A Chlorate-Resistant Mutant Defective in the Regulation of Nitrate Reductase Gene Expression in Arabidopsis Defines a New HY Locus

Abstract

Light acts both directly as a signal and indirectly through photosynthesis to regulate the expression of genes encoding nitrate reductase (NR). Here, we report the isolation and characterization of a novel chlorate-resistant mutant that is defective in the regulation of NR gene expression. The response of NR2, but not NR1 or the gene encoding nitrate reductase (NiR), to light signals was impaired in this Arabidopsis mutant, designated cr88. In addition to NR2, the light regulation of the genes encoding the chlorophyll a/b binding protein (CAB) and the small subunit of ribulose bisphosphate carboxylase (RBCS) was also impaired in this mutant. These results suggest that the pathway through which light regulates the expression of NR2, CAB, and RBCS genes is different from those that regulate the expression of NR1 and NiR. An examination of the deetiolation process under different light spectrum showed that cr88 is defective in red light-mediated deetiolation. Complementation tests with various long hypocotyl (hy) mutants indicated that CR88 identifies a new HY locus. The possible functions of CR88 are discussed.

The chlorate‐resistant and photomorphogenesis‐defective mutant cr88 encodes a chloroplast‐targeted HSP90

“…In addition, NR activity of transgenic T5.5 plants was restored to wildtype levels in response to nitrate (Table 1). This con®rms our earlier conclusion that both the chlorate resistance and yellow phenotypes are caused by the same mutation (Lin and Cheng, 1997).…”

“…The yellow-green phenotype of cr88 is most pronounced in cotyledons and young leaves (Lin and Cheng, 1997), suggesting that CR88 gene expression may be developmentally regulated. To investigate this possibility, we performed a time course study of CR88 gene expression using RNA blot analysis.…”

“…In cotyledons and young leaves, plastids are less developed than those of the wild type (Lin and Cheng, 1997). In addition, mutation decreased the expression of light-induced genes encoding the chlorophyll a/b binding protein (CAB), the small subunit of ribulose biphosphate carboxylase (RBCS), and nitrate reductase 2 (NR2), but not that of the chalcone synthase (CHS) and NR1, under all light conditions tested (Cao et al, 2000;Lin and Cheng, 1997). These phenotypes led us to propose that CR88 is a component of the pathway controlling photomorphogenesis (Lin and Cheng, 1997).…”

“…Previously, we demonstrated that cr88 is a recessive allele (Lin and Cheng, 1997) that maps to the north arm of chromosome 2 where it is linked closely to marker m246 (Cao et al, 2000). To locate CR88 more precisely, the markers Mi320, Mi421, CDs3, IGS1, and m246 were used to probe 600 F 2 plants exhibiting the cr88 phenotype.…”

“…In addition, mutation decreased the expression of light-induced genes encoding the chlorophyll a/b binding protein (CAB), the small subunit of ribulose biphosphate carboxylase (RBCS), and nitrate reductase 2 (NR2), but not that of the chalcone synthase (CHS) and NR1, under all light conditions tested (Cao et al, 2000;Lin and Cheng, 1997). These phenotypes led us to propose that CR88 is a component of the pathway controlling photomorphogenesis (Lin and Cheng, 1997). By analyzing the epistatic relationship between cr88 and cop1 and between cr88 and hy5, we concluded that CR88 is likely to act downstream of COP1 to regulate a subset of photomorphogenesis responses and acts in a pathway independent of HY5 to control hyopcotyl elongation in red light (Cao et al, 2000).…”