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Overview on Peroxiredoxin.过氧化物酶体增殖物激活受体概述。
Mol Cells. 2016 Jan;39(1):1-5. doi: 10.14348/molcells.2016.2368.
2
The Functional Analysis of Histone Acetyltransferase MOF in Tumorigenesis.组蛋白乙酰转移酶MOF在肿瘤发生中的功能分析
Int J Mol Sci. 2016 Jan 14;17(1):99. doi: 10.3390/ijms17010099.
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Transcript Quantification by RNA-Seq Reveals Differentially Expressed Genes in the Red and Yellow Fruits of Fragaria vesca.通过RNA测序进行转录本定量分析揭示了野草莓红果和黄果中差异表达的基因。
PLoS One. 2015 Dec 4;10(12):e0144356. doi: 10.1371/journal.pone.0144356. eCollection 2015.
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LSD1 is essential for oocyte meiotic progression by regulating CDC25B expression in mice.在小鼠中，赖氨酸特异性去甲基化酶1（LSD1）通过调节细胞周期蛋白依赖性激酶25B（CDC25B）的表达对卵母细胞减数分裂进程至关重要。
Nat Commun. 2015 Dec 2;6:10116. doi: 10.1038/ncomms10116.
5
Sirt6 depletion causes spindle defects and chromosome misalignment during meiosis of mouse oocyte.沉默调节蛋白6缺失导致小鼠卵母细胞减数分裂过程中纺锤体缺陷和染色体排列异常。
Sci Rep. 2015 Oct 20;5:15366. doi: 10.1038/srep15366.
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Apoptosis in mammalian oocytes: a review.哺乳动物卵母细胞中的细胞凋亡：综述
Apoptosis. 2015 Aug;20(8):1019-25. doi: 10.1007/s10495-015-1136-y.
7
miR-214-mediated downregulation of RNF8 induces chromosomal instability in ovarian cancer cells.miR-214介导的RNF8下调诱导卵巢癌细胞中的染色体不稳定。
Cell Cycle. 2014;13(22):3519-28. doi: 10.4161/15384101.2014.958413.
8
N-acetylcysteine improves function and follicular survival in mice ovarian grafts through inhibition of oxidative stress.N-乙酰半胱氨酸通过抑制氧化应激改善小鼠卵巢移植后的功能及卵泡存活率。
Reprod Biomed Online. 2015 Jan;30(1):101-10. doi: 10.1016/j.rbmo.2014.09.013. Epub 2014 Oct 7.
9
Depletion of pericentrin in mouse oocytes disrupts microtubule organizing center function and meiotic spindle organization.小鼠卵母细胞中中心蛋白的缺失会破坏微管组织中心功能和减数分裂纺锤体组织。
Mol Reprod Dev. 2014 Nov;81(11):1019-29. doi: 10.1002/mrd.22422. Epub 2014 Sep 29.
10
Adenanthin targets peroxiredoxin I/II to kill hepatocellular carcinoma cells.腺嘌呤靶向过氧化物还原酶I/II以杀死肝癌细胞。
Cell Death Dis. 2014 Sep 4;5(9):e1400. doi: 10.1038/cddis.2014.345.

组蛋白乙酰转移酶KAT8通过调节活性氧水平对小鼠卵母细胞发育至关重要。

Histone acetyltransferase KAT8 is essential for mouse oocyte development by regulating reactive oxygen species levels.

作者信息

Yin Shi, Jiang Xiaohua, Jiang Hanwei, Gao Qian, Wang Fang, Fan Suixing, Khan Teka, Jabeen Nazish, Khan Manan, Ali Asim, Xu Peng, Pandita Tej K, Fan Heng-Yu, Zhang Yuanwei, Shi Qinghua

机构信息

Molecular and Cell Genetics Laboratory, The CAS Key Laboratory of Innate Immunity and Chronic Diseases, Hefei National Laboratory for Physical Sciences at Microscale, School of Life Sciences, CAS Center for Excellence in Molecular Cell Science, University of Science and Technology of China, Collaborative Innovation Center of Genetics and Development, Collaborative Innovation Center for Cancer Medicine, Hefei, Anhui 230027, China.

USTC-Shenyang Jinghua Hospital Joint Center of Human Reproduction and Genetics, Shenyang, Liaoning 110000, China.

出版信息

Development. 2017 Jun 15;144(12):2165-2174. doi: 10.1242/dev.149518. Epub 2017 May 15.

DOI:10.1242/dev.149518
PMID:28506985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5482993/
Abstract

Proper oocyte development is crucial for female fertility and requires timely and accurate control of gene expression. K (lysine) acetyltransferase 8 (KAT8), an important component of the X chromosome dosage compensation system in , regulates gene activity by acetylating histone H4 preferentially at lysine 16. To explore the function of KAT8 during mouse oocyte development, we crossed mice with mice to specifically delete in oocytes. Oocyte deletion resulted in female infertility, with follicle development failure in the secondary and preantral follicle stages. RNA-seq analysis revealed that deficiency in oocytes results in significant downregulation of antioxidant genes, with a consequent increase in reactive oxygen species. Intraperitoneal injection of the antioxidant N-acetylcysteine rescued defective follicle and oocyte development resulting from deficiency. Chromatin immunoprecipitation assays indicated that KAT8 regulates antioxidant gene expression by direct binding to promoter regions. Taken together, our findings demonstrate that KAT8 is essential for female fertility by regulating antioxidant gene expression and identify KAT8 as the first histone acetyltransferase with an essential function in oogenesis.

摘要

适当的卵母细胞发育对于女性生育能力至关重要，并且需要对基因表达进行及时且准确的调控。赖氨酸（K）乙酰转移酶8（KAT8）是[物种名称未给出]中X染色体剂量补偿系统的重要组成部分，它通过优先在赖氨酸16位点乙酰化组蛋白H4来调节基因活性。为了探究KAT8在小鼠卵母细胞发育过程中的功能，我们将[小鼠品系1未给出]小鼠与[小鼠品系2未给出]小鼠杂交，以在卵母细胞中特异性删除[KAT8未给出]。卵母细胞中[KAT8未给出]的缺失导致雌性不育，在次级卵泡和窦前卵泡阶段卵泡发育失败。RNA测序分析表明，卵母细胞中[KAT8未给出]的缺乏导致抗氧化基因显著下调，从而使活性氧增加。腹腔注射抗氧化剂N - 乙酰半胱氨酸挽救了因[KAT8未给出]缺乏而导致的卵泡和卵母细胞发育缺陷。染色质免疫沉淀分析表明，KAT8通过直接结合启动子区域来调节抗氧化基因的表达。综上所述，我们的研究结果表明，KAT8通过调节抗氧化基因表达对雌性生育能力至关重要，并确定KAT8是首个在卵子发生中具有重要功能的组蛋白乙酰转移酶。