Transcriptional regulation of the stress-responsive light harvesting complex genes inChlamydomonas reinhardtii

Dissipating excess energy of light is critical for photosyn-thetic organisms to keep the photosynthetic apparatus func-tional and less harmful under stressful environmental conditions. In the green alga Chlamydomonas reinhardtii, efficient energy dissipation is achieved by a process called non-photochemical quenching (NPQ), in which a distinct member of light harvesting complex, LHCSR, is known to play a key role. Although it has been known that two very closely related genes (LHCSR3.1 and LHCSR3.2) encoding LHCSR3 protein and another paralogous gene LHCSR1 are present in the C. reinhardtii genome, it is unclear how these isoforms are differentiated in terms of transcriptional regu-lation and functionalization. Here, we show that transcripts of both of the isoforms, LHCSR3.1 and LHCSR3.2, are accu-mulated under high light stress. Reexamination of the gen-omic sequence and gene models along with survey of sequence motifs suggested that these two isoforms shared an almost identical but still distinct promoter sequence and a completely identical polypeptide sequence, with more di-vergent 30-untranscribed regions. Transcriptional induction under high light condition of both isoforms was suppressed by treatment with a photosystem II inhibitor, 3-(3,4-dichlor-ophenyl)-1,1-dimethylurea (DCMU), and a calmodulin in-hibitor W7. Despite a similar response to high light, the inhibitory effects of DCMU and W7 to the LHCSR1 transcript accumulation were limited compared to LHCSR3 genes. These results suggest that the transcription of LHCSR para-logs in C. reinhardtii are regulated by light signal and differ-entially modulated via photosynthetic electron transfer and calmodulin-mediated calcium signaling pathway(s)