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

• Published in: Plant and cell physiology Vol. 55; no. 7; pp. 1304 - 1310
• Main Authors: Maruyama, Shinichiro, Tokutsu, Ryutaro, Minagawa, Jun
• Format: Journal Article
• Language: English
• Published: Japan 01.07.2014
• Subjects: Base Sequence; Calcium Signaling - drug effects; Chlamydomonas reinhardtii - drug effects; Chlamydomonas reinhardtii - genetics; Chlamydomonas reinhardtii - physiology; Chlamydomonas reinhardtii - radiation effects; Diuron - pharmacology; Electron Transport; Enzyme Inhibitors - pharmacology; Gene Expression Regulation, Plant; Herbicides - pharmacology; Light; Light-Harvesting Protein Complexes - chemistry; Light-Harvesting Protein Complexes - genetics; Models, Molecular; Molecular Sequence Data; Multigene Family; Photosynthesis; Photosystem II Protein Complex - drug effects; Phylogeny; Protein Isoforms; Sequence Alignment; Sequence Analysis, DNA; Stress, Physiological; Sulfonamides - pharmacology; Calcium signaling; Photosynthetic electron flow; Light harvesting complex; Transcriptional regulation; High light stress; Non-photochemical quenching
• ISSN: 0032-0781; 1471-9053
• DOI: 10.1093/pcp/pcu068

Dissipating excess energy of light is critical for photosynthetic organisms to keep the photosynthetic apparatus functional 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 regulation and functionalization. Here, we show that transcripts of both of the isoforms, LHCSR3.1 and LHCSR3.2, are accumulated under high light stress. Reexamination of the genomic 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 divergent 3'-untranscribed regions. Transcriptional induction under high light condition of both isoforms was suppressed by treatment with a photosystem II inhibitor, 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU), and a calmodulin inhibitor 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 paralogs in C. reinhardtii are regulated by light signal and differentially modulated via photosynthetic electron transfer and calmodulin-mediated calcium signaling pathway(s).