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Screening of genes involved in chromosome segregation in meiosis I

ABSTRACT: Prophase I of meiosis involves dynamic chromosome segregation processes including synapsis, meiotic recombination, and cohesion. Genetic defects in genes participating in these processes consistently cause reproduction failure in mice. To identify candidate genes responsible for infertility or recurrent pregnancy loss in humans, we performed expression profiling of male and female gonads of mice undergoing meiotic prophase I. Both male and female gonads at 15.5 days postcoitum, neonatal day 1 and 10 weeks postpartum were dissected from mice for RNA extraction and subjected to hybridization on Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Makiko Tsutsumi

PROVIDER: E-GEOD-35734 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Screening of genes involved in chromosome segregation during meiosis I: in vitro gene transfer to mouse fetal oocytes.

Tsutsumi Makiko M Kowa-Sugiyama Hiroe H Bolor Hasbaira H Kogo Hiroshi H Inagaki Hidehito H Ohye Tamae T Yamada Kouji K Taniguchi-Ikeda Mariko M Toda Tatsushi T Kurahashi Hiroki H

Journal of human genetics 20120531 8

The events that take place during the prophase of meiosis I are essential for the correct segregation of homologous chromosomes. Defects in these processes likely contribute to infertility or recurrent pregnancy loss in humans. To screen for candidate genes for reproductive failure due to meiotic defects, we have analyzed the gene expression patterns in fetal, neonatal and adult gonads of both male and female mice by microarray and thereby identified 241 genes that are expressed specifically dur ...[more]

PMID: 22648182

Similar Datasets

Screening of genes involved in chromosome segregation in meiosis I

Project description:Prophase I of meiosis involves dynamic chromosome segregation processes including synapsis, meiotic recombination, and cohesion. Genetic defects in genes participating in these processes consistently cause reproduction failure in mice. To identify candidate genes responsible for infertility or recurrent pregnancy loss in humans, we performed expression profiling of male and female gonads of mice undergoing meiotic prophase I.

2012-06-04 | GSE35734 | GEO

Screening of genes involved in chromosome segregation in meiosis I

2010-03-31 | GSE19532 | GEO

Screening of genes involved in chromosome segregation in meiosis I

Project description:Prophase I of male meiosis involves dynamic chromosome segregation processes during early spermatogenesis, including synapsis, meiotic recombination, and cohesion. Genetic defects in genes participating in these processes consistently cause reproduction failure in mice. To identify candidate genes responsible for infertility in humans, we performed expression profiling of mouse spermatogenic cells undergoing meiotic prophase I. Cell fractions enriched in spermatogonia, leptotene/zygotene spermatocytes, or pachytene spermatocytes were separately isolated from mouse testes for RNA extraction. To minimize the contamination of other cell types, we fractionated the testicular cells undergoing the first round of spermatogenesis using Percoll gradient procedure. The cell fractions were characterized by morphological analysis by phase contrast microscopy and Nomarski interference microscopy, and then expression of cell lineage- and spermatogenesis stage-specific genes were examined by RT-PCR. The most enriched fractions for spermatogonia (fraction2 from day8), leptotene/zygotene spermatocytes (fraction5 from day12), and pachytene spermatocytes (fraction8 from day15) were subjected to hybridization on Affymetrix microarrays.

2010-03-31 | E-GEOD-19532 | biostudies-arrayexpress

MEIOC interacting proteins during meiotic prophase I

Project description:The meiosis-specific chromosomal events of homolog pairing, synapsis, and recombination occur over an extended meiotic prophase I. In this study, we show that, in mice, maintenance of an extended meiotic prophase I requires the gene Meioc, a germ-cell specific factor conserved in most metazoans. Using immunoprecipitation and quantitative mass spectrometry, we identify proteins that interact with MEIOC in the mouse germ line.

2017-03-27 | PXD005473 | Pride

SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice [RNA-seq]

Project description:Homologous pairing and synapsis are essential in meiotic prophase I during spermatogenesis. However, the underlying mechanisms of how alternative splicing (AS) functions in homologous pairing and synapsis remain largely unclear. We reveal that SRSF1 is essential for gene expression and AS in homologous pairing and synapsis. Conditional knockout (cKO) of Srsf1 in mouse germ cells impaired homologous pairing and synapsis, leading to non-obstructive azoospermia (NOA). SRSF1 was required for initial homology recognition, telomere-led chromosome movement, and synaptonemal complex (SC) assembly. Moreover, SRSF1 interacted with TRA2B and U2AF2, directly binding and regulating the expression of Dmc1, Sycp1, Sun1, and Majin via AS to implement homologous pairing and synapsis during the meiotic prophase I program. Altogether, our data reveal the critical role of an SRSF1-mediated post-transcriptional regulatory mechanism in homologous pairing and synapsis during meiotic prophase I, providing a framework for elucidating the molecular mechanisms underlying the post-transcriptional network of male meiosis.

2024-01-09 | GSE227403 | GEO

SRSF1 is crucial for male meiosis through alternative splicing during homologous pairing and synapsis in mice [CLIP-seq]

2024-01-08 | GSE227303 | GEO

Expression data from gonads of Meioc+/+ and Meioc-/-mice

Project description:Meiosis is a specialized division that is specifically engaged in germ cells. This program is finely and dichotomically regulated: germ cells enter meiosis at fetal life in ovaries (13.5 dpc) and only at post-natal life in testes (8 dpp). We used microarrays to determine the gene expression modifications in Meioc mutant gonads displaying early meiotic defects. 14.5 dpc ovaries and 8 dpp testes from Meioc+/+ and Meioc-/- mice (NMRI) were dissected and processed for RNA extraction and hybridization on Affymetrix microarrays. Two pools were analysed for each genotype and each sex. We sought to constitutes pairs (A and B) of wild type and knock-out pools from embryos and pups that were homogenous for developmental stages and from matched littermates. 10 ovaries from 5 embryos composed each pool for females and 4 testes from 4 pups composed each pool for males.

2015-11-19 | E-GEOD-66880 | biostudies-arrayexpress

Dynamic Reorganization of the Genome Shapes the Recombination Landscape in Meiotic Prophase

Project description:In meiotic prophase, chromosomes are organized into compacted loop arrays to promote homolog pairing and recombination. Here, we probe the architecture of the mouse spermatocyte genome in early and late meiotic prophase using Hi-C. We show that early-prophase chromosomes are arranged as linear arrays of 0.8-1 Mb loops, which extend to 1.5-2 Mb in late prophase as chromosomes compact and homologs undergo synapsis. Topologically associating domains (TADs) are lost in meiotic prophase, suggesting that assembly of the meiotic chromosome axis dramatically reduces the dynamics of chromosome-associated cohesin complexes. While TADs are lost, physically-separated A and B compartments are maintained in meiotic prophase. Moreover, meiotic DNA breaks and inter-homolog crossovers preferentially form in the gene-dense A compartment, revealing a role for chromatin organization in meiotic recombination. Finally, direct detection of inter-homolog contacts genome-wide reveals the structural basis for homolog alignment and juxtaposition by the synaptonemal complex.

2018-11-17 | GSE122622 | GEO

SWI/SNF chromatin remodeling complex coordinates the meiotic gene activation via promoter remodeling and Meiosin activation in female germline

Project description:In mammals, primordial germ cells (PGCs) enter meiosis and differentiate to primary oocytes in embryonic ovaries. Previously, we demonstrated that SWI/SNF chromatin remodeling complex is required for induction of the meiotic prophase genes and meiotic initiation in female germline, using conditional knockout (CKO) mice lacking the Smarcb1 (also known as Snf5) gene, which encodes a core subunit of the SWI/SNF complex. Here, we show that the meiotic prophase genes expressed at lower levels in the Snf5 CKO females can be classified into two groups, based on the promoter accessibility. The promoters of 74% of these genes showed lower accessibility in the mutant mice whereas those of remaining genes were opened equivalently in control and the mutant mice. The former genes include the Meiosin that encodes the transcription regulator essential for activation of the meiotic prophase genes. Furthermore, the promoters of the former and the latter genes were largely modified with H3K27me3/bivalent histone marks and H3K4me3, respectively. Collectively, we provide the mechanistic model by which SWI/SNF complex remodels the meiotic prophase genes repressed by polycomb repressive complex (PRC), including the Meiosin, and then MEIOSIN together with STRA8 activates the meiotic prophase genes in female germline.

2022-11-17 | GSE203588 | GEO

TOPBP1 Shapes XY Silencing Dynamics Independently of Sex Body Formation to Ensure Male Fertility

Project description:In mammals and several other taxa, the ability of males to cope with the limited synapsis of the X and Y chromosomes during prophase I of meiosis relies on the process of meiotic sex chromosome inactivation (MSCI). Components of the somatic DNA damage response machinery, including ATR, TOPBP1, MDC1 and BRCA1 play key roles in MSCI, although how they establish XY silencing remains incompletely understood. In particular, it remains unclear how DDR factors coordinate XY silencing with DNA repair, chromosome synapsis and the formation of the sex body, a distinct phase-separated sub-nuclear structure formed during prophase I to house the unsynapsed XY bivalent. Here we report a mutant mouse (Topbp1B5/B5), harboring mutations in the BRCT5 domain of Topbp1, that shows impaired XY silencing but grossly normal sex body formation. While Topbp1B5/B5 mice are viable, without detectable somatic defects, males are completely infertile. Distinct from mice lacking ATR or TOPBP1 specifically during meiosis, Topbp1B5/B5 males exhibit normal chromosome synapsis and canonical markers of DNA repair in early prophase I. ATR signaling is mostly intact in Topbp1B5/B5 spermatocytes, although specific ATR-dependent events are disrupted, including localization of the RNA:DNA helicase Senataxin to chromatin loops of the XY. Strikingly, while Topbp1B5/B5 spermatocytes are able to initiate MSCI the completion of gene silencing is defective, with a subset of X chromosome genes displaying distinct patterns of transcriptional deregulation. These findings suggest a non-canonical role for the ATR-TOPBP1 signaling axis in XY silencing dynamics at advanced stages in pachynema. This is the first DDR mutant that separates XY silencing from sex body formation, as well as TOPBP1’s role in spermatogenesis from its roles in organismal viability.

2024-02-09 | PXD042199 | Pride

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