crp1 maps to chromosome 7L. crp1 is a nuclear mutation that causes the loss of the cytochrome f/b6 complex and a decrease in photosystem I. These protein losses are due to a defect in the processing and translation of specific chloroplast mRNAs (manuscript in preparation). This mutation was unmasked in crosses with TB-7Lb. Therefore, it maps to the long arm of chromosome 7.
crp1 is allelic to hcf111. hcf111, a mutation isolated by Cook and Miles (MNL63:65-66), and crp1 map to the same chromosome arm (7L). Like crp1, hcf111 is also deficient in the cytochrome f/b6 complex. We have determined that hcf111 shares the defect in chloroplast RNA processing previously seen only in crp1. Because the map position and phenotypes of the two mutations were similar, it seemed likely that they represented two alleles of the same gene. In complementation tests, six different crosses between pairs of heterozygous plants each yielded one-quarter mutant progeny. Therefore, crp1 and hcf111 do not complement and are most likely allelic.
cps1 maps to chromosome 1L. cps1 is a nuclear gene that is required for chloroplast protein synthesis (A. Barkan, Plant Cell 5:389-402). Crosses of five cps1/+ plants by TB-1La pollen yielded pale green seedlings with hypoploid morphology and lacking Rubisco. Therefore, cps1 maps to the long arm of chromosome 1.
hcf6 is allelic to pet3-1 and pet3-2. pet3-1 and pet3-2 are two independent alleles of a gene, pet3, that is required specifically for the accumulation of the chloroplast cytochrome f/b6 complex. Both alleles were obtained from Mutator lines and both block the accumulation of the cytochrome f/b6 complex at a post-translational step (Voelker and Barkan, in preparation). Complementation tests were performed between these mutations and hcf6, an EMS-induced mutation isolated by Don Miles (University of Missouri) that also lacks the cytochrome f/b6 complex. Three crosses between plants heterozygous for pet3-1 and hcf6 and one cross between plants heterozygous for pet3-2 and hcf6 each yielded one quarter mutant progeny. Therefore, pet3 and hcf6 mutations do not complement and are most likely allelic.
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