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Title: UV hyper-resistance in Prochlorococcus MED4 results from a single base pair deletion just upstream of an operon encoding nudix hydrolase and photolyase

Journal Article · · Environmental Microbiology
 [1];  [2];  [2];  [3];  [2];  [2];  [2];  [3];  [3];  [2]
  1. Massachusetts Inst. of Technology (MIT), Cambridge, MA (United States); DOE/OSTI
  2. Massachusetts Inst. of Technology (MIT), Cambridge, MA (United States)
  3. Harvard Medical School, Boston, MA (United States)

Exposure to solar radiation can cause mortality in natural communities of pico-phytoplankton, both at the surface and to a depth of at least 30 m. DNA damage is a significant cause of death, mainly due to cyclobutane pyrimidine dimer formation, which can be lethal if not repaired. While developing a UV mutagenesis protocol for the marine cyanobacterium Prochlorococcus, we isolated a UV-hyper-resistant variant of high light-adapted strain MED4. The hyper-resistant strain was constitutively upregulated for expression of the mutT-phrB operon, encoding nudix hydrolase and photolyase, both of which are involved in repair of DNA damage that can be caused by UV light. Photolyase (PhrB) breaks pyrimidine dimers typically caused by UV exposure, using energy from visible light in the process known as photoreactivation. Nudix hydrolase (MutT) hydrolyses 8-oxo-dGTP, an aberrant form of GTP that results from oxidizing conditions, including UV radiation, thus impeding mispairing and mutagenesis by preventing incorporation of the aberrant form into DNA. These processes are error-free, in contrast to error-prone SOS dark repair systems that are widespread in bacteria. The UV-hyper-resistant strain contained only a single mutation: a 1 bp deletion in the intergenic region directly upstream of the mutT-phrB operon. Two subsequent enrichments for MED4 UV-hyper-resistant strains from MED4 wild-type cultures gave rise to strains containing this same 1 bp deletion, affirming its connection to the hyper-resistant phenotype. These results have implications for Prochlorococcus DNA repair mechanisms, genome stability and possibly lysogeny.

Research Organization:
Massachusetts Institute of Technology (MIT), Cambridge, MA (United States)
Sponsoring Organization:
USDOE Office of Science (SC), Biological and Environmental Research (BER). Earth and Environmental Systems Science Division
OSTI ID:
1625899
Journal Information:
Environmental Microbiology, Journal Name: Environmental Microbiology Journal Issue: 7 Vol. 12; ISSN 1462-2912
Publisher:
WileyCopyright Statement
Country of Publication:
United States
Language:
English

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Cited By (6)

Substrate ambiguity among the nudix hydrolases: biologically significant, evolutionary remnant, or both? journal November 2012
Temporal dynamics of Prochlorococcus ecotypes in the Atlantic and Pacific oceans journal May 2010
Sequence analysis of a complete 1.66 Mb Prochlorococcus marinus MED4 genome cloned in yeast journal August 2012
Toward a genetic system in the marine cyanobacterium Prochlorococcus journal April 2020
The spontaneous mutation frequencies of Prochlorococcus strains are commensurate with those of other bacteria: Mutation frequencies in Prochlorococcus journal September 2011
Closely related phytoplankton species produce similar suites of dissolved organic matter journal March 2014

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