Dicer interacts with SIRT7 and regulates H3K18 deacetylation in response to DNA damaging agents

doi:10.1093/nar/gkv1504

科研成果详情

题名	Dicer interacts with SIRT7 and regulates H3K18 deacetylation in response to DNA damaging agents
作者	Zhang, Pei-Ying 1,2; Li, Guiling3; Deng, Zhu-Jun 1,2; Liu, Li-Yuan 4; Chen, Li 1,2; Tang, Jun-Zhou 5; Wang, Yu-Qun4; Cao, Su-Ting4; Fang, Yu-Xiao 1,2; Wen, Fuping 1; Xu, Yunsheng1,6; Chen, Xiaoming 1,7; Shi, Ke-Qing4; Li, Wen-Feng8; Xie, Congying8; Tang, Kai-Fu1,2,3
发表日期	2016-05-05
发表期刊	NUCLEIC ACIDS RESEARCH 影响因子和分区
语种	英语
原始文献类型	Article
其他关键词	RNA-POLYMERASE-I ; GENE-EXPRESSION ; STRESS ; COMPLEXES ; HETEROCHROMATIN ; RECOMBINATION ; INTERFERENCE ; RIBONUCLEASE ; METHYLATION ; BIOGENESIS
摘要	Dicer participates in heterochromatin formation in fission yeast and plants. However, whether it has a similar role in mammals remains controversial. Here we showed that the human Dicer protein interacts with SIRT7, an NAD(+)-dependent H3K18Ac (acetylated lysine 18 of histone H3) deacetylase, and holds a proportion of SIRT7 in the cytoplasm. Dicer knockdown led to an increase of chromatin-associated SIRT7 and simultaneously a decrease of cytoplasmic SIRT7, while its overexpression induced SIRT7 reduction in the chromatin-associated fraction and increment in the cytoplasm. Furthermore, DNA damaging agents promoted Dicer expression, leading to decreased level of chromatin-associated SIRT7 and increased level of H3K18Ac, which can be alleviated by Dicer knockdown. Taken together with that H3K18Ac was exclusively associated with the chromatin, our findings suggest that Dicer induction by DNA damaging treatments prevents H3K18Ac deacetylation, probably by trapping more SIRT7 in the cytoplasm.
资助项目	National Sciences Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81171967, 31271383, 81572780, 31200976]; National Major Special Science and Technology Project [2013ZX10002002]; Zhejiang Provincial National Sciences Foundation [LZ16H160004]
出版者	OXFORD UNIV PRESS
出版地	OXFORD
ISSN	0305-1048
EISSN	1362-4962
卷号	44 期号:8 页码:3629-3642
DOI	10.1093/nar/gkv1504
页数	14
WOS类目	Biochemistry & Molecular Biology
WOS研究方向	Biochemistry & Molecular Biology
WOS记录号	WOS:000376389000022
收录类别	SCIE ; PUBMED ; SCOPUS
URL	查看原文
PubMed ID	26704979
PMC记录号	PMC4856966
SCOPUSEID	2-s2.0-84966392085
自科自定义期刊分类	T3(B)类
通讯作者地址	[Tang, Kai-Fu]Institute of Translational Medicine,Hospital of Wenzhou Medical University,Wenzhou,325015,China
Scopus学科分类	Genetics
TOP期刊	TOP期刊
引用统计	被引频次：46[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/18597
专题	温州医科大学基因组医学研究院其他_浙江省肿瘤医院（浙江省癌症中心）
通讯作者	Tang, Kai-Fu
作者单位	1.Institute of Translational Medicine,Hospital of Wenzhou Medical University,Wenzhou,325015,China; 2.Cancer Center,Hospital of Wenzhou Medical University,Wenzhou,325015,China; 3.Institute of Genomic Medicine,Wenzhou Medical University,Wenzhou,325015,China; 4.Department of Infection and Liver Diseases,Hospital of Wenzhou Medical University,Wenzhou,325015,China; 5.Research Institute of Surgery,Daping Hospital,Third Military Medical University,Chongqing,400042,China; 6.Department of Dermato-Venereology,Hospital of Wenzhou Medical University,Wenzhou,325015,China; 7.Department of Pediatric Surgery,Hospital of Wenzhou Medical University,Wenzhou,325015,China; 8.Department of Radiation Oncology,Hospital of Wenzhou Medical University,Wenzhou,325015,China
第一作者单位	温州医科大学; 其他_浙江省肿瘤医院（浙江省癌症中心）
通讯作者单位	温州医科大学
第一作者的第一单位	温州医科大学
推荐引用方式 GB/T 7714	Zhang, Pei-Ying,Li, Guiling,Deng, Zhu-Jun,et al. Dicer interacts with SIRT7 and regulates H3K18 deacetylation in response to DNA damaging agents[J]. NUCLEIC ACIDS RESEARCH,2016,44(8):3629-3642.
APA	Zhang, Pei-Ying., Li, Guiling., Deng, Zhu-Jun., Liu, Li-Yuan., Chen, Li., ... & Tang, Kai-Fu. (2016). Dicer interacts with SIRT7 and regulates H3K18 deacetylation in response to DNA damaging agents. NUCLEIC ACIDS RESEARCH, 44(8), 3629-3642.
MLA	Zhang, Pei-Ying,et al."Dicer interacts with SIRT7 and regulates H3K18 deacetylation in response to DNA damaging agents".NUCLEIC ACIDS RESEARCH 44.8(2016):3629-3642.