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Genes involved in invasion and metastasis such as matrilysin (), gelatinase (MMP9), matrix metalloproteinase 10 and 12 were upregulated in most tumours. Several other expression profiling studies have been undertaken which identified differentially expressed genes between serous and mucinous carcinomas; and also identified differences in gene expression during progression of ovarian carcinoma.
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We did not observe increased levels of synthetic incompatibilities for the heterogametic sex, suggesting that Haldane’s rule may not apply for within-species variation of our study species. However, when we examined the genetic basis of female sterility we found evidence consistent with the dominance hypothesis of Haldane’s rule. This is because female-specific synthetic sterility involved recessive alleles in each case. As there is evidence of female-biased expression patterns on the X chromosome (), our findings are also consistent with the faster-X hypothesis. Had the faster male hypothesis held, we would have expected to observe greater levels of male sterility. Note that while our study reveals the recessivity of standing epistatic fitness variation, it does not directly explain what causes Haldane’s rule.
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The chromosomes involved in DBM incompatibilities are important to Haldane’s rule. This rule states that if only one sex of a hybrid is sterile or inviable, it tends to be the heterogametic sex (). Four alternative hypotheses that explain Haldane’s rule are: faster-X, faster male, meiotic drive, and dominance (). The faster-X hypothesis is sensitive to demography and it posits that rates of adaptive change differ between X-linked and autosomal loci (). The faster male hypothesis posits that male traits may evolve faster due to sexual selection and the sensitivity of spermatogenesis to new mutations (). Divergence of meiotic drive suppression systems can cause hybrid sterility and lethality, and segregation distortion of sex chromosomes can distort sex ratios away from 50:50 (; ; ; ). Finally, the dominance hypothesis states that if alleles causing interspecific incompatibilities behave recessively in hybrids, then the heterogametic sex will be more likely to be affected (). Data from a wide variety of taxa support the dominance hypothesis (; ; ), as do theoretical models with a firm grounding in DBM incompatibilities (). Drosophila have an XY system in which males are the heterogametic sex. Because recessive X-linked alleles cannot be masked in Drosophila males, sex-specific patterns can arise when epistasis involves the X chromosome. While Haldane’s rule is known to apply to between-species incompatibilities, it is unknown whether it applies to within-species sterility and lethality. Note, however, that the dominance theory does not make any predictions about the dominance of incompatible alleles within species. Recent work in Tribolium castaneum suggests that Haldane’s rule may apply to within-species incompatibilities between different populations (). However, sterility in other heterogametic-male species (such as Homo sapiens) seems to be female-biased ().
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A majority of X-autosome interactions were recessive (requiring homozygous autosomes) and both X-2nd and X-3rd interactions were observed. Of the 154 lines tested in Set 2, 92 did not exhibit any synthetic lethality (). Of the remaining synthetic lethal lines, 22 (35.5%) exhibited dominant synthetic lethality and 40 (64.5%) exhibited recessive lethality. Here, dominance and recessivity refers to the number of autosomal copies required for synthetic lethality (all lines tested were homozygous for an extracted X chromosome). One caveat is that our methodology may overestimate the frequency of synthetic lethals. This is because Mendelian segregation alone can cause a genotype to be absent (even if 60 flies were assayed per cross). Three times as many X-autosome combinations involving the 2nd chromosome resulted in recessive synthetic lethality relative to combinations involving the 3rd chromosome (two-tailed p-value Drosophila melanogaster second chromosome is slightly larger than the third chromosome (and thus a larger target for epistatic interactions), this alone is an insufficient explanation for the observed differences in X-2nd vs. X-3rd synthetic lethality. Finally, an appreciable number of lines (16) exhibited both X-2nd and X-3rd interactions, suggesting that complex epistasis may underlie synthetic lethality in these lines.
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Additionally, genomic conflict, in the form of competition among oötids for inclusion into the pronucleus, potentially plays a role in Haldane's rule in marsupials (reviewed in ). Centromeric sequences involved in spindle fiber attachment have been shown to be involved in such competition in mammals (; ). Separated by 1–2 My (), 2 wallaby sister species, Macropus rufogriseus and M. eugenii, differ greatly in the repeat content of their centromeric sequences (; ). Interspecific crosses between these species produce infertile male and female hybrids that display extensive chromosomal remodeling and genomic instability, for example, changes in chromatin structure and the amplification of satellite repeats and transposable elements (). The effects of genomic instability may contribute to Haldane's rule in marsupials if centromeric misalignment of the X and Y chromosomes during metaphase in hybrids leads to the failure of spermatogenesis (; ; ). Furthermore, meiotic inactivation of sex chromosomes in male hybrids, a process crucial for male fertility in mammals (), could be delayed or derailed by the decondensation or amplification of centromeric regions. In marsupials, meiotic sex chromosome inactivation occurs before the X–Y associations that lead to the formation of the sex chromatin beginning at midpachytene (). A delay in the formation of the sex chromatin may trigger the late-pachytene meiotic checkpoint and lead to spermatocyte apoptosis and reduced fertility, a phenomenon attributable to chromosomal asynapsis in placental mammals (). If true, this mechanism would be consistent with more general “faster heterogametic sex” hypotheses that propose the XY sex evolves faster because of the conflicting pressures that the X and Y chromosomes experience to distort the sex ratio (; ; ).