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Meiosis is essential for reproduction in sexually reproducing organisms. A key stage in meiosis is the synapsis of maternal and paternal homologous chromosomes, accompanied by exchange of genetic material to generate crossovers. A decade ago, studies found that when chromosomes fail to synapse, the many hundreds of genes housed within them are transcriptionally inactivated. This process, meiotic silencing, is conserved in all mammals studied to date, but its purpose is not yet defined. Here, I review the molecular genetics of meiotic silencing and consider the many potential functions that it could serve in the mammalian germ line. In addition, I discuss how meiotic silencing influences sex differences in meiotic infertility and the profound impact that meiotic silencing has had on the evolution of mammalian sex chromosomes. [ABSTRACT FROM AUTHOR]

During male meiosis in mammals the X and Y chromosomes become condensed to form the sex body (XY body), which is the morphological manifestation of the process of meiotic sex chromosome inactivation (MSCI). An increasing number of sex body located proteins are being identified, but their functions in relation to MSCI are unclear. Here we demonstrate that assaying male sex body located proteins during XY female mouse meiosis, where MSCI does not take place, is one way in which to begin to discriminate between potential functions. We show that a newly identified protein, "Asynaptin" (ASY), detected in male meiosis exclusively in association with the X and Y chromatin of the sex body, is also expressed in pachytene oocytes of XY females where it coats the chromatin of the asynapsed X in the absence of MSCI. Furthermore, in pachytene oocytes of females carrying a reciprocal autosomal translocation, ASY associates with asynapsed autosomal chromatin. Thus the location of ASY to the sex body during male meiosis is likely to be a response to the asynapsis of the non-homologous regions [outside the pseudoautosomal region (PAR)] of the heteromorphic X-Y bivalent, rather than being related to MSCI. In contrast to ASY, the previously described sex body protein XY77 proved to be male sex body specific. Potential functions for MSCI and the sex body are discussed together with the possible roles of these two proteins. [ABSTRACT FROM AUTHOR]

X chromosome inactivation ensures equal dosage of X-linked genes between male and female mammals. Two new studies have shown that the initiation of inactivation is preceded by X chromosome pairing; their results implicate this pairing in the choice and counting functions of X chromosome inactivation. [Copyright &y& Elsevier]

Summary: In female marsupials, X chromosome inactivation (XCI) is imprinted, affecting the paternal X chromosome. One model, supported by recent studies , proposes that XCI in marsupials is achieved through inheritance of an already silent X chromosome from the father , with XCI initiated by meiotic sex chromosome inactivation (MSCI) . This model is appealing because marsupials have no Xist gene and the marsupial inactive X chromosome is epigenetically dissimilar to that of mice, apparently lacking repressive histone marks such as H3K27 trimethylation . A central prediction of the meiotic inactivation model of XCI is that silencing of genes on the X chromosome, initiated during male meiosis, is stably maintained during subsequent spermiogenesis. Here we characterize XCI in the male germline and female soma of the marsupial Monodelphis domestica. Contrary to the meiotic inactivation model, we find that X genes silenced by MSCI are reactivated after meiosis and are subsequently inactivated in the female. A reexamination of the female somatic inactive marsupial X chromosome reveals that it does share common properties with that of eutherians, including H3K27 trimethylation and targeting to the perinucleolar compartment. We conclude that aspects of the XCI process are more highly conserved in therian mammals than previously thought. [Copyright &y& Elsevier]

Summary Somatic X dosage compensation requires two mechanisms: X inactivation balances X gene output between males (XY) and females (XX), while X upregulation, hypothesized by Ohno and documented in vivo, balances X gene with autosomal gene output. Whether X dosage compensation occurs in germ cells is unclear. We show that mouse and human germ cells exhibit non-canonical X dosage states that differ from the soma and between the sexes. Prior to genome-wide reprogramming, X upregulation is present, consistent with Ohno's hypothesis. Subsequently, however, it is erased. In females, erasure follows loss of X inactivation, causing X dosage excess. Conversely, in males, erasure leads to permanent X dosage decompensation. Sex chromosomally abnormal models exhibit a “sex-reversed” X dosage state: XX males, like XX females, develop X dosage excess, while XO females, like XY males, develop X dosage decompensation. Thus, germline X dosage compensation states are determined by X chromosome number, not phenotypic sex. These unexpected differences in X dosage compensation states between germline and soma offer unique perspectives on sex chromosome infertility. [ABSTRACT FROM AUTHOR]