fL were significantly different (TR = 0.47 +/- 0.02 and 0.40 +/- 0.02, respectively), while this was not the case between G0f and G1fH. Our results demonstrate the existence of genotypes controlling B TR in this native population of maize.
Measuring meiotic drive
4400Robbins, LGP, G.; Bonaccorsi, S.; Pimpinelli, S., Genetics, 142:645-647. 1996-01-18 00:00:00.
LAURENCE HURST’S (1996) letter re-examines our data on the effect of Stellate copy number on the meiotic parameters of Mystal- (= su(ste)-) males (PALUMBO et al. 1994). In our analysis, we found a tight correlation of fertility and disjunction with Stellate copy number, with both being normal at low copy numbers. In contrast, we found only a weak correlation of meiotic drive and Stellate copy number, with substantial sperm lethality projected to exist even at Stellate copy number = 0. We argue that the absence of crystal, not the presence of Stellate, is the proximate cause of drive in crystal males. HURST argues that the data support the hypothesis (HURST 1992) that Stellate causes drive.
Meiotic drive in fungi: Chromosomal elements that cause fratricide and distort genetic ratios
4399Raju, NB, Journal of Genetics, 75:287-296. 1996-01-17 00:00:00.
Fungal Spore killers (Sk), studied most extensively in Neurospora and to a lesser extent in Podospora, Gibberella and Cochliobolus, cause the death of ascospores (= meiospores) that do not contain the killer (Sk(K)) element. When a Spore killer is heterozygous (Sk(K) x Sk(S)) in Neurospora, every ascus (= meiocyte) contains four normal-sized, black, viable ascospores (Sk(K)), and four ascospores that are tiny, unpigmented and unviable (Sk(S)). Killing of sensitive nuclei is expressed postmeiotically, and results in gross distortion of segregation ratios for Sk-linked genes. A sensitive nucleus that would otherwise die is rescued if a killer nucleus is also enclosed in the same ascospore. In Neurospora, Sk is centromere-linked (linkage group III), and when heterozygous, shows a recombination block in a 30-map-unit region spanning the centromere of linkage group III. There is no ascospore death or recombination block in killer x killer or sensitive x sensitive crosses. Spore killers are Fairly common in Gibberella fujikuroi and Neurospora sitophila but extremely rare in N. intermedia, and have not yet been found among natural isolates of N. crassa.
Epistatic control of non-mendelian inheritance in mouse interspecific crosses
4398Montagutelli, XT, R.; Nadeau, J. H., Genetics, 143:1739-1752. 1996-01-16 00:00:00.
Strong deviation of allele frequencies from Mendelian inheritance favoring Mus spretus-derived alleles has been described previously for X-linked loci in four mouse interspecific crosses. We reanalyzed data for three of these crosses focusing on the location of the gene(s) controlling deviation on the X-chromosome and the genetic basis for incomplete deviation. At least two loci control deviation on the X chromosome, one near Xist (the candidate gene controlling X inactivation) and the other more centromerically located. In all three crosses, strong epistasis was found between loci near Xist and marker loci on the central portion of chromosome 2. The mechanism for this deviation from Mendelian expectations is not yet known but it is probably based on lethality of embryos carrying particular combinations of alleles rather than true segregation distortion during oogenesis in F-1 hybrid females.
The effect of B chromosomes on mating success of the grasshopper Eyprepocnemis plorans
4397Martin, SA, P.; HenriquesGil, N., Genetica, 97:197-203. 1996-01-15 00:00:00.
The mating ability of E. plorans was tested in laboratory conditions in six experimental units composed of ten males and fifteen females during 31 days. When significant differences were found (three from the six cages, and in totals) they involved a decrease of matings involving males with B chromosomes. The same tendency seems to exist in females, but to a lesser extent, so that a significant effect is only detected when the totals are considered. Accessory chromosomes also delay, in both sexes, the occurrence of the first mating. No mating preferences depending on the number of Bs were detected.
Analysis of meiotic segregation, using single-sperm typing: Meiotic drive at the myotonic dystrophy locus
4396Leeflang, EPM, M. S.; Arnheim, N., American Journal of Human Genetics, 59:896-904. 1996-01-14 00:00:00.
Meiotic drive at the myotonic dystrophy (DM) locus has recently been suggested as being responsible for maintaining the frequency, in the human population, of DM chromosomes capable of expansion to the disease state. In order to test this hypothesis, we have studied samples of single sperm from three individuals heterozygous at the DM locus, each with one allele larger and one allele smaller than 19 CTG repeats. To guard against the possible problem of differential PCR amplification rates based on the lengths of the alleles, the sperm were also typed at another closely linked marker whose allele size was unrelated to the allele size at the DM locus. Using statistical models specifically designed to study single-sperm segregation data, we find no evidence of meiotic segregation distortion. The upper limit of the two-sided 95% confidence interval for the estimate of the common segregation probability for the three donors is at or below .515 for all models considered, and no statistically significant difference from .5 is detected in any of the models. This suggests that any greater amount of segregation distortion at the myotonic dystrophy locus must result from events following sperm ejaculation. The mathematical models developed make it possible to study segregation distortion with high resolution by using sperm-typing data from any locus.
The mouse t-complex-encoded protein Tctex-1 is a light chain of brain cytoplasmic dynein
4395King, SMD, J. F.; Benashski, S. E.; Lye, R. J.; PatelKing, R. S.; Pfister, K. K., Journal of Biological Chemistry, 271:32281-32287. 1996-01-13 00:00:00.
Mammalian brain cytoplasmic dynein contains three light chains of M(r) = 8,000, 14,000, add 22,000 (King, S. M., Barbarese, E., Dillman, J. F., III, Patel-King, R. S., Carson, J. H., and Pfister, K. Kr (1996) J. Biol. Chem. 271, 19358-19366). Peptide sequence data (16/16 residues correct) implicate the M(r) = 14,000 polypeptide as Tctex-1, a protein encoded within the mouse t-complex. Tctex-1 cosediments with microtubules and is eluted with ATP or salt but not with GTP as expected for a dynein subunit, The ATP-eluted protein precisely cosediments with known cytoplasmic dynein proteins in sucrose density gradients, Tctex-1 also is immunoprecipitated from brain and other tissue homogenates by a monoclonal antibody raised against the 74-kDa cytoplasmic dynein intermediate chain, Quantitative densitometry indicates that Tctex-1 is a stoichiometric component of the dynein complex, As Tctex-1 is a candidate for involvement in the transmission ratio distortion (meiotic drive) of mouse t-haplotypes, these results suggest that cytoplasmic dynein dysfunction may play an important role in non-mendelian chromosome segregation.
Further evidence consistent with Stellate’s involvement in meiotic drive
4394Hurst, LD, Genetics, 142:641-643. 1996-01-12 00:00:00.
STELLATE is an X-linked multicopy gene found in Drosophila melanogaster and is one of the most bizarre gene arrays yet described (for details see HARDY et al. 1984; LIVAK 1984, 1990; DANILEVSKAYA et al. 1991; BAW~REVA et al. 1992; SHEVELYOV 1992; PALUMBO et al. 1994). The activity of Stellate is restricted to spermatogenesis. However, the transcription and translation of Stellate is inhibited in most males by a Y-linked multicopy gene, Suppressor of Stellate (Su(Ste)) alias crystal (q) . If Stellate is not suppressed, then the protein product (homologous to the beta subunit of casein kinase 11) is produced at levels dependent upon the copy number of Stellate. If Stellate copy number is relatively low, then linear crystals form and the males are of reduced, but nonzero, fertility. In high copy number (up to 200), however, the protein forms a star-shaped crystal in sperm, and the males are typically sterile. An understanding of this system is hence potentially of importance for the study of both intra- and inter-specific sterility and hence of HALDANE’S Rule
Evidence for B chromosome drive suppression in the grasshopper Eyprepocnemis plorans
4393Herrera, JAL, M. D.; Cabrero, J.; Shaw, M. W.; Camacho, J. P. M., Heredity, 76:633-639. 1996-01-11 00:00:00.
The grasshopper Eyprepocnemis plorans is polymorphic for both a B chromosome and a heterochromatic segment of chromatin on the smallest autosome. Females transmit these to their offspring more frequently after copulating with a male from a population without Bs than after copulating with a male from their own population. Paternity analyses using the heterochromatic segment as a marker showed that the effect of male on female transmission does not depend on fertilization because it occurs even when all the eggs are fertilized by sperm from another mating. The possible mechanisms include behavioural differences in mating and transfer of substances affecting female meiosis in male ejaculate. The data support the idea that the B chromosome is initially subject to meiotic drive in populations in which it has not previously existed, and that genes which suppress this drive are then selected.
Segregation distortion of the CTG repeats at the myotonic dystrophy locus
4392Chakraborty, RS, D. N.; Deka, R.; Yu, L. M.; Shriver, M. D.; Ferrell, R. E., American Journal of Human Genetics, 59:109-118. 1996-01-10 00:00:00.
Myotonic dystrophy (DM), an autosomal dominant neuromuscular disease, is caused by a CTG-repeat expansion, with affected individuals having greater than or equal to 50 repeats of this trinucleotide, at the DMPK locus of human chromosome 19q13.3. Severely affected individuals die early in life; the milder form of this disease reduces reproductive ability. Alleles in the normal range of CTG repeats are not as unstable as the (CTG)(greater than or equal to 50) alleles. In the DM families, anticipation and parental bias of allelic expansions have been noted. However, data on mechanism of maintenance of DM in populations are conflicting. We present a maximum-likelihood model for examining segregation distortion of CTG-repeat alleles in normal families. Analyzing 726 meiotic events in 95 nuclear families from the CEPH panel pedigrees, we find evidence of preferential transmission of larger alleles (of size less than or equal to 29 repeats) from females (the probability of transmission of larger alleles is .565 +/- 0.03, different from .5 at P approximate to .028). There is no evidence of segregation distortion during male meiosis. We propose a hypothesis that preferential transmission of larger CTG-repeat alleles during female meiosis can compensate for mutational contraction of repeats within the normal allelic size range, and reduced viability and fertility of affected individuals. Thus, the pool of premutant alleles at the DM locus can be maintained in populations, which can subsequently mutate to the full mutation status to give rise to DM.
The inheritance of B chromosomes in Allium schoenoprasum L
4391Bougourd, SMP, A. B., Chromosome Research, 4:151-158. 1996-01-09 00:00:00.
The inheritance of B chromosomes has been investigated in Allium schoenoprasum from the River Wye, Powys; controlled crosses between plants of known B chromosome constitution were carried out, and the numbers of Bs present in the progenies scored. There was considerable heterogeneity in B chromosome transmission rates across the range of B chromosome numbers, through both the male and female lines, and in crosses involving odd and even numbers of Bs. The mean B number of the progeny was lower than the Mendelian expectation in 41 of the 57 crosses, significantly so in about a third of cases. No progeny had a mean B number significantly higher than expected. The mean transmission rate per B was not significantly different between parents with different numbers of Bs, in either the male or female line, or between plants carrying odd or even numbers of Bs. Transmission through the male line (0.43) was higher than through the female line (0.35), but not significantly so. The overall mean transmission rate per B (0.4), estimated from all crosses, was significantly lower than the expected rate of 0.5. This study provides conclusive evidence that B chromosomes in A. schoenoprasum from the River Wye lack an effective accumulation mechanism and, furthermore, show significant losses during transmission to the progeny of controlled crosses.
Low frequency of mouse t haplotypes in wild populations is not explained by modifiers of meiotic drive
4390Ardlie, KGS, L. M., Genetics, 144:1787-1797. 1996-01-08 00:00:00.
t haplotypes are naturally occurring forms of mouse chromosome 17 that show non-Mendelian transmission from heterozygous +/t males. In laboratory studies, transmission ratios of greater than or equal to 0.90 or higher are typically observed. With transmission ratios of this level, theoretical analyses predict high frequencies of t haplotypes (similar to 75%) in wild populations. In contrast, empirical frequencies of only 15-25% are typically found. This has led to the suggestion that modifiers of drive may play a role in reducing t frequencies. We have measured transmission ratio distortion (TRD) levels in wild +/t mice to examine this hypothesis. TRD was very high in both litters collected from wild-caught pregnant females, and in wild litters bred in the laboratory (mean = 0.9). Contrary to the results of other studies, we found no difference in TRD levels between semilethal and lethal t haplotypes nor between litters conceived from cycling or postpartum estrus. We found three litters with aberrantly low TRDs that were all multiply sired, although the role this might play in natural populations is unknown. These findings show a general absence of modifiers of drive in natural populations and suggest that other factors are responsible for the low observed frequencies of wild t haplotypes.
Gene transfer into the Medfly, Ceratitis capitata, using a Drosophila hydei transposable element.
6269T. G. Loukeris, I. Livadaras, B. Arca, S. Zabalou and C. Savakis, Science, 270:2002-2005. 1995-12-22 16:35:47.
Exogenous functional DNA was introduced into the germline chromosomes of the Mediterranean fruit fly (medfly) Ceratitis capitata with a germline transformation system based on the transposable element Minos from Drosophila hydei. Transformants were identified as phenotypic revertants of a white-eyed mutation carried by the recipient strain. Clusters of transformants were detected among the progeny of 390 individuals screened for germline transformation. Five independent and phenotypically active integration events were identified, in each of which a single copy of the transposon was inserted into a different site of the medfly genome. Molecular analysis indicates that they represent transposase-mediated insertions of the transposon into medfly chromosomes.
Meiotic drive in female mice: An essay
4407Ruvinsky, A, Mammalian Genome, 6:315-320. 1995-01-05 00:00:00.
Since the rediscovery of Mendel's laws, geneticists have accumulated various examples in which equal meiotic segregation in heterozygotes is violated. However, only a few natural meiotic drive systems have been characterized in detail and the majority of these are sex chromosome linked (Hurst and Pomiankovski 1991a). In animals, only two autosomal meiotic drive systems have been thoroughly investigated: the t complex in Mus musculus (Lyon 1991; Silver 1993) and the Segregation Distorter system (SD) in Drosophila melanogaster (Lyttle 1991). Both affect heterozygous males. Recently Agulnik and associates (1990a, 1993c, 1993d) have found and described a new meiotic drive system that disturbs normal segregation in heterozygous female mice. The system is the main target of this review, which also includes a comparative analysis of other drive systems to establish a likely scenario of their origin, evolution, and stability in natural populations.
Sex-ratio distortion in Drosophila simulans – cooccurrence of a meiotic drive and a suppressor of drive
4406Mercot, HA, A.; Jacques, M.; Montchampmoreau, C., Journal of Evolutionary Biology, 8:283-300. 1995-01-04 00:00:00.
A sex-ratio distortion factor was found at high frequency in D. simulans strains from Seychelles and New Caledonia. This factor is poorly or not expressed within those strains which are resistant to it. Its presence was detected by crossing females from New Caledonia or the Seychelles with males from a different geographic origin. Most of the Fl males obtained produced an excess of females (up to 99%) in their progeny. The two strains are infected with Wolbachia, but these micro-organismms are not involved in the sex-ratio distortion. The sex-ratio factor is shown to be an X-linked meiotic driver; nuclear resistance factor(s) act by suppressing the drive. It is likely that the same X-located driver invaded the two populations, which subsequently developed resistance factor(s) against it.
Tctex2 – a sperm tail surface protein mapping to the t-complex
4405Huw, LYG, A. S.; Willison, K.; Artzt, K., Developmental Biology, 170:183-194. 1995-01-03 00:00:00.
Transmission ratio distortion (TRD) in mouse t-haplotypes remains the most significant example of meiotic drive in vertebrates. While the underlying mechanism that fuels it is still mysterious, TRD is clearly a complex multigene phenomenon. The characterization of Tctex2 (t-complex testis expressed 2) shows it to be one of several candidates for involvement in TRD, Tctex2 maps to the t-complex and encodes a membrane-associated protein found exclusively on the sperm tail. The t-haplotype form of Tctex2 is aberrant in both the level of its expression and its primary amino acid sequence, but is nonetheless translated and transported to its normal location. The multiple amino acid changes in the t-form make it extremely unlikely that it can function normally and, since it is found on sperm tails, suggest that it may actively interfere with the development of normal gamete function in males. The possible role of Tctex2 in t-complex transmission ratio distortion and sterility is discussed. (C) 1995 Academic Press, Inc.
Meiotic drive an Myotonic Dystrophy – Reply
4404Carey, NJ, K.; Nokelainen, P.; Peltonen, L.; Savontaus, M. L.; Juvonen, V.; Anvret, M.; Grandell, U.; Chotai, K.; Robertson, E.; Middletonprice, H.; Malcolm, S., Nature Genetics, 10:133-133. 1995-01-02 00:00:00.
Myotonic dystrophy (DM) is a trinucleotide disorder and in sub-clinical individuals there is considerable variation in the length of the CTG repeat. Two groups have recently analysed the patterns of segregation of different sized alleles at this locus and both report an excess of the longer version of the allele in the progeny of sub-clinical individuals1•2• This excess they claim to be due to meiotic drive1•2• Our re-analysis of these two studies indic
Ascoycete spore killers: Chromosomal elements that distort genetic ratios among the products of meiosis
4417Raju, NB, Mycologia, 86:461-473. 1994-01-15 00:00:00.
Spore killers (Sk), studied most extensively in Neurospora, are also known in Podospora, Gibberella and Cochliobolus. Spore killers are no doubt present in natural populations of other fungi. Criteria are outlined here for recognizing their presence and distinguishing them from other causes of ascospore death. Killing occurs when one parent carries the killer element (Sk(K)) and the other carries the sensitive counterpart (Sk(S)). When heterozygous, every ascus contains four normal-sized, viable ascospores and four ascospores that are tiny, undeveloped, and inviable. Spore killers are expressed postmeiotically causing the death of ascospores that do not receive the killer element and resulting in gross distortion of allele ratios for Sk-linked genes. There is little or no ascospore death in homozygous killer x killer or sensitive x sensitive crosses. Sk(K) is centromere-linked in linkage group III of Neurospora crassa and N. intermedia. When Sk is heterozygous, crossing over is blocked in a 30 map unit region that spans the centromere. A sensitive nucleus that would otherwise die is rescued, unchanged, if a killer nucleus is also included in the same ascospore. This has been shown for a developmental giant-ascospore mutant of N, crassa and for the naturally heterokaryotic ascospores of N. tetrasperma and Podospora anserina. As with other segregation-distorters in animals and plants, fungal Spore killers have been found only among strains from nature. Spore killers are fairly common in N. sitophila and Gibberella fujikuroi, but none have been found among natural isolates of N. crassa. In N. intermedia, most strains are sensitive to killing and killers are extremely rare. Some neutral strains are found in nature. These neither kill nor are killed. Resistance to killing is conferred by loci linked to the Sk region. The significance of fungal Spore killers for the individual organism and for populations is discussed.
Characterization of 2 Segregation Distorter revertants: Evidence that the tandem duplication is necessary for SD activity in Drosophila melanogaster
4416Palopoli, MFD, P.; Wu, C. I., Genetics, 136:209-215. 1994-01-14 00:00:00.
Segregation Distorter (SD) is a naturally occurring system of meiotic drive in Drosophila melanogaster. Males heterozygous for an SD second chromosome and a normal homolog (SD+) transmit predominantly SD-bearing sperm. To accomplish this, the Segregation distorter (Sd) locus induces the dysfunction of those spermatids that receive the SD+ chromosome. Recently, P. A. Powers and B. Ganetzky isolated overlapping DNA clones spanning the region of DNA known to contain the Sd gene and identified a 5-kb tandem duplication that is present on all SD chromosomes examined, but is apparently absent from wild-type chromosomes. Here we report a molecular analysis of two spontaneous revertants from an Australian SD chromosome (SD-Arm28). Both of these revertants have lost the 5-kb tandem duplication along with the ability to distort transmission; the critical observation, however, is that they retain the DNA haplotype in the flanking regions (both proximally and distally) that is characteristic of the original SD-Arm28. We propose unequal sister chromatid exchange between the tandem repeats as the only plausible explanation for loss of a repeat while retaining flanking markers. This provides direct evidence that the tandem duplication is indeed necessary for the Sd phenotype. Further, we examined testes-specific levels of both RNA and protein for the nearby Topoisomerase 2 gene. Neither revealed a consistent difference between SD and SD+ strains. We also measured testes-specific levels of RNA using the tandem duplication itself as probe. Our results suggest that there is strong up-regulation of one or several 2.0-2.3-kb transcripts from the duplicated region in the testes of an SD strain. Whether it is this overexpression of transcripts that causes segregation distortion remains to be investigated.
Functional identification of the Segregation Distorter locus of Drosophila melanogaster by germline transformation
4415McLean, JRM, C. J.; Powers, P. A.; Ganetzky, B., Genetics, 137:201-209. 1994-01-13 00:00:00.
Segregation Distorter (SD) is a meiotic drive system in D. melanogaster that results in the failure of SD/SD+ males to transmit SD+ homologs owing to the induced dysfunction of spermatids carrying the normal chromosome. Segregation distorter (Sd), the gene primarily responsible for this distorted transmission, is associated with a novel 12-kb restriction fragment containing a tandem duplication of a 5-kb wild-type segment of genomic DNA. When introduced into appropriate genetic backgrounds by germline transformation, this 12-kb fragment causes full levels of distortion and directs the expression of an Sd-specific 4-kb transcript. Transformants that have lost part of this segment are unable to cause distortion and do not express the 4-kb transcript. These results identify the tandem duplication as Sd.
Selfish DNA as method of pest control
4414Hastings, IM, Philosophical Transactions of the Royal Society B-Biological Sciences, 344:313-324. 1994-01-12 00:00:00.
The inheritance of most genes is tightly controlled, governed by the rules of mendelian inheritance if nuclear or uniparental inheritance if cytoplasmic. A few notable genes and cytoplasmic genomes have escaped this regulation. Such genes may spread by increasing their own rate of transmission despite reducing host fitness and may be regarded as 'selfish'. Their population genetics are described and it appears they may impose a significant genetic load on the host population. Modern molecular techniques may enable similar loads to be imposed on pest species either by transferring selfish genes between species, or by linking deleterious genes to a selfish locus. Alternatively, 'modifier' genes that eliminate the virulent, or disease vectorial capacity, of the pest population may be introduced by linkage to a selfish locus. Selfish elements present in multiple copies may be preferable to single-copy elements as the former are capable of a larger reduction in host fitness. The practical application of these agents depends on five factors: (i) the rate of 'reversion' to a non-selfish form; (ii) the evolution of host repressor systems; (iii) their effect on host fitness, which determines their rate of invasion; (iv) the mechanism regulating host population size in the field; and (v) their ease of manipulation in the laboratory. The first two factors are the most uncertain in most systems, but should be amenable to experimental analysis. It is proposed that the development of such techniques may result in powerful new methods of population control which may be applied to both agricultural pests and disease vectors.
Meiotic drive at the myotonic dystrophy locus
4413Gennarelli, MD, B.; Baiget, M.; Martorell, L.; Novelli, G., Journal of Medical Genetics, 31:980-980. 1994-01-11 00:00:00.
The mutation underlying myotonic dystrophy (DM, MIM* 160900) is the expansion of a CTG trinucleotide repeat sequence at the 3' untranslated region of a protein kinase gene (MT-PK).' The kinetics of this process is influenced by the sex of the transmitting parent and size of the parental allele.2 Congenital DM (CDM) occurs almost always with maternal transmission. Only two patients with CDM have proven paternal inheritance.5' Maternal transmission is considered to be the result of a large intergenerational increase of the CTG repeat size,7 while repeat length contractions are more likely inherited if the mutated allele is of paternal origin.8 However, the range of expansions is wider for alleles transmitted by fathers with fewer than 100 repeats (range 41 to 95).9 This has suggested a male bias in the generation of new contracted or expanded DM alleles.'° Carey et all' described an unusual segregation of the MT-PK alleles with a CTG number > 19 in healthy persons heterozygous for repeats in the wild type size range, and suggested the possibility of meiotic drive at the DM locus
Y-linked suppressors of the sex-ratio trait in Drosophila mediopunctata
4412Decarvalho, ABK, L. B., Heredity, 73:573-579. 1994-01-10 00:00:00.
X-linked meiotic drive causing female-biased progenies is known to occur in nine Drosophila species and is called 'sex-ratio'. In D. mediopunctata this trait is associated with the X:21 chromosome inversion and has variable expression. We describe here a powerful Y-linked suppressor system of sex-ratio expression in this species. There are two types of Y chromosomes (suppressor and nonsuppressor) and two types of X:21 chromosomes (suppressible and unsuppressible). Sex-ratio expression is suppressed in males with the 21 (suppressible)/Y-suppressor genotype, whereas the remaining three genotypes produce female-biased progenies.
The evolution of lethals in the t-haplotype system of the mouse
4411Charlesworth, B, Proceedings of the Royal Society B-Biological Sciences, 258:101-107. 1994-01-09 00:00:00.
The evolution of lethal haplotypes in the t-haplotype segregation distortion system of Mus is examined by mathematical and computer models. The models assume that there is reproductive compensation for the loss of lethal embryos, such that the net reproductive success of a female is not reduced in proportion to the frequency of lethal offspring which she produces. The initial population consists of a mixture of wildtype and homozygous male-sterile t-haplotypes. The failure of sterile males to reproduce may cause a higher fitness cost to mothers heterozygous for t-haplotypes than does elimination of a recessive lethal. Under certain conditions, a recessive lethal will spread and come to a polymorphic equilibrium. Wildtype, lethal and non-lethal haplotypes are all present at this equilibrium. Ifa second lethal mutation arises on a non-lethal t-haplotype in such an equilibrium population, it will increase in frequency and eventually displace the non-lethal t-haplotypes. A third lethal t-haplotype introduced at a low frequency into an equilibrium with two lethals can sometimes be selected for, although this is less likely if compensation is strong. The theoretical predictions are compared with data on natural populations.
Hypothetical sisterkiller
4409Butcher, DLD, H. W., Nature, 369:26-26. 1994-01-07 00:00:00.
It was premature of Hurst in his News and Views article I to accept Haig's claim2 that a hypothetical meiotic drive element, SisterKiller, can lead to evolution from one-step to multi-step meiosis. The basis of Haig's claim is that a SisterKiller allele that causes a gamete to kill its sister gamete can invade and go to fixation in a population using one-step meiosis, whereas in a population using multi-step meiosis, Sister Killer cannot invade. Hurst concludes that SisterKiller could have caused the evolution of multi-step meiosis. The conditions under which this is true are more restrictive than Haig suggests.
Bewildering Bs – An impression of the 1st B-chromosome conference
4408Beukeboom, LW, Heredity, 73:328-336. 1994-01-06 00:00:00.
Ever since their first discovery B chromosomes have attracted attention. Why are they so appealing? The standard chromosomes of an organism are A chromosomes; B chromosomes are extra to this normal complement. In the B chromosome 'bible' (Jones & Rees, 1982) Bs are defined as dispensable supernumerary chromosomes that are not homologous and do not pair with A chromosomes. They have been further characterized as (1) morphologically different from As (usually smaller), (2) being inherited in a nonMendelian fashion, (3) not (or only rarely) having nucleolus organisers, (4) often displaying nondisjunction at anaphase of mitosis resulting in frequencies varying between organs in the same individual, (5) reducing fertility and growth when present in high numbers, and (6) carrying no genes with major effects. These features of Bs were recently discussed at an international conference and the main ideas presented by the participants are reported here. From 21 to 25 September 19
Eradication of the screwworm from Libya using the sterile insect technique
25558M. Vargas-Terán, B. S. Hursey and E. P. Cunningham, Parasitology Today, 10:119-122. 1994-01-01 09:06:27.
The introduction in 1988 of the New World screwworrn into Libya presented a serious threat to the livestock and wildlife sectors of the African continent Mediterranean and the region. In this article, MoisPs Vargas-Terin, Brian 8. Hursey and Edward P. Cunningham describe the action taken to determine the extent of the problem, to prevent the spread of the infestation and to eradicate the fly from the region using the sterile insect technique. New World screwworm hominivorax; myiasis is caused by the larval stage of the fly (Cochliomyia Coquerel) infesting the tissues of living animals. It is an obligate parasite and the female may oviposit in any wound or abrasion in mammals, including humans. Its natural distribution extends from the state of Minnesota, USA, southwards as far as Buenos Aires, A.rgentina, and includes the Caribbean region.
The Segregation Distorter (SD) complex and the accumulation of deleterious genes in laboratory strains of Drosophila melanogaster
4423Dominguez, AS, E.; Albornoz, J.; Gutierrez, A., Theoretical and Applied Genetics, 87:479-486. 1993-01-21 00:00:00.
Segregation Distorter (SD) associated with the second chromosome of D. melanogaster is found in nature at equilibrium frequencies lower than 5%. We report extremely high frequencies of SD (30-50%) in two selected strains, established in 1976, and show it to be responsible for the accumulation of deleterious genes in chromosome II. Samples of chromosomes extracted over a 4-year period were characterized with respect to distortion, sensitivity, lethality, sterility, and inversions. SD chromosomes were inversion-free as they have been shown to be in the Mediterranean area. The cosmopolitan inversion In(2L)t was found associated with SD+ chromosomes. Lines polymorphic for SD have accumulated linked lethal and female-sterile genes approaching a near balanced system. It is proposed that deleterious genes linked in coupling to SD were accumulated by the balancing effect of distortion, while drift and restricted recombination account for the accumulation of deleterious genes linked in repulsion by a mechanism similar to Muller's ratchet. Our results should not be viewed as a particular case as SD chromosomes associated with detrimental genes and inversions are present in almost all populations around the world. The system could evolve in the way we describe whenever equilibrium conditions are broken down in small populations and lead to an increase in SD frequency.
