The X and Y Chromosomes Assemble into H2A.Z-Containing Facultative Heterochromatin following Meiosis

Greaves, Ian K.; Rangasamy, Danny; Devoy, Michael; Graves, Jennifer A. Marshall; Tremethick, David J.

doi:10.1128/mcb.01407-06

Cited by 23 publications

(35 citation statements)

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“…polymerase II, and are enriched for several repressive chromatin marks present on the sex body, including histone H3 dimethylated at lysine 9 (H3K9me2) and CBX1 (chromobox protein homolog 1, previously known as HP1) (Baarends et al, 2007;Greaves et al, 2006;Khalil et al, 2004;Namekawa et al, 2006;Turner et al, 2006). However, the X and Y chromosomes are continually remodelled during the transition between meiosis and spermiogenesis, and histone modifications associated with transcriptionally active chromatin [e.g.…”

Section: Introductionmentioning

confidence: 99%

“…However, the X and Y chromosomes are continually remodelled during the transition between meiosis and spermiogenesis, and histone modifications associated with transcriptionally active chromatin [e.g. histone acetylation and histone H3 dimethylated on lysine 4 (H3K4me2)] are also enriched on PMSC in round spermatids (Baarends et al, 2007;Greaves et al, 2006;Khalil and Driscoll, 2006). These epigenetic changes could explain why XY spermatid silencing is less complete than MSCI, and might reflect a need to retain expression of some X-and Yencoded genes that are essential for spermiogenesis.…”

Section: Introductionmentioning

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: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

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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“…Le traitement différentiel des deux chromosomes X au cours de la fécondation et du développement embryonnaire précoce et une telle dynamique d'inactivation tone (H3K4me, H3.3, H4A.Z) [18,19,22,23]. Ces microARN pourraient avoir un rôle clé, soit dans le processus de la MSCI, soit dans la régulation post-transcriptionelle des ARNm autosomiques dans les stages postméiotiques de la spermatogenèse.…”

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Le modèle de l’inactivation du chromosome X chez la souris

et al. 2012

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“…In one school of thought, the paternal germ line marks the Xist gene for expression in the female embryo, but the mark is not read until later in preimplantation development (17). Another model suggests that X p silencing mechanistically follows from meiotic sex chromosome inactivation in the male germ line (16,(33)(34)(35)(36)(37) and is a direct extension of the postmeiotic sex Significance Mammals with imprinted X inactivation demonstrate exclusive silencing of the paternal X chromosome. X-inactivation-specific transcript (Xist) RNA directs this silencing and is imprinted to be expressed only from the father's X chromosome.…”

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Xist imprinting is promoted by the hemizygous (unpaired) state in the male germ line

Sun

Payer

Namekawa

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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This contribution is part of the special series of Inaugural Articles by members of the National Academy of Sciences elected in 2015. Contributed by Jeannie T. Lee, October 1, 2015 (sent for review July 29, 2015; reviewed by Nora Engel and Kathrin Plath)The long noncoding X-inactivation-specific transcript (Xist gene) is responsible for mammalian X-chromosome dosage compensation between the sexes, the process by which one of the two X chromosomes is inactivated in the female soma. Xist is essential for both the random and imprinted forms of X-chromosome inactivation. In the imprinted form, Xist is paternally marked to be expressed in female embryos. To investigate the mechanism of Xist imprinting, we introduce Xist transgenes (Tg) into the male germ line. Although ectopic high-level Xist expression on autosomes can be compatible with viability, transgenic animals demonstrate reduced fitness, subfertility, defective meiotic pairing, and other germ-cell abnormalities. In the progeny, paternal-specific expression is recapitulated by the 200-kb Xist Tg. However, Xist imprinting occurs efficiently only when it is in an unpaired or unpartnered state during male meiosis. When transmitted from a hemizygous father (+/Tg), the Xist Tg demonstrates paternalspecific expression in the early embryo. When transmitted by a homozygous father (Tg/Tg), the Tg fails to show imprinted expression. Thus, Xist imprinting is directed by sequences within a 200-kb X-linked region, and the hemizygous (unpaired) state of the Xist region promotes its imprinting in the male germ line.Xist | imprinting | X inactivation | transgenerational inheritance | meiotic silencing by unpaired DNA

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The X and Y Chromosomes Assemble into H2A.Z-Containing Facultative Heterochromatin following Meiosis

Cited by 23 publications

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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

Le modèle de l’inactivation du chromosome X chez la souris

Xist imprinting is promoted by the hemizygous (unpaired) state in the male germ line

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