SYMPK is essential for meiosis in mouse germ cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE133155 | GEO | 2019/06/22
REPOSITORIES: GEO
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Project description:Male germ cell meiosis is essential for generating haploid spermatozoa in mice. Here, we investigate the essential role of DIS3 in male germ cell meiosis in mice. Conditional inactivation of DIS3 in spermatocytes with Stra8-cre transgenic mice have severely impaired meiotic progression, which results in defective meiosis and spermatogenesis. RNA-seq analysis reveals that Dis3 deficiency causes significant dysregulation of the expression of transcripts in mutant testes. Meiosis-associated genes are significantly decreased in the absence of DIS3. Therefore, we show that DIS3 ribonuclease plays a critical role in germ cell meiosis during spermatogenesis in mice.
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Project description:SYMPK is essential for meiosis in mouse germ cells
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Project description:Germ cell connectivity via intercellular bridges is a widely conserved feature but its functional significance is poorly understood. Intercellular bridges are essential for fertility in male mice as genetic ablation of a critical bridge component, TEX14, causes loss of germ cell connectivity and meiotic failure, however the underlying reasons are unknown. A screen for meiosis-defective mouse mutants yielded a sterile mutant harboring a point mutation in Tex14 that leads to a partial loss of germ cell intercellular bridges. We utilized the Tex14 hypomorphs with reduced intercellular bridges, along with Tex14-null mice that completely lack bridges to examine the roles of germ cell connectivity during adult spermatogenesis. Complete or partial loss of intercellular bridges does not severely deplete spermatogonia, but spermatocytes are unable to undergo meiotic DNA replication and enter meiotic prophase. Phenotypic severity correlates with the extent of intercellular bridge depletion, with Tex14 hypomorphs containing a relatively larger number of spermatocytes undergoing meiosis, thus allowing us to assess impacts on meiotic progression. Tex14-deficient germ cells that enter prophase form meiotic breaks and initiate synapsis, but later exhibit synaptic failures and retain unrepaired breaks. Strikingly, Tex14-deficient germ cells derepress LINE1 retrotransposons and accumulate LINE1-encoded proteins during meiosis. Single-cell RNA-sequencing of testes from Tex14 hypomorphs show that intercellular bridge depletion modestly impacts the RNA landscape in early germ cell stages, while mutant cells that progress to late spermatocyte and post-meiotic spermatid stages broadly upregulate retrotransposons and dysregulate gene expression. RNA-sequencing confirms extensive sharing of transcripts between normal spermatids and demonstrates its partial attenuation in Tex14 hypomorphs, indicating that intercellular bridges enable exchange of cytoplasmic material between connected germ cells in testes. Tex14 hypomorphs display a progressive decline in germ cell numbers starting from the spermatocyte stage, with a complete lack of elongating spermatids, and are therefore sterile. Our findings reveal that the regulation of meiosis is non-cell-intrinsic and inform a model in which intercellular bridges orchestrate critical meiotic events and protect germline genome integrity during spermatogenesis, possibly by facilitating the exchange of regulatory factors.
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Project description:In many metazoans, germ cells are separated from somatic lineages early in development and maintain their identity throughout life. Here we show that a Polycomb group (PcG) component, Enhancer of Zeste [E(z)] H3K27me3-specific methyltransferase, maintains germline identity in Drosophila adult testes. We find excessive early-stage somatic gonadal cells in E(z) mutant testes, which originate from both over-proliferative cyst stem cells and germ cells turning on an early-stage somatic cell marker. Using complementary lineage-tracing experiments in E(z) mutant testes, a portion of excessive early-stage somatic gonadal cells are found to derive from early-stage germ cells, including germline stem cells. Interestingly, knocking down E(z) specifically in somatic cells caused this germline-to-soma change, suggesting a non-cell autonomous role of E(z) to antagonize somatic identity in germ cells. Using fly testis specifically expressing E(z) shmiR RNAi in germ cells by nos promoter driven GAL4>UAS system, ChIPseq with H3K27me3 antibody was performed, where H3K27me3 is only detected in somatic cells.
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