The Cia5 gene controls formation of the carbon concentrating mechanism in Chlamydomonas reinhardtii

Abstract

Wild-type Chlamydomonas reinhardtii cells shifted from high concentrations (5%) of CO 2 to low, ambient levels (0.03%) rapidly increase transcription of mRNAs from several CO 2-responsive genes. Simultaneously, they develop a functional carbon concentrating mechanism that allows the cells to greatly increase internal levels of CO 2 and HCO 3 ؊ . The cia5 mutant is defective in all of these phenotypes. A newly isolated gene, designated Cia5, restores transformed cia5 cells to the phenotype of wild-type cells. The 6,481-bp gene produces a 5.1-kb mRNA that is present constitutively in light in high and low CO 2 both in wild-type cells and the cia5 mutant. It encodes a protein that has features of a putative transcription factor and that, likewise, is present constitutively in low and high CO 2 conditions. Complementation of cia5 can be achieved with a truncated Cia5 gene that is missing the coding information for 54 C-terminal amino acids. Unlike wild-type cells or cia5 mutants transformed with an intact Cia5 gene, cia5 mutants complemented with the truncated gene exhibit constitutive synthesis of mRNAs from CO 2-responsive genes in light under both high and low CO 2 conditions. These discoveries suggest that posttranslational changes to the C-terminal domain control the ability of CIA5 to act as an inducer and directly or indirectly control transcription of CO 2-responsive genes. Thus, CIA5 appears to be a master regulator of the carbon concentrating mechanism and is intimately involved in the signal transduction mechanism that senses and allows immediate responses to fluctuations in environmental CO 2 and HCO 3 ؊ concentrations.

Thylakoid Lumen Carbonic Anhydrase (CAH3) Mutation Suppresses Air-Dier Phenotype of LCIB Mutant in Chlamydomonas reinhardtii

“…Even though the data presented here help identify the position of LCIB in the pathway for Ci uptake and accumulation by placing its function downstream of CAH3, the actual function of LCIB remains a mystery, as does how the single mutation in LCIB eliminates almost all Ci accumulation to the same extent as the cia5 mutant, in which almost no limiting-CO 2 -induc- ible genes are expressed Xiang et al, 2001). LCIB is essential in L-CO 2 conditions, and we hypothesize that LCIB might be involved in somehow preventing the loss of CAH3-generated CO 2 that is not captured by Rubisco in the pyrenoid, either by preventing its diffusion from the pyrenoid or by recapturing any CO 2 escaping from the pyrenoid or from thylakoids outside the pyrenoid.…”

Novel metabolism in Chlamydomonas through the lens of genomics

“…The cia5 (ccm1) mutant of Chlamydomonas cannot acclimate to limiting [CO 2 ] and the CIA5 protein is probably a transcription factor that is crucial for acclimation [21,22]. The pmp1 mutant was reported to be a high Figure 1, LCIB, LCIC and LCID appear to be localized in the plastid, and are soluble polypeptides that function in some unknown way to enable Ci transport.…”

Light and CO2/cAMP Signal Cross Talk on the Promoter Elements of Chloroplastic β-Carbonic Anhydrase Genes in the Marine Diatom Phaeodactylum tricornutum

“…The enhancer region is controlled by two critical elements denoted enhancer-element consensus (Kucho et al, 2003), to which a class of basic-ZIP transcription factors, enhancer-element-consensus binding proteins, interact (Yoshioka et al, 2004). A zinc finger protein, CCM1/Cia5, has been found to be involved in the up-regulation of most low-CO 2 -inducible genes, strongly suggesting that CCM1/Cia5 is a master regulator for the transcriptional response of the Chlamydomonas CCM, but the mechanism of the initial CO 2 signal perception is still unknown (Fukuzawa et al, 2001;Xiang et al, 2001). …”