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High light‐induced hydrogen peroxide production in C hlamydomonas reinhardtii is increased by high CO 2 availability
Author(s) -
Roach Thomas,
Na Chae Sun,
KriegerLiszkay Anja
Publication year - 2015
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12768
Subject(s) - chlamydomonas reinhardtii , hydrogen peroxide , photosystem ii , reactive oxygen species , photosynthesis , chemistry , superoxide , chloroplast , quenching (fluorescence) , photochemistry , wild type , oxygen evolution , mutant , oxygen , biophysics , dcmu , photosystem i , biochemistry , enzyme , biology , fluorescence , gene , electrochemistry , organic chemistry , physics , electrode , quantum mechanics
Summary The production of reactive oxygen species ( ROS ) is an unavoidable part of photosynthesis. Stress that accompanies high light levels and low CO 2 availability putatively includes enhanced ROS production in the so‐called Mehler reaction. Such conditions are thought to encourage O 2 to become an electron acceptor at photosystem I, producing the ROS superoxide anion radical ( O 2 · − ) and hydrogen peroxide (H 2 O 2 ). In contrast, here it is shown in Chlamydomonas reinhardtii that CO 2 depletion under high light levels lowered cellular H 2 O 2 production, and that elevated CO 2 levels increased H 2 O 2 production. Using various photosynthetic and mitochondrial mutants of C. reinhardtii , the chloroplast was identified as the main source of elevated H 2 O 2 production under high CO 2 availability. High light levels under low CO 2 availability induced photoprotective mechanisms called non‐photochemical quenching, or NPQ , including state transitions ( qT ) and high energy state quenching ( qE ). The qE ‐deficient mutant npq4 produced more H 2 O 2 than wild‐type cells under high light levels, although less so under high CO 2 availability, whereas it demonstrated equal or greater enzymatic H 2 O 2 ‐degrading capacity. The qT ‐deficient mutant stt7‐9 produced the same H 2 O 2 as wild‐type cells under high CO 2 availability. Physiological levels of H 2 O 2 were able to hinder qT and the induction of state 2, providing an explanation for why under high light levels and high CO 2 availability wild‐type cells behaved like stt7‐9 cells stuck in state 1.