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www.plantcell.org/cgi/doi/10.1105/tpc.106.041541
One of the mechanisms plants have developed for chloroplast protection against oxidative damage involves a 2-Cys
peroxiredoxin, which has been proposed to be reduced by ferredoxin and plastid thioredoxins, Trx x and CDSP32, the FTR/
Trx pathway. We show that rice (Oryza sativa) chloroplast NADPH THIOREDOXIN REDUCTASE (NTRC), with a thioredoxin
domain, uses NADPH to reduce the chloroplast 2-Cys peroxiredoxin BAS1, which then reduces hydrogen peroxide. The
presence of both NTR and Trx-like domains in a single polypeptide is absolutely required for the high catalytic efficiency of
NTRC. An Arabidopsis thaliana knockout mutant for NTRC shows irregular mesophyll cell shape, abnormal chloroplast
structure, and unbalanced BAS1 redox state, resulting in impaired photosynthesis rate under low light. Constitutive
expression of wild-type NTRC in mutant transgenic lines rescued this phenotype. Moreover, prolonged darkness followed
by light/dark incubation produced an increase in hydrogen peroxide and lipid peroxidation in leaves and accelerated
senescence of NTRC-deficient plants. We propose that NTRC constitutes an alternative system for chloroplast protection
against oxidative damage, using NADPH as the source of reducing power. Since no light-driven reduced ferredoxin is
produced at night, the NTRC-BAS1 pathway may be a key detoxification system during darkness, with NADPH produced by
the oxidative pentose phosphate pathway as the source of reducing power.
This work was supported by Grant BIO2004-02023 from the Ministerio de
Educación y Ciencia (Spain) and Grant CVI-182 from Junta de Andalucía
(Spain). J.M.P.-R. was supported by a predoctoral fellowship from the
Ministerio de Educación y Ciencia, M.C.S. by a postdoctoral fellowship
from Fundación Carolina (Spain), and K.K. by a predoctoral fellowship
from the Consejo Superior de Investigaciones Científicas (Spain).
Peer reviewed