Pleiotropic deficiencies of the laccase-derepressed mutant lah-1 are caused by constitutively increased expression of the cross-pathway control gene cpc-1 in Neurospora crassa.
In Neurospora crassa, expression of the laccase gene is induced by treatment with the protein synthesis inhibitor cycloheximide (CHX). This expression is mediated by CPC1, which acts as a general transcriptional activator when mycelia are treated with CHX or starved for any one of the amino acids. A laccase-derepressed mutant, lah-1, shows pleiotropic deficiencies in growth, hyphal morphology, CHX sensitivity, and production of protoperithecia. Moreover, in the lah-1 mutant, transcript levels of CHX-inducible genes, including lacc, tub-2, tef-1, and amino acid biosynthetic genes such as cpc-1, trp-3, and arg-12, are increased without exposure to CHX. All of the defects exhibited in the lah-1 mutant are suppressed by a mutation in the cpc-1 locus. These findings suggest that the cpc-1 mutation is epistatic to the lah-1 mutation and that the pleiotropic defects in the lah-1 mutant are attributable to constitutive expression of CPCI. These conclusions are supported by a developmental Northern blot analysis of the CHX-inducible genes. Based on these results, the lah-1 gene product appears to regulate expression of the cpc-1 gene negatively. Expression of the CHX-inducible genes was induced by CHX treatment in the lah-1 cpc-1 mutant, as well as in the cpc-1 mutant. This observation indicates that LAH1 is not a component of CHX-responsive pathway itself.
Department of Regulation Biology, Faculty of Science, Saitama University, Urawa, Japan.
T
T
Harashima
H
H
Inoue
D003513:Cycloheximide / Q000494:pharmacology; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000502:physiology; D004843:Epistasis, Genetic; D005656:Fungal Proteins / Q000235:genetics* / Q000502:physiology; D015966:Gene Expression Regulation, Fungal / Q000187:drug effects; D042845:Laccase; D009154:Mutation / Q000502:physiology*; D009492:Neurospora crassa / Q000201:enzymology / Q000235:genetics* / Q000254:growth & development; D010088:Oxidoreductases / Q000235:genetics*; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D012331:RNA, Fungal / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis; D013489:Suppression, Genetic
D004268:DNA-Binding Proteins; D005656:Fungal Proteins; D011500:Protein Synthesis Inhibitors; D012331:RNA, Fungal; D012333:RNA, Messenger; D003513:Cycloheximide; D010088:Oxidoreductases; D042845:Laccase