SETDB1 Regulates Porcine Spermatogonial Adhesion and Proliferation through Modulating MMP3/10 Transcription

Liu, Ruifang; Liu, Zidong; Guo, Ming; Zheng, Yi

doi:10.3390/cells11030370

Cited by 4 publications

(1 citation statement)

References 52 publications

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“…Setdb1, also termed ESET, is a histone methyltransferase and it participates in silencing genes through H3K9 trimethylation in the promoter region [ 9 ]. Setdb1 is involved in many pathological and physiological processes, such as carcinogenesis [ 10 , 11 ], cell lineage differentiation during embryogenesis [ 12 ], X chromosome inactivation [ 13 ], and transcriptional regulation [ 14 , 15 ]. Importantly, several studies have reported that Setdb1 plays a crucial role in bone formation.…”

Section: Introductionmentioning

confidence: 99%

Methyltransferase Setdb1 Promotes Osteoblast Proliferation by Epigenetically Silencing Macrod2 with the Assistance of Atf7ip

Zhang

et al. 2022

Cells

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Bone loss caused by mechanical unloading is a threat to prolonged space flight and human health. Epigenetic modifications play a crucial role in varied biological processes, but the mechanism of histone modification on unloading-induced bone loss has rarely been studied. Here, we discovered for the first time that the methyltransferase Setdb1 was downregulated under the mechanical unloading both in vitro and in vivo so as to attenuate osteoblast proliferation. Furthermore, we found these interesting processes depended on the repression of Macrod2 expression triggered by Setdb1 catalyzing the formation of H3K9me3 in the promoter region. Mechanically, we revealed that Macrod2 was upregulated under mechanical unloading and suppressed osteoblast proliferation through the GSK-3β/β-catenin signaling pathway. Moreover, Atf7ip cooperatively contributed to osteoblast proliferation by changing the localization of Setdb1 under mechanical loading. In summary, this research elucidated the role of the Atf7ip/Setdb1/Macrod2 axis in osteoblast proliferation under mechanical unloading for the first time, which can be a potential protective strategy against unloading-induced bone loss.

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Section: Introductionmentioning

confidence: 99%

Methyltransferase Setdb1 Promotes Osteoblast Proliferation by Epigenetically Silencing Macrod2 with the Assistance of Atf7ip

Zhang

et al. 2022

Cells

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The functions of SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) in biological process and disease

Luo,

Wu,

Zhu

et al. 2023

Epigenetics & Chromatin

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Histone methyltransferase SETDB1 (SET domain bifurcated histone lysine methyltransferase 1, also known as ESET or KMT1E) is known to be involved in the deposition of the di- and tri-methyl marks on H3K9 (H3K9me2 and H3K9me3), which are associated with transcription repression. SETDB1 exerts an essential role in the silencing of endogenous retroviruses (ERVs) in embryonic stem cells (mESCs) by tri-methylating H3K9 (H3K9me3) and interacting with DNA methyltransferases (DNMTs). Additionally, SETDB1 is engaged in regulating multiple biological processes and diseases, such as ageing, tumors, and inflammatory bowel disease (IBD), by methylating both histones and non-histone proteins. In this review, we provide an overview of the complex biology of SETDB1, review the upstream regulatory mechanisms of SETDB1 and its partners, discuss the functions and molecular mechanisms of SETDB1 in cell fate determination and stem cell, as well as in tumors and other diseases. Finally, we discuss the current challenges and prospects of targeting SETDB1 for the treatment of different diseases, and we also suggest some future research directions in the field of SETDB1 research.

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Deletion of Hnrnpk Gene Causes Infertility in Male Mice by Disrupting Spermatogenesis

Guo

et al. 2022

Cells

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HnRNPK is a heterogeneous nuclear ribonucleoprotein (hnRNP) that has been firmly implicated in transcriptional and post-transcriptional regulation. However, the molecular mechanisms by which hnRNPK orchestrates transcriptional or post-transcriptional regulation are not well understood due to early embryonic lethality in homozygous knockout mice, especially in a tissue-specific context. Strikingly, in this study, we demonstrated that hnRNPK is strongly expressed in the mouse testis and mainly localizes to the nucleus in spermatogonia, spermatocytes, and round spermatids, suggesting an important role for hnRNPK in spermatogenesis. Using a male germ cell-specific hnRNPK-depleted mouse model, we found that it is critical for testicular development and male fertility. The initiation of meiosis of following spermatogenesis was not affected in Hnrnpk cKO mice, while most germ cells were arrested at the pachytene stage of the meiosis and no mature sperm were detected in epididymides. The further RNA-seq analysis of Hnrnpk cKO mice testis revealed that the deletion of hnRNPK disturbed the expression of genes involved in male reproductive development, among which the meiosis genes were significantly affected, and Hnrnpk cKO spermatocytes failed to complete the meiotic prophase. Together, these results identify hnRNPK as an essential regulator of spermatogenesis and male fertility.

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SETDB1 Regulates Porcine Spermatogonial Adhesion and Proliferation through Modulating MMP3/10 Transcription

Cited by 4 publications

References 52 publications

Methyltransferase Setdb1 Promotes Osteoblast Proliferation by Epigenetically Silencing Macrod2 with the Assistance of Atf7ip

Methyltransferase Setdb1 Promotes Osteoblast Proliferation by Epigenetically Silencing Macrod2 with the Assistance of Atf7ip

The functions of SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) in biological process and disease

Deletion of Hnrnpk Gene Causes Infertility in Male Mice by Disrupting Spermatogenesis

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