Mitochondrial activity in illuminated leaves of chlorophyll-deficient mutant rice (<Emphasis Type="Italic">OsCHLH</Emphasis>) seedlings |
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| Authors: | Chang-Hyo Goh Kouji Satoh Shoshi Kikuchi Seong-Cheol Kim Suk-Min Ko Hong-Gyu Kang Jong-Seong Jeon Cheol Soo Kim Youn-Il Park |
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| Institution: | (1) Environmental Biotechnology National Core Research Center, Gyeongsang National University, Jinju, 660-701, Korea;(2) Department of Molecular Genetics, National Institute of Agrobiological Sciences, Tsukuba Ibaraki, 305-8602, Japan;(3) National Institute of Subtropical Agriculture, Rural Development Administration, 316 Ayeonnno, Jeju, 690-150, Korea;(4) Subtropical Horticulture Research Institute, Jeju National University, Jeju, 690-756, Korea;(5) Plant Metabolism Research Center and Graduate School of Biotechnology, Kyung Hee University, Yongin, 446-701, Korea;(6) Department of Plant Biotechnology and Agricultural Plant Stress Research Center, Chonnam National University, Gwangju, 500-757, Korea;(7) Department of Biology, Chungnam National University, Daejeon, 305-764, Korea;(8) Present address: Research Institute for Basic Sciences, Jeju National University, Jeju, 690-756, Korea |
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| Abstract: | The rice CHLH gene encodes the Mg2+-chelatase H subunit, which is involved in chlorophyll biosynthesis. Growth of the chlorophyll-deficient oschlh mutant is supported by mitochondrial activity. In this study, we investigated the activity of mitochondrial respiration in
the illuminated leaves during oschlh seedling development. Growth of mutant plants was enhanced in the presence of 3% sucrose, which may be used by mitochondria
to meet cellular energy requirements. ATP content in these mutants was, however, significantly lowered in light conditions.
Low cytosolic levels of NADH in illuminated oschlh mutant leaves further indicated the inhibition of mitochondrial metabolism. This down-regulation was particularly evident
for oxidative stress-responsive genes in the mutant under light conditions. Hydrogen peroxide levels were higher in oschlh mutant leaves than in wild-type leaves; this increase was largely caused by the impairment of the expression of the antioxidant
genes, such as OsAPX1, OsRAC1, and OsAOXc in knockout plants. Moreover, treatment of mesophyll protoplasts with ascorbic acid or catalase recovered ATP content in
the mutants. Taken together, these results suggest that the light-mediated inhibition of mitochondrial activity leads to stunted
growth of CHLH rice seedlings. |
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