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Chlamydomonas reinhardtii is an unicellular green alga that is widely used for studying photosynthetic physiology, molecular biology, biochemistry, genomics, and toxicology. To improve our knowledge of molecular and metabolic events in response to environmental changes, we must first identify the factors that control the expression of these processes. For this purpose, we have developed an efficient screening method to isolate mutant strains sensitive to light regulation. We identified four mutants that showed an altered response to light. Two of these, cpi and cmv, affect the synthesis of plastoquinone, while lin, a mutant deficient in phycocyanobilin synthesis, and kos, an auxin-resistant mutant, are defective in the synthesis of phycocyanin. In addition, we are characterizing in detail two phycobilisome-defective mutants, mwt and mcy. mwt carries a deletion of the entire bapA gene and a nonsense mutation in the gene encoding the light-harvesting alpha-subunit ApcA1. This strain is incapable of synthesizing phycobiliprotein and of assembling phycobilisomes on the thylakoid membranes. The mcy strain is partially defective in the synthesis of an apcA1-like protein, resulting in a low level of phycobilin synthesis. Both mutants grow at a rate similar to wild type and under the same conditions. The effects of a dark treatment of mwt suggest that the mutation probably affects the stability of the apcA1 polypeptide. Light stabilizes the mcy mutant and does not cause further decreases in the levels of the ApcA1 polypeptide. The apcA1 polypeptide is not detectable in the cells of the mwt mutant, suggesting that the mutation affects the stability of the alpha-subunit. Although the mutation does not inactivate a maturase involved in the carotenoid pathway of plastidial isoprenoids, it does affect the conversion of precurs
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