Bidirectional transcription of a novel chimeric gene mapping to mouse chromosome Yq

Ellis, Peter J. I.; Ferguson, Lydia; Clemente, Emily J; Affara, Nabeel A.

doi:10.1186/1471-2148-7-171

Cited by 33 publications

(45 citation statements)

References 38 publications

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“…These include the Ssty gene family, Asty, Orly and Sly, all of which are transcribed specifically in the testis and are absent in the MSYqtestis (Conway et al, 1994;Toure et al, 2005;Ellis et al, 2007). A good candidate gene is Sly, which encodes a protein (SLY1) that is present in the both the nucleus and cytoplasm of round and early elongating spermatids (Reynard et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…The subcellular localisation and function of the SSTY1 protein in spermatids is unknown, although the levels of this protein are increased by approximately twofold in the 2/3MSYq-testis (Toure et al, 2004b). The biological role of the Asty and Orly genes are also unknown, but might act as non-coding RNAs as these genes have no identifiable open reading frame (Touré et al, 2005;Ellis et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

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Increased sex chromosome expression and epigenetic abnormalities in spermatids from male mice with Y chromosome deletions

Reynard¹,

Turner²

2009

Journal of Cell Science

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During male meiosis, the X and Y chromosomes are transcriptionally silenced, a process termed meiotic sex chromosome inactivation (MSCI). Recent studies have shown that the sex chromosomes remain substantially transcriptionally repressed after meiosis in round spermatids, but the mechanisms involved in this later repression are poorly understood. Mice with deletions of the Y chromosome long arm (MSYq–) have increased spermatid expression of multicopy X and Y genes, and so represent a model for studying post-meiotic sex chromosome repression. Here, we show that the increase in sex chromosome transcription in spermatids from MSYq– mice affects not only multicopy but also single-copy XY genes, as well as an X-linked reporter gene. This increase in transcription is accompanied by specific changes in the sex chromosome histone code, including almost complete loss of H4K8Ac and reduction of H3K9me3 and CBX1. Together, these data show that an MSYq gene regulates sex chromosome gene expression as well as chromatin remodelling in spermatids.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Increased sex chromosome expression and epigenetic abnormalities in spermatids from male mice with Y chromosome deletions

Reynard¹,

Turner²

2009

Journal of Cell Science

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“…Sly1 is a full-length isoform and encodes a ,40 kDa protein (referred to as SLY1), detected by our anti-SLY1 antibody (Reynard et al, 2009). Exons 5-6, which arose from a duplication of exons 3-4 (Ellis et al, 2007), are spliced out in the Sly2 isoform. Our anti-SLY1 antibody does not detect SLY2 protein but Sly2 can be translated: a transgene-derived SLY2 protein fused to a FLAG tag was detectable by an anti-FLAG antibody (supplementary material Fig.…”

Section: Characterization Of a New Shsly Line In Which Sly1 But Not Smentioning

confidence: 99%

Deficiency of the multi-copy mouse Y gene Sly causes sperm DNA damage and abnormal chromatin packaging

Riel

Yamauchi

Sugawara

et al. 2012

Journal of Cell Science

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SummaryIn mouse and man Y chromosome deletions are frequently associated with spermatogenic defects. Mice with extensive deletions of nonpairing Y chromosome long arm (NPYq) are infertile and produce sperm with grossly misshapen heads, abnormal chromatin packaging and DNA damage. The NPYq-encoded multi-copy gene Sly controls the expression of sex chromosome genes after meiosis and Sly deficiency results in a remarkable upregulation of sex chromosome genes. Sly deficiency has been shown to be the underlying cause of the sperm head anomalies and infertility associated with NPYq gene loss, but it was not known whether it recapitulates sperm DNA damage phenotype. We produced and examined mice with transgenically (RNAi) silenced Sly and demonstrated that these mice have increased incidence of sperm with DNA damage and poorly condensed and insufficiently protaminated chromatin. We also investigated the contribution of each of the two Sly-encoded transcript variants and noted that the phenotype was only observed when both variants were knocked down, and that the phenotype was intermediate in severity compared with mice with severe NPYq deficiency. Our data demonstrate that Sly deficiency is responsible for the sperm DNA damage/chromatin packaging defects observed in mice with NPYq deletions and point to SLY proteins involvement in chromatin reprogramming during spermiogenesis, probably through their effect on the post-meiotic expression of spermiogenic genes. Considering the importance of the sperm epigenome for embryonic and fetal development and the possibility of its inter-generational transmission, our results are important for future investigations of the molecular mechanisms of this biologically and clinically important process.

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“…An alternative hypothesis was formulated by Ellis et al (2005) that the gene amplification on the mouse X was a consequence of a genomic conflict between X and Y chromosomes (see also Evidence for functional differences between haploid cells). In support of this, the most highly ampliconic genes on the mouse became amplified shortly after Sly arose in the Y chromosome (Ellis et al 2007(Ellis et al , 2011. These hypotheses are not mutually exclusive: Sly, one of the participants in the proposed genomic conflict is believed to act via modulation of PMSC .…”

Section: Sex Chromosome Transcriptional Activity In Spermatidsmentioning

confidence: 81%

Transcriptional dynamics of the sex chromosomes and the search for offspring sex-specific antigens in sperm

Ellis¹,

Yu²,

Zhang³

2011

Reproduction

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The ability to pre-select offspring sex via separation of X-and Y-bearing sperm would have profound ramifications for the animal husbandry industry. No fully satisfactory method is as yet available for any species, although flow sorting is commercially viable for cattle. The discovery of antigens that distinguish X-and Y-bearing sperm, i.e. offspring sex-specific antigens (OSSAs), would allow for batched immunological separation of sperm and thus enable a safer, more widely applicable and high-throughput means of sperm sorting. This review addresses the basic processes of spermatogenesis that have complicated the search for OSSAs, in particular the syncytial development of male germ cells, and the transcriptional dynamics of the sex chromosomes during and after meiosis. We survey the various approaches taken to discover OSSA and propose that a whole-genome transcriptional approach to the problem is the most promising avenue for future research in the field.

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Bidirectional transcription of a novel chimeric gene mapping to mouse chromosome Yq

Cited by 33 publications

References 38 publications

Increased sex chromosome expression and epigenetic abnormalities in spermatids from male mice with Y chromosome deletions

Increased sex chromosome expression and epigenetic abnormalities in spermatids from male mice with Y chromosome deletions

Deficiency of the multi-copy mouse Y gene Sly causes sperm DNA damage and abnormal chromatin packaging

Transcriptional dynamics of the sex chromosomes and the search for offspring sex-specific antigens in sperm

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