Kaiso, a critical regulator of spermatogenesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA436947 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6806314_1.fastq.gz | Fastqsanger.gz | |||
| SRR6806314_2.fastq.gz | Fastqsanger.gz | |||
| SRR6806315_1.fastq.gz | Fastqsanger.gz | |||
| SRR6806315_2.fastq.gz | Fastqsanger.gz |
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Project description:Spermatogenesis is a highly coordinated process by which diploid spermatogonia (2n) differentiate into mature haploid (1n) spermatozoa in the seminiferous epithelium. Here, we show that Kaiso (Zbtb33) is critical to spermatogenesis, via binding to KBEs (Kaiso-binding elements) in the 5’ upstream regulatory regions of Gdnf and Plzf to repress their expression, promoting the differentiation of spermatogonial stem cells (SSCs). In Kaiso-/Y mice, Plzf and Gdnf were derepressed in both SSCs and Sertoli cells, explaining the increased number of SSCs observed in these abnormal mice. We also found that Bcl6, an antiapoptotic spermatocyte survival factor, represses the Crem pathway genes. In particular, Kaiso represses Bcl6 by binding two KBEs in the Bcl6 5’ upstream regulatory region and first intron, thus indirectly derepressing Crem and Crem pathway genes. In Kaiso-/Y mice, Bcl6 is overexpressed, and these mice lack differentiated post-mitotic cells and consequently, are infertile. Interestingly, epigenetic “marks,” histone post-translational modifications such as lysine methylation, within histone H3 (H3K27me3), of the promoters of Kaiso target genes, were found transgenerationally heritable, prior to “wash out” during generations 1-3 in Kaiso-/Y mice, thus impacting Kaiso target gene expression. Consequently, Kaiso, by repressing Plzf, Gdnf, and Bcl6, indirectly upregulates Crem, and thereby plays a critical role not only in SSC differentiation, but also in post-meiotic events during spermatogenesis.
2021-03-05 | GSE111409 | GEO
Project description:Absence of the epigenetic regulator Kaiso suppresses Wnt driven intestinal tumourigenesis. To identify genes regulated by Kaiso we generated wild type and Kaiso-/- mice for microarray expression analysis to identify genes derepressed in the absence of Kaiso.
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Project description:The mammalian Y chromosome plays a critical role in spermatogenesis. However, the exact functions of each gene in the Y chromosome have not been completely elucidated, partly owing to difficulties in gene targeting analysis for the Y chromosome. Zfy was first proposed to be a sex determination factor, but its function in spermatogenesis has been recently elucidated. Nevertheless, Zfy gene targeting analysis has not been performed thus far. Here, we adopted the highly efficient CRISPR/Cas9 system to generate individual Zfy1 or Zfy2 knockout (KO) mice, and Zfy1 and Zfy2 double knockout (Zfy1/2-DKO) mice. While individual Zfy1 or Zfy2-KO mice did not show any significant phenotypic alterations in fertility, Zfy1/2-DKO mice were infertile and displayed abnormal sperm morphology, fertilization failure, and early embryonic development failure. Mass spectrometric screening, followed by confirmation with western blot analysis, showed that PLCZ1, PLCD4, PRSS21, and HTT protein expression was significantly deceased in spermatozoa from Zfy1/2-DKO mice compared with those from wild type mice. These results are consistent with the phenotypic changes seen in the double mutant mice. Collectively, our strategy and findings revealed that Zfy1 and Zfy2 have redundant functions in spermatogenesis, facilitating a better understanding of fertilization failure and early embryonic development failure.
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