α-Tocopherol Is Essential for Acquired Chill-Light Tolerance in the Cyanobacterium Synechocystis sp. Strain PCC 6803
Author(s) -
Yang Yang,
Chuntao Yin,
Weizhi Li,
Xudong Xu
Publication year - 2007
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.01577-07
Subject(s) - synechocystis , strain (injury) , biology , mutant , cyanobacteria , tocopherol , wild type , escherichia coli , biochemistry , bacteria , microbiology and biotechnology , genetics , gene , antioxidant , vitamin e , anatomy
UnlikeEscherichia coli , the cyanobacteriumSynechocystis sp. strain PCC 6803 is insensitive to chill (5°C) in the dark but rapidly losses viability when exposed to chill in the light (100 μmol photons m−2 s−1 ). Preconditioning at a low temperature (15°C) greatly enhances the chill-light tolerance ofSynechocystis sp. strain PCC 6803. This phenomenon is called acquired chill-light tolerance (ACLT). Preconditioned wild-type cells maintained a substantially higher level of α-tocopherol after exposure to chill-light stress. Mutants unable to synthesize α-tocopherol, such as slr1736, slr1737, slr0089, and slr0090 mutants, almost completely lost ACLT. When exposed to chill without light, these mutants showed no or a slight difference from the wild type. When complemented, the slr0089 mutant regained its ACLT. Copper-regulated expression of slr0090 from PpetE controlled the level of α-tocopherol and ACLT. We conclude that α-tocopherol is essential for ACLT ofSynechocystis sp. strain PCC 6803. The role of α-tocopherol in ACLT may be based largely on a nonantioxidant activity that is not possessed by other tocopherols or pathway intermediates.
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