Upregulation of PHLDA2 in Dicer knockdown HEK293 cells

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	Upregulation of PHLDA2 in Dicer knockdown HEK293 cells
	Tang, Kai-Fu ; Wang, Yan ; Wang, Pengfei ; Chen, Min ; Chen, Yao ; Hu, Huai-Dong ; Hu, Peng ; Wang, Bo ; Yang, Wenjie ; Ren, Hong ; K. F. Tang ; H. Ren
摘要	It has been reported that RNAi-dependent chromatin silencing in vertebrates is not restricted to the centromeres. To address whether RNAi machinery could regulate the chromatin structure of imprinted genes, we knocked down Dicer in HEK293 cells and found that the expression of PHLDA2, one of the several genes in the imprinted gene domain of 11p15.5, was specifically upregulated. This was accompanied by a shift towards more activated chromatin at PHLDA2 locus as indicated by change in H3K9 acetylation, however, the methylation state at this locus was not affected. Furthermore, we found that PHLDA2 was downregulated in growth-arrested HEK293 cells induced by either serum deprivation or contact inhibition. This suggests that PHLDA2 upregulation might be a direct result of Dicer depletion rather than the consequence of growth arrest induced by Dicer knockdown. Considering the reports that there is consistent placental outgrowth in PHLDA2 knockout mice and that PHLDA2 overexpression in mice causes growth inhibition, we speculate that PHLDA2 may be a candidate for contributing to the reduced growth rate of Dicer-deficient cells and the very early embryonic lethality in Dicer knockout mice.; It has been reported that RNAi-dependent chromatin silencing in vertebrates is not restricted to the centromeres. To address whether RNAi machinery could regulate the chromatin structure of imprinted genes, we knocked down Dicer in HEK293 cells and found that the expression of PHLDA2, one of the several genes in the imprinted gene domain of 11p15.5, was specifically upregulated. This was accompanied by a shift towards more activated chromatin at PHLDA2 locus as indicated by change in H3K9 acetylation, however, the methylation state at this locus was not affected. Furthermore, we found that PHLDA2 was downregulated in growth-arrested HEK293 cells induced by either serum deprivation or contact inhibition. This suggests that PHLDA2 upregulation might be a direct result of Dicer depletion rather than the consequence of growth arrest induced by Dicer knockdown. Considering the reports that there is consistent placental outgrowth in PHLDA2 knockout mice and that PHLDA2 overexpression in mice causes growth inhibition, we speculate that PHLDA2 may be a candidate for contributing to the reduced growth rate of Dicer-deficient cells and the very early embryonic lethality in Dicer knockout mice. (c) 2007 Elsevier B.V. All rights reserved.
关键词	PHLDA2 Dicer genomic imprinting embryonic lethality growth arrest
学科领域	系统生物学/生物信息学
	2007-05-01
语种	英语
发表期刊	BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
ISSN	0304-4165
卷号	1770 期号:5 页码:820-825
期刊论文类型	Article
收录类别	SCI
WOS记录号	WOS:000245832500011
引用统计	被引频次：12[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	http://ir.psych.ac.cn/handle/311026/5827
专题	中国科学院心理研究所回溯数据库(1956-2010)
通讯作者	K. F. Tang; H. Ren
作者单位	1.Chongqing Med Univ, Inst Viral Hepatitis, Affiliated Hosp 2, Key Lab Mol Biol Infect Dis,State Minist Educ, Chongqing 400010, Peoples R China 2.Chongqing Med Univ, Dept Emergency, Affiliated Hosp 2, Chongqing 400010, Peoples R China 3.Chongqing Med Univ, Dept Endocrinol, Affiliated Hosp 2, Chongqing 400010, Peoples R China 4.Chinese Acad Sci, Inst Psychol, Beijing 100101, Peoples R China 5.Tulane Univ, Sch Publ Hlth & Trop Med, Dept Epidemiol, New Orleans, LA 70112 USA
推荐引用方式 GB/T 7714	Tang, Kai-Fu,Wang, Yan,Wang, Pengfei,et al. Upregulation of PHLDA2 in Dicer knockdown HEK293 cells[J]. BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS,2007,1770(5):820-825.
APA	Tang, Kai-Fu.,Wang, Yan.,Wang, Pengfei.,Chen, Min.,Chen, Yao.,...&H. Ren.(2007).Upregulation of PHLDA2 in Dicer knockdown HEK293 cells.BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS,1770(5),820-825.
MLA	Tang, Kai-Fu,et al."Upregulation of PHLDA2 in Dicer knockdown HEK293 cells".BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS 1770.5(2007):820-825.

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