In the chlorophyll cycle, chlorophyll b is synthesized from chlorophyll a (forward reaction) by chlorophyllide a oxygenase (CAO) and chlorophyll b is reconverted to chlorophyll a (backward reaction) by chlorophyll b reductase (NOL, NYC1) and 7-hydroxyl chlorophyll a reductase (HCAR). Activity of the forward and backward reactions alters the levels of chlorophyll a and chlorophyll b which is associated with the changes of chlorophyll a/b ratio. The level of light harvesting complexes, which forms the antenna of photosystem II (PSII), is primarily regulated by the chlorophyll cycle. Stabilization of light harvesting chlorophyll a/b binding protein complexes (LHCII) is corelated with accumulation of chlorophyll b indicating that LHCII formation is regulated by chlorophyll b synthesis. In contrast, degradation of chlorophyll b is the initial step of LHCII degradation during senescence, indicating that chlorophyll b degradation regulates the degradation of LHCII. This study aimed to clarify the regulation mechanisms of the formation and degradation of LHCs by the chlorophyll cycle. In the first part, I examined detail of LHCII formation and its effect on the structure and stoichiometry of both photosystems when chlorophyll b synthesis was triggered by the expression of the full length CAO in the Arabidopsis chlorophyll b less mutant ch1-1. Out results show that accompanied with biosynthesis of chlorophyll b, LHCs apoproteins were accumulated. Formation of LHCII trimer was associated to the core antenna of PSII to form PSII-LHCII supercomplexes. Peripheral antenna of photosystem I (PSI) and II increased after chlorophyll b synthesis. I also found that PSI/PSII ratio was altered accompanied by the synthesis of chlorophyll b. In the second part, I examined the effect of chlorophyll b on the accumulation NYC1 which is responsible for the degradation of LHCII during leaf senescence. In this study, I introduced BC domain of CAO fused with GFP into Arabidopsis mutant ch1-1, 5 which was named BCG plant, in which chlorophyll b was over-produced. Analysis of my results show that NYC1 was over-accumulated in BCG plant, but not in ch1-1 after dark incubation; however, the mRNA level increased in both BCG and ch1-1 after dark incubation. Interestingly, LHCII protein level did not corelate with NYC1 protein level; chlorophyll fluorescence of dark adapted plant (Fo) displayed high co-relationship with accumulation of NYC1 suggesting NYC1 level is related to the energetically uncoupled LHC. (主査) 教授 田中 歩, 教授 山口 淳二, 准教授 田中 亮一 生命科学院（生命科学専攻）