Aym1, a mouse meiotic gene identified by virtue of its ability to activate early meiotic genes in the yeast Saccharomyces cerevisiae

Malcov, Mira; Cesarkas, Karen; Stelzer, Gil; Shalom, Sarah; Dicken, Yosef; Naor, Yaniv; Goldstein, Ronald S.; Sagee, Shira; Kassir, Yona; Don, Jeremy

doi:10.1016/j.ydbio.2004.08.026

Cited by 10 publications

(9 citation statements)

References 38 publications

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“…Although lamins are not present in yeast, the single-celled eukaryote has been used commonly to examine the function of mammalian transcription factors including those with no yeast counterparts [35-39]. With this goal in mind, the lamin A bait protein was constructed by fusing human lamin A to the Gal4 DNA-binding domain (Gal4DBD) and under the control of the constitutive ADH1 promoter.…”

Section: Resultsmentioning

confidence: 99%

A-type nuclear lamins act as transcriptional repressors when targeted to promoters

Lee¹,

Welton²,

Smith³

et al. 2009

Experimental Cell Research

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Regions of heterochromatin are often found at the periphery of the mammalian nucleus, juxtaposed to the nuclear lamina. Genes in these regions are likely maintained in a transcriptionally silent state, although other locations at the nuclear periphery associated with nuclear pores are sites of active transcription. As primary components of the nuclear lamina, A-and B-type nuclear lamins are intermediate filament proteins that interact with DNA, histones and known transcriptional repressors, leading to speculation that they may promote establishment of repressive domains. However, no direct evidence of a role for nuclear lamins in transcriptional repression has been reported. Here we find that human lamin A, when expressed in yeast and cultured human cells as a fusion protein to the Gal4 DNA-binding domain (DBD), can mediate robust transcriptional repression of promoters with Gal4 binding sites. Full repression by lamin A requires both the coiled-coil rod domain and the C-terminal tail domain. In human cells, other intermediate filament proteins such as lamin B and vimentin are unable to confer robust repression as Gal4-DBD fusions, indicating that this property is specific to A-type nuclear lamins. These findings indicate that A-type lamins can promote transcriptional repression when in proximity of a promoter.

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Section: Resultsmentioning

confidence: 99%

A-type nuclear lamins act as transcriptional repressors when targeted to promoters

Lee¹,

Welton²,

Smith³

et al. 2009

Experimental Cell Research

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“…How Tcte3 is involved in the apoptotic process of male germ cells is not understood. However, Tcte3 could directly induce meiotic gene activation, because Tcte3 can bind to the IME2 promoter which is involved in the expression of meiotic genes in yeast (Malcov et al 2004).…”

Section: Discussionmentioning

confidence: 99%

Disruption of the murine dynein light chain gene Tcte3-3 results in asthenozoospermia

Rashid

Grzmil²,

Drenckhahn³

et al. 2010

Reproduction

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To elucidate the role of the mouse gene Tcte3 (Tctex2), which encodes a putative light chain of the outer dynein arm of cilia and sperm flagella, we have inactivated this gene in mice using targeted disruption. Breeding of heterozygous males and females resulted in normal litter size; however, we were not able to detect homozygous Tcte3-deficent mice using standard genotype techniques. In fact, our results indicate the presence of at least three highly similar copies of the Tcte3 gene (Tcte3-1, Tcte3-2, and Tcte3-3) in the murine genome. Therefore, quantitative real-time PCR was established to differentiate between mice having one or two targeted Tcte3-3 alleles. By this approach, Tcte3-3 K/K animals were identified, which were viable and revealed no obvious malformation. Interestingly, some homozygous Tcte3-3-deficient male mice bred with wild-type female produced no offspring while other Tcte3-3-deficient males revealed decreased sperm motility but were fertile. In infertile Tcte3-3 K/K males, spermatogenesis was affected and sperm motility was reduced, too, resulting in decreased ability of Tcte3-3-deficient spermatozoa to move from the uterus into the oviduct. Impaired flagellar motility is not correlated with any gross defects in the axonemal structure, since outer dynein arms are detectable in sperm of Tcte3-3 K/K males. However, in infertile males, deficient Tcte3-3 function is correlated with increased apoptosis during male germ cell development, resulting in a reduction of sperm number. Moreover, multiple malformations in developing haploid germ cells are present. Our results support a role of Tcte3-3 in generation of sperm motility as well as in male germ cell differentiation.

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“…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). RFX4 belongs to the regulatory factor X (RFX) family of transcription factors with testis expression that has been implicated in the regulation of spermatogenesis .…”

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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Aym1, a mouse meiotic gene identified by virtue of its ability to activate early meiotic genes in the yeast Saccharomyces cerevisiae

Cited by 10 publications

References 38 publications

A-type nuclear lamins act as transcriptional repressors when targeted to promoters

A-type nuclear lamins act as transcriptional repressors when targeted to promoters

Disruption of the murine dynein light chain gene Tcte3-3 results in asthenozoospermia

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

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