Exploiting genetic variation for more efficient photosynthesis is an underexplored route towards new crop varieties. This study demonstrates the genetic dissection of higher plant photosynthesis efficiency down to the genomic DNA level, by confirming that allelic sequence variation at the Arabidopsis thaliana YELLOW SEEDLING1 (YS1) gene explains natural diversity in photosynthesis acclimation to high irradiance. We use a genome-wide association study to identify quantitative trait loci (QTLs) involved in the Arabidopsis photosynthetic acclimation response. Candidate genes underlying the QTLs are prioritized according to functional clues regarding gene ontology, expression and function. Reverse genetics and quantitative complementation confirm the candidacy of YS1, which encodes a pentatrico-peptide-repeat (PPR) protein involved in RNA editing of plastid-encoded genes (anterograde signalling). Gene expression analysis and allele sequence comparisons reveal polymorphisms in a light-responsive element in the YS1 promoter that affect its expression, and that of its downstream targets, resulting in the variation in photosynthetic acclimation.
A new class of glycerol non-utilizing mutants, designated glcC, has been isolated. The glcC gene was mapped in linkage group VI and mutants were found to complement the reference strains glcA2 (linkage group V) and glcB33 (linkage group I) in diploids. The new mutants were unable to grow on glycerol. However, in contrast to theglcA andglcB phenotype these mutants did grow well on dihydroxyacetone and D-galacturonate. By in vivo 3C NMR spectroscopy it was shown that the glcC mutant did not take up glycerol but did take up dihydroxyacetone. The latter substrate was converted intracellularly into glycerol which was then catabolized as normal. I N T R O D U C T I O NGlycerol metabolism in filamentous fungi has thus far been studied most extensively in Neurospora crassa. Evidence was presented for a catabolic pathway involving phosphorylation to glycerol 3-phosphate and subsequent oxidation of glycerol 3-phosphate in the mitochondria to dihydroxyacetone phosphate (Courtright, 1975). This route was indeed confirmed as glycerol non-utilizing mutants were isolated that lacked either glycerol kinase (glpl) or the mitochondria1 membrane-bound flavoprotein glycerol-3-phosphate dehydrogenase (glp2) (Holm et al., 1976; Denor & Courtright, 1978, 1982. However, Viswanath-Reddy et al. (1977) and Tom et al. (1978) have also suggested that there is an alternative route in which glycerol is utilized by a direct NADP+-dependent oxidation to glyceraldehyde which is similar to the NAD+-dependent oxidation to dihydroxyacetone in Schizosaccharomycespombe and in some other yeasts (Marshall et al., 1985).In Aspergillus nidulans Payton (1978) isolated two classes of glycerol non-utilizing mutants, glcA and glcB, after mutation and filtration enrichment in a glycerol medium. Filtration enrichment in a D-galaCtUrOnate medium, however, resulted only in mutants of the glcB genotype (Uitzetter et al., 1986). We have recently found biochemical evidence that in A . nidulans glycerol is also catabolized through phosphorylation (glcA) and oxidation (glcB) (J. Visser & coworkers, unpublished results). In this fungus the presence of a NADP+-dependent glycerol dehydrogenase was also established. The latter enzyme is involved in the conversion of dihydroxyacetone into glycerol. The interaction between D-galacturonate breakdown and glycerol catabolism was also previously shown (Uitzetter et al., 1986). The uronic acid is catabolized through glyceraldehyde and pyruvate, the former compound being further metabilized through glycerol. In this study we describe the isolation and characterization of a new class of glycerol non-utilizing mutants (glcC) in addition to the two genotypes already described. METHODSStrains and mutagenesis. The strains of Aspergillus were all derived from the original Glasgow strains (Pontecorvo et al., 1953). The strain used for mutagenesis was H542 (pabaAl a l X 4 sB43) from which the glycerol non-utilizing strain H913 was derived. The wild-type control was WG096 (pabaAI yA2). The glycerol non- 0001-4482 0 1988 SGM
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