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* Environmental Sciences and ** Life Sciences Divisions, Oak Ridge
National Laboratory, Oak Ridge, TN 37831; Communicated by Todd R. Klaenhammer, North Carolina State
University, Raleigh, NC, January 22, 2003 (received for review October
14, 2002)
Deinococcus radiodurans R1 (DEIRA) is a
bacterium best known for its extreme resistance to the lethal effects
of ionizing radiation, but the molecular mechanisms underlying this
phenotype remain poorly understood. To define the repertoire of DEIRA
genes responding to acute irradiation (15 kGy), transcriptome dynamics were examined in cells representing early, middle, and late phases of
recovery by using DNA microarrays covering
Microbiology
Transcriptome dynamics of Deinococcus radiodurans
recovering from ionizing radiation
,
,
,
,
,
,
, and
Center for
Microbial Ecology, Michigan State University, East
Lansing, MI 48824; 
Center for
Biotechnology Information, National Institutes of Health, Bethesda, MD
20894; and § Uniformed Services University of the Health
Sciences, Bethesda, MD 20814
94% of its predicted genes. At least at one time point during DEIRA recovery, 832 genes (28% of the genome) were induced and 451 genes (15%) were repressed 2-fold or more. The expression patterns of the majority of the induced
genes resemble the previously characterized expression profile of
recA after irradiation. DEIRA recA, which is
central to genomic restoration after irradiation, is substantially
up-regulated on DNA damage (early phase) and down-regulated before the
onset of exponential growth (late phase). Many other genes were
expressed later in recovery, displaying a growth-related pattern of
induction. Genes induced in the early phase of recovery included those
involved in DNA replication, repair, and recombination, cell wall
metabolism, cellular transport, and many encoding uncharacterized
proteins. Collectively, the microarray data suggest that DEIRA cells
efficiently coordinate their recovery by a complex network, within
which both DNA repair and metabolic functions play critical roles.
Components of this network include a predicted distinct ATP-dependent
DNA ligase and metabolic pathway switching that could prevent
additional genomic damage elicited by metabolism-induced free radicals.
Y.L. and J.Z. contributed equally to this work.
To whom correspondence should be addressed regarding
microarray analysis and reprints. E-mail: zhouj{at}ornl.gov.
¶
Present address: Biological Sciences Division,
Pacific Northwest National Laboratory, Richland, WA 99352.
www.pnas.org/cgi/doi/10.1073/pnas.0630387100
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