Meisetz, A Novel Histone Tri-Methyltransferase, Regulates Meiosis-Specific Epigenesis

Hayashi, Kozaburo; Matsui, Yasuhisa

doi:10.4161/cc.5.6.2572

Cited by 43 publications

(41 citation statements)

References 75 publications

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“…Using this technique, we were able to visualize the chromatin localization patterns. As predicted for H3-K4 methylation based on its previously identified association with gene transcription [37][38][39], H3-K4 mono-, di, and trimethylation appeared to be preferentially associated with euchromatic regions (Fig. 2).…”

Section: Dynamic Modulation Of H3-k4 Mono- Di- and Trimethylation Dmentioning

confidence: 70%

Dynamic Regulation of Histone H3 Methylation at Lysine 4 in Mammalian Spermatogenesis1

Godmann

Auger

Ferraroni-Aguiar

et al. 2007

Biology of Reproduction

134

104

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Spermatogenesis is a highly complex cell differentiation process that is governed by unique transcriptional regulation and massive chromatin alterations, which are required for meiosis and postmeiotic maturation. The underlying mechanisms involve alterations to the epigenetic layer, including histone modifications and incorporation of testis-specific nuclear proteins, such as histone variants and protamines. Histones can undergo methylation, acetylation, and phosphorylation among other modifications at their N-terminus, and these modifications can signal changes in chromatin structure. We have identified the temporal and spatial distributions of histone H3 mono-, di-, and trimethylation at lysine 4 (K4), and the lysine-specific histone demethylase AOF2 (amine oxidase flavin-containing domain 2, previously known as LSD1) during mammalian spermatogenesis. Our results reveal tightly regulated distributions of H3-K4 methylation and AOF2, and that H3-K4 methylation is very similar between the mouse and the marmoset. The AOF2 protein levels were found to be higher in the testes than in the somatic tissues. The distribution of AOF2 matched the cell- and stage-specific patterns of H3-K4 methylation. Interaction studies revealed unique epigenetic regulatory complexes associated with H3-K4 methylation in the testis, including the association of AOF2 and methyl-CpG-binding domain protein 2 (MBD2a/b) in a complex with histone deacetylase 1 (HDAC1). These studies enhance our understanding of epigenetic modifications and their roles in chromatin organization during male germ cell differentiation in both normal and pathologic states.

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Section: Dynamic Modulation Of H3-k4 Mono- Di- and Trimethylation Dmentioning

confidence: 70%

Dynamic Regulation of Histone H3 Methylation at Lysine 4 in Mammalian Spermatogenesis1

Godmann

Auger

Ferraroni-Aguiar

et al. 2007

Biology of Reproduction

134

104

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“…The unpaired chromosomes often formed domains of silenced chromatin, sometimes termed "pseudosex bodies" (40). However, unlike the fertile controls but similar to Prdm9 −/− null mutants (41), the early pachytene spermatocytes from sterile males rarely displayed a discernible sex body ( Fig. 2 A and B).…”

Section: Rates Of Double-strand Breaks and Meiotic Recombination Do Notmentioning

confidence: 98%

Mechanistic basis of infertility of mouse intersubspecific hybrids

Bhattacharyya

Gregorová

Mihola

et al. 2013

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

164

228

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According to the Dobzhansky-Muller model, hybrid sterility is a consequence of the independent evolution of related taxa resulting in incompatible genomic interactions of their hybrids. The model implies that the incompatibilities evolve randomly, unless a particular gene or nongenic sequence diverges much faster than the rest of the genome. Here we propose that asynapsis of heterospecific chromosomes in meiotic prophase provides a recurrently evolving trigger for the meiotic arrest of interspecific F1 hybrids. We observed extensive asynapsis of chromosomes and disturbance of the sex body in >95% of pachynemas of Mus m. musculus × Mus m. domesticus sterile F1 males. Asynapsis was not preceded by a failure of double-strand break induction, and the rate of meiotic crossing over was not affected in synapsed chromosomes. DNA double-strand break repair was delayed or failed in unsynapsed autosomes, and misexpression of chromosome X and chromosome Y genes was detected in single pachynemas and by genome-wide expression profiling. Oocytes of F1 hybrid females showed the same kind of synaptic problems but with the incidence reduced to half. Most of the oocytes with pachytene asynapsis were eliminated before birth. We propose the heterospecific pairing of homologous chromosomes as a preexisting condition of asynapsis in interspecific hybrids. The asynapsis may represent a universal mechanistic basis of F1 hybrid sterility manifested by pachytene arrest. It is tempting to speculate that a fast-evolving subset of the noncoding genomic sequence important for chromosome pairing and synapsis may be the culprit. meiosis | meiotic sex chromosome inactivation | Prdm9 | chromosome substitution strains | Haldane's rule H ybrid sterility (HS) is a postzygotic reproductive isolation mechanism contributing to the genesis of new species. It occurs when two parental forms, each which is fertile, produce a sterile hybrid. The widespread occurrence of HS in animal and plant species puzzled evolutionary biologists until Theodosius Dobzhansky and later Herman Muller devised a two-gene model now termed "Dobzhansky-Muller (D-M) incompatibility" (1, 2). The model postulates functional incompatibility of a minimum of two interacting genes that, after independent evolution in two related taxa, lose their ability to cooperate when combined in a hybrid (3, 4). HS almost invariably obeys the Haldane's rule of preferential impairment of the heterogametic (XY or ZW) sex (5); hence male sterility occurs predominantly in mammalian or Drosophila hybrids, whereas in birds and Lepidoptera female hybrids are most often affected (5, 6). HS is under the control of multiple genes, a disproportionally large number of which are located on the X chromosome (7,8). The development of methods of molecular genetics renewed interest in HS (4), and, as a result, OdsH, Ovd, and JYalpha HS genes defined by their DNA sequence were identified in Drosophila (9-11). We identified Prdm9 as a vertebrate HS gene in mouse intersubspecific hybrids (12, 13). Although generalizati...

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“…These include Morc2b, Aym1 and Rfx4. Morc2b is one of the genes identified by ChIP, and it has been linked with Prdm9 male infertility alleles of the histone H3 methyltransferase Prdm9 (Hayashi and Matsui, 2006;Mihola et al, 2009). Aym1 was identified in a screen for mouse genes that could activate promoters of early meiotic genes in S. cerevisiae (Malcov et al, 2004).…”

Section: Mybl1 Influences Diverse Genes and Biological Pathways In Spmentioning

confidence: 99%

A-MYB (MYBL1) transcription factor is a master regulator of male meiosis

et al. 2011

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SUMMARYThe transcriptional regulation of mammalian meiosis is poorly characterized, owing to few genetic and ex vivo models. From a genetic screen, we identify the transcription factor MYBL1 as a male-specific master regulator of several crucial meiotic processes. Spermatocytes bearing a novel separation-of-function allele ( Mybl1 repro9 ) had subtle defects in autosome synapsis in pachynema, a high incidence of unsynapsed sex chromosomes, incomplete double-strand break repair on synapsed pachytene chromosomes and a lack of crossing over. MYBL1 protein appears in pachynema, and its mutation caused specific alterations in expression of diverse genes, including some translated postmeiotically. These data, coupled with chromatin immunoprecipitation (ChIP-chip) experiments and bioinformatic analysis of promoters, identified direct targets of MYBL1 regulation. The results reveal that MYBL1 is a master regulator of meiotic genes that are involved in multiple processes in spermatocytes, particularly those required for cell cycle progression through pachynema.

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Meisetz, A Novel Histone Tri-Methyltransferase, Regulates Meiosis-Specific Epigenesis

Cited by 43 publications

References 75 publications

Dynamic Regulation of Histone H3 Methylation at Lysine 4 in Mammalian Spermatogenesis1

Dynamic Regulation of Histone H3 Methylation at Lysine 4 in Mammalian Spermatogenesis1

Mechanistic basis of infertility of mouse intersubspecific hybrids

A-MYB (MYBL1) transcription factor is a master regulator of male meiosis

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