Genetic control of chlorophyll biosynthesis in chlamydomonas: analysis of a mutant affecting synthesis of delta-aminolevulinic acid.
A Mendelian mutation, r-1, in Chlamydomonas reinhardtii has been isolated which elevates protoporphyrin accumulation of the Mendelian protoporphyrin mutants brS-1 and brC-1 more than 20 fold. This increased protoporphyrin accumulation is shown to result from increased delta-aminolevulinic acid synthesis in the double mutants brS-1 r-1 and brC-1 r-1 over that of brS-1 and brC-1 alone. By itself, the r-1 mutation has no detectable protoporphyrin accumulation and has reduced levels of delta-aminolevulinic acid synthesizing activity, chlorophyll, protoheme, and cytochrome oxidase activity. The low levels of chlorophyll and protoheme in r-1 can be increased by feeding delta-aminolevulinic acid. We hypothesize that r-1 may be a mutation of the gene coding for the delta-aminolevulinic acid synthesizing enzyme which reduces the sensitivity of this enzyme to feedback inhibition by protoporphyrin or heme as well as reducing the overall activity of the enzyme. Evidence is also presented for a single delta-aminolevulinic acid synthesizing enzyme serving both chlorophyll and heme biosynthesis.
D000624:5-Aminolevulinate Synthetase / Q000378:metabolism; D000622:Aminolevulinic Acid / Q000096:biosynthesis*; D002696:Chlamydomonas / Q000201:enzymology / Q000378:metabolism* / Q000648:ultrastructure; D002734:Chlorophyll / Q000096:biosynthesis*; D002736:Chloroplasts / Q000648:ultrastructure; D003576:Electron Transport Complex IV / Q000378:metabolism; D005796:Genes; D006418:Heme / Q000096:biosynthesis; D007982:Levulinic Acids / Q000096:biosynthesis*; D009154:Mutation; D000623:Porphobilinogen Synthase / Q000378:metabolism; D011524:Protoporphyrins / Q000096:biosynthesis
D007982:Levulinic Acids; D011524:Protoporphyrins; D002734:Chlorophyll; D006418:Heme; D000622:Aminolevulinic Acid; D003576:Electron Transport Complex IV; D000624:5-Aminolevulinate Synthetase; D000623:Porphobilinogen Synthase