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Upregulation of PHLDA2 in Dicer knockdown HEK293 cells

文献类型:期刊论文

作者Tang, Kai-Fu; Wang, Yan; Wang, Pengfei; Chen, Min; Chen, Yao; Hu, Huai-Dong; Hu, Peng; Wang, Bo; Yang, Wenjie; Ren, Hong
刊名BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
出版日期2007-05-01
卷号1770期号:5页码:820-825
关键词PHLDA2 Dicer genomic imprinting embryonic lethality growth arrest
ISSN号0304-4165
文献子类Article
英文摘要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.
学科主题系统生物学/生物信息学
语种英语
WOS记录号WOS:000245832500011
公开日期2011-08-22
源URL[http://ir.psych.ac.cn/handle/311026/5827]  
专题心理研究所_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
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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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来源:心理研究所

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