Mechanism of thermotolerance induction by split-dose hyperthermia in Deinococcus radiodurans DNA repair deficient mutants
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Updated: Aug 30, 2026

Measuring DNA Damage and Repair in Mouse Splenocytes After Chronic In Vivo Exposure to Very Low Doses of Beta- and Gamma-Radiation
Published on: July 3, 2015
Kazuki Harada1, Mami Ando, Tomoko Fujimura-Ito
1Department of Food Science and Technology, National Fisheries University, Independent Administrative Institution, The Ministry of Agriculture, Forestry and Fisheries of Japan, Shimonoseki-shi, Yamaguchi, Japan. kazuki@fish-u.ac.jp
Abstract:
We examined the phenomenon of thermotolerance induction in the radioresistant prokaryote, Deinococcus radiodurans, which was initially exposed to 30 min at 52 degrees C followed by various intervals up to 6 h at 30 degrees C in TGY medium and then re-exposed to 52 degrees C for various periods, i.e., split-dose hyperthermia. This thermotolerance induction was analyzed in DNA repair deficient mutants (strain 302, 251, UVS25, rec30 and KH840) and the wild-type strain MR1. The strain UVS25 is a double mutant for the mtcA and uvsD genes, and strain rec30 is a mutant for the deinococcal recA gene. The induction was suppressed to 1/10 and 1/25 in strains UVS25 and rec30 respectively, as compared with the maximum level in the wild-type strain MR1. However, the induction in strain 302 (mutant for the uvrA gene) was not suppressed. Therefore, we conclude that proteins synthesized during the interexposure interval, i.e., the products of the uvsD (UV endonuclease beta) and recA (RecA protein) genes contribute to the induction of thermotolerance in D. radiodurans.
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