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Carotenoid isomerase (CRTISO) has been suggested to protect photosystem II (PS II) from photodamage, probably through its product lutein. However, the mechanism of the photoprotection still remains to be further elucidated. In this work, we cloned a point mutated gene reported to encode a CRTISO which is responsible for the accumulation of lutein in rice mutant zel1 by a map-based cloning approach. The mutant phenotype was rescued by transformation with the corresponding gene of the wild type (WT). The activity of photosynthetic oxygen evolution was evidently suppressed in zel1. The amount of the core protein of PS II CP47 was much lower in all the PS II complexes especially in the LHCII-PS II supercomplexes and CP43-free PS II of zel1 than that of WT. On the other hand, the amount of another core protein of PS II CP43 of zel1 was decreased in the higher supercomplexes, whereas it was increased in the lower ones and PS II monomer. The immunodetection displayed that CP43, CP47, and the oxygen-evolving extrinsic proteins PsbO and PsbP were reduced, but the amount of reaction center protein D1 did not show significant change in zel1. Northern blot analysis showed that the transcriptional level of CP43 was down-regulated but not that of CP47 or D1 in zel1. In addition, the plastoquinone (PQ) Q(A) was in a reduced state in zel1. On the basis of the results, we suggest that CRTISO might function in regulating the transcription of CP43 and the translation of CP47 by affecting the redox state of the PQ to stabilize the extrinsic proteins of oxygen evolution complexes in the rice plant.

The role of carotenoid isomerase in maintenance of photosynthetic oxygen evolution in rice plant