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제107회 대한화학회 학술발표회, 총회 및 기기전시회 Defects in non-photochemical quenching of excessive light energy absorbed by chlorophyll result in the increased production of superoxide from photosystem II in PsbS lacking rice mutant leaves

2011년 3월 15일 09시 15분 08초
INOR2-6 이곳을 클릭하시면 발표코드에 대한 설명을 보실 수 있습니다.
금 11시 : 30분
무기화학 - Inorganic/Material Science in Energy Applications II
저자 및
M. Hall, 윤웅찬1, S. Jansson, 이춘환2
Umeå University, Sweden, Sweden
1부산대학교 화학과, Korea
2부산대학교 분자생물학과, Korea
Higher plants develop a variety of photoprotective mechanisms against photoinhibition or the light-dependent loss of photosynthetic efficiency. One of the mechanisms against photoinhibition is non-photochemical quenching, especially energy-dependent quenching (qE) of chlorophyll fluorescence. This component depends on three major parameters: the development of transthylakoid proton gradient (ΔpH), the amount of pigments involved in xanthophyll cycle, and the existence of a PsbS subunit in PSII. A rice PsbS T-DNA knock-out line and several RNAi lines were isolated and were deficient in energy-dependent part (qE) of NPQ. The growth rate of young seedlings lacking PsbS was reduced under fluctuating high light condition and photosystem II in detached leaves was more sensitive to photoinhibitory illumination compared to wild-type. Singlet oxygen, superoxide anion radical and hydrogen peroxide levels were determined in leaves histochemically and by fluorescence sensors. PsbS-deficient plants produced more superoxide anion radical and consequently more hydrogen peroxide in chloroplasts and superoxide dismutase activity was increased. The site for superoxide anion radical in PsbS-less plants appeared to be PSII. Genome-wide analysis of the gene expression pattern of the PsbS-KO rice plants shows that lack of PsbS protein led to changes on the transcript level of the 587 genes, presumably as a result of the produced superoxide anion radical in the chloroplast. These data indicate that the specific reactive oxygen species induce specific signaling pathways which activate defense mechanism.