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.
Disclaimer>

Putting the brake on drive: meiotic drive of t haplotypes in natural populations of mice

4365
Ardlie, 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

4383
Carvalho, 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

4382
Braidotti, 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

4381
Atlan, 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

4389
Rubinsztein, 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

4388
Presgraves, 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

4387
OwusuDaaku, 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

4386
OwusuDaaku, 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

4385
MontchampMoreau, 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

4384
Inglehearn, 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

4403
VanBoven, 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

4402
vanBoven, 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)

4401
Rosato, 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

4400
Robbins, 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

4399
Raju, 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

4398
Montagutelli, 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

4397
Martin, 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

4396
Leeflang, 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

4395
King, 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

4394
Hurst, 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

« First ‹ Previous 1 9 99 107 108 109 110 111 118 Next › Last »