H2O2-induced cross-protection against UV-C killing in Escherichia coli is blocked in a lexA (Def) background.
Pretreatment with 2.5 mM H2O2 protects E. coli cells against UV-C killing, a phenomenon independent of LexA cleavage. In this paper, we observe that this cross-protection response is neither dependent on the dinY gene product nor on the system that controls dinY, since H2O2 is able to induce cross-protection but not to induce the dinY gene in a lexA-noninducible strain [lexA (Ind-)]. Moreover, this response is not induced in a lexA (Def) background, suggesting that the expression of the SOS regulon may inhibit this cross-protection response.
Asad
L M
LM
Departamento de Biofísica e Biometria, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, RJ, Brazil.
de Carvalho
A A
AA
Felzenszwalb
I
I
Leitão
A C
AC
Asad
N R
NR
D001426:Bacterial Proteins / Q000235:genetics*; D004307:Dose-Response Relationship, Radiation; D004926:Escherichia coli / Q000187:drug effects* / Q000235:genetics / Q000528:radiation effects*; D005798:Genes, Bacterial; D005819:Genetic Markers; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D011837:Radiation-Protective Agents / Q000494:pharmacology; D012097:Repressor Proteins / Q000235:genetics; D012697:Serine Endopeptidases / Q000235:genetics*; D014466:Ultraviolet Rays; D000099160:LexA Repressor Protein
D001426:Bacterial Proteins; D005819:Genetic Markers; D006861:Hydrogen Peroxide; D011837:Radiation-Protective Agents; D012097:Repressor Proteins; D012697:Serine Endopeptidases; D000099160:LexA Repressor Protein