scholarly journals Natural variation of the Y chromosome suppresses sex ratio distortion and modulates testis-specific gene expression in Drosophila simulans

Heredity ◽  
2013 ◽  
Vol 111 (1) ◽  
pp. 8-15 ◽  
Author(s):  
A T Branco ◽  
Y Tao ◽  
D L Hartl ◽  
B Lemos
1997 ◽  
Vol 87 (6) ◽  
pp. 617-623 ◽  
Author(s):  
K. O. Owusu-Daaku ◽  
R. J. Wood ◽  
R. D. Butler

AbstractReciprocal 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 Fl, 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 Fl 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.


Author(s):  
Yehonatan Alcalay ◽  
Silke Fuchs ◽  
Roberto Galizi ◽  
Federica Bernardini ◽  
Roya Elaine Haghighat-Khah ◽  
...  

Sex-ratio distorters based on X-chromosome shredding are more efficient than sterile male releases for population suppression. X-shredding is a form of sex distortion that skews spermatogenesis of XY males towards the preferential transmission of Y-bearing gametes, resulting in a higher fraction of sons than daughters. Strains harboring X-shredders on autosomes were first developed in the malaria mosquito Anopheles gambiae, resulting in strong sex-ratio distortion. Since autosomal X-shredders are transmitted in a Mendelian fashion and can be selected against, their frequency in the population declines once releases are halted. However, unintended transfer of X-shredders to the Y-chromosome could produce an invasive meiotic drive element, that benefits from its biased transmission to the predominant male-biased offspring and its effective shielding from female negative selection. Indeed, linkage to the Y-chromosome of an active X-shredder instigated the development of the nuclease-based X-shredding system. Here, we analyze mechanisms whereby an autosomal X-shredder could become unintentionally Y-linked after release by evaluating the stability of an established X-shredder strain that is being considered for release, exploring its potential for remobilization in laboratory and wild-type genomes of An. gambiae and provide data regarding expression on the mosquito Y-chromosome. Our data suggest that an invasive X-shredder resulting from a post-release movement of such autosomal transgenes onto the Y-chromosome is unlikely.


2020 ◽  
Vol 37 (12) ◽  
pp. 3453-3468 ◽  
Author(s):  
Charlotte Moretti ◽  
Mélina Blanco ◽  
Côme Ialy-Radio ◽  
Maria-Elisabetta Serrentino ◽  
Clara Gobé ◽  
...  

Abstract Transmission distorters (TDs) are genetic elements that favor their own transmission to the detriments of others. Slx/Slxl1 (Sycp3-like-X-linked and Slx-like1) and Sly (Sycp3-like-Y-linked) are TDs, which have been coamplified on the X and Y chromosomes of Mus species. They are involved in an intragenomic conflict in which each favors its own transmission, resulting in sex ratio distortion of the progeny when Slx/Slxl1 versus Sly copy number is unbalanced. They are specifically expressed in male postmeiotic gametes (spermatids) and have opposite effects on gene expression: Sly knockdown leads to the upregulation of hundreds of spermatid-expressed genes, whereas Slx/Slxl1-deficiency downregulates them. When both Slx/Slxl1 and Sly are knocked down, sex ratio distortion and gene deregulation are corrected. Slx/Slxl1 and Sly are, therefore, in competition but the molecular mechanism remains unknown. By comparing their chromatin-binding profiles and protein partners, we show that SLX/SLXL1 and SLY proteins compete for interaction with H3K4me3-reader SSTY1 (Spermiogenesis-specific-transcript-on-the-Y1) at the promoter of thousands of genes to drive their expression, and that the opposite effect they have on gene expression is mediated by different abilities to recruit SMRT/N-Cor transcriptional complex. Their target genes are predominantly spermatid-specific multicopy genes encoded by the sex chromosomes and the autosomal Speer/Takusan. Many of them have coamplified with not only Slx/Slxl1/Sly but also Ssty during muroid rodent evolution. Overall, we identify Ssty as a key element of the X versus Y intragenomic conflict, which may have influenced gene content and hybrid sterility beyond Mus lineage since Ssty amplification on the Y predated that of Slx/Slxl1/Sly.


1995 ◽  
Vol 8 (3) ◽  
pp. 283-300 ◽  
Author(s):  
Herve Mercot ◽  
Anne Atlan ◽  
Micheline Jacques ◽  
Catherine Montchamp-Moreau

Genetics ◽  
1981 ◽  
Vol 98 (2) ◽  
pp. 317-334
Author(s):  
Terrence W Lyttle

ABSTRACT Laboratory populations of Drosophila melanogaster were challenged by pseudo-Y drive, which mimics true Y-chromosome meiotic drive through the incorporation of Segregation Distorter (SD) in a T(Y;2) complex. This causes extreme sex-ratio distrotion and can ultimately lead to population extinction. Populations normally respond by the gradual accumulation of drive suppressors, and this reduction in strength of distortion allows the sex ratio to move closer to the optimal value of 1:1. One population monitored, however, was rapidly able to neutralize the effects of sex-ratio distortion by the accumulation of sex-chromosome aneuploids (XXY, XYY). This apparently occurs because XX-bearing eggs, produced in relatively high numbers (~4%) by XXY genotypes, become the main population source of females under strong Y-chromosome drive. Computer simulation for a discrete generation model incorporating random mating with differences in fitness and segregation permits several predictions that can be compared to the data. First, sex-chromosome aneuploids should rapidly attain equilibrium, while stabilizing the population at ~60% males. This sex ratio should be roughly independent of the strength of the meiotic drive. Moreover, conditions favoring the accumulation of drive suppressors (e.g., weak distortion, slow population extinction) are insufficient for maintaining aneuploidy, while conditions favoring aneuploidy (e.g., strong distortion, low production of females) lead to population extinction before drive suppressors can accumulate. Thus, the different mechanisms for neutralizing sex-ratio distortion are complementary. In addition, Y drive and sex-chromosome aneuploidy are potentially co-adaptive, since under some conditions neither will survive alone. Finally, these results suggest the possibility that genetic variants promoting sex-chromosome nondisjunction may have a selective advantage in natural populations faced with sex-ratio distortion.


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