HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: M800123-MCP200v1 8/3/481    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Glossary Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lu, H. Articles by Hua, Y. Search for Related Content PubMed PubMed Citation Articles by Lu, H. Articles by Hua, Y. Social Bookmarking                      What's this?

Molecular & Cellular Proteomics 8:481-494, 2009.
© 2009 by The American Society for Biochemistry and Molecular Biology, Inc.

---

Research

Deinococcus radiodurans PprI Switches on DNA Damage Response and Cellular Survival Networks after Radiation Damage^*,S

Huiming Lu^,,¶, Guanjun Gao^,¶,||, Guangzhi Xu, Lu Fan, Longfei Yin, Binghui Shen^, and Yuejin Hua^,**

From the Institute of Nuclear-Agricultural Sciences, Key Laboratory of Chinese Ministry of Agriculture for Nuclear-Agricultural Sciences, Zhejiang University, Hangzhou 310029, China and Department of Radiation Biology, City of Hope National Medical Center and Beckman Research Institute, Duarte, California 91010

Preliminary findings indicate that PprI is a regulatory protein that stimulates transcription and translation of recA and other DNA repair genes in response to DNA damage in the extremely radioresistant bacterium Deinococcus radiodurans. To define the repertoire of proteins regulated by PprI and investigate the in vivo regulatory mechanism of PprI in response to radiation, we performed comparative proteomics analyses on wild type (R1) and a pprI knock-out strain (YR1) under conditions of ionizing irradiation. Results of two-dimensional electrophoresis and MALDI-TOF MS or MALDI-TOF/TOF MS indicated that in response to low dose ray exposure 31 proteins were significantly up-regulated in the presence of PprI. Among them, RecA and PprA are well known for their roles in DNA replication and repair. Others are involved in six different pathways, including stress response, energy metabolism, transcriptional regulation, signal transduction, protein turnover, and chaperoning. The last group consists of many proteins with uncharacterized functions. Expression of an additional four proteins, most of which act in metabolic pathways, was down-regulated in irradiated R1. Additionally phosphorylation of two proteins was under the control of PprI in response to irradiation. The different functional roles of representative PprI-regulated genes in extreme radioresistance were validated by gene knock-out analysis. These results suggest a role, either directly or indirectly, for PprI as a general switch to efficiently enhance the DNA repair capability and extreme radioresistance of D. radiodurans via regulation of a series of pathways.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				M. Baudet, P. Ortet, J.-C. Gaillard, B. Fernandez, P. Guerin, C. Enjalbal, G. Subra, A. de Groot, M. Barakat, A. Dedieu, et al. Proteomics-based Refinement of Deinococcus deserti Genome Annotation Reveals an Unwonted Use of Non-canonical Translation Initiation Codons Mol. Cell. Proteomics, February 1, 2010; 9(2): 415 - 426. [Abstract] [Full Text] [PDF]

				D. Sheng, J. Jao, M. Li, P. Xu, and J. Zhang RecX is Involved In the Switch between DNA Damage Response and Normal Metabolism in D. radiodurans J. Biochem., September 1, 2009; 146(3): 337 - 342. [Abstract] [Full Text] [PDF]