Mutants of Neurospora crassa defective in regulation of blue light perception
Molecular and General Genetics, ISSN: 0026-8925, Vol: 254, Issue: 2, Page: 111-118
1997
- 43Citations
- 28Captures
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Metrics Details
- Citations43
- Citation Indexes42
- 42
- CrossRef29
- Patent Family Citations1
- Patent Families1
- Captures28
- Readers28
- 28
Article Description
A new selection system was used to isolate mutants deficient in regulation of blue light perception in Neurospora crassa. This selection system has two possible applications and was used for the isolation of either blind or constitutive mutants. We isolated 17 UV-induced mutants that showed the pleiotropic white collar (WC) phenotype and were completely blocked in transduction of the light signal. From the segregation pattern in sexual crosses, we tentatively assigned the 17 mutants to either the wc-1 or wc-2 gene. Furthermore, two Neurospora mutants, ccb-1 and ccb-2, were isolated that showed constitutive carotenoid biosynthesis in the dark. Analysis of these mutants for transcripts of the carotenoid biosynthesis genes al-3 and al-1 revealed no higher steady-state levels in the dark than in the control strain. The mutant ccb-2 showed major differences in mRNA levels only for conidiation and developmental genes. The lack of a specific change in mRNA levels in response to light, and the mutant phenotype, which seems to reflect a step in conidiation, indicate a role for the ccb-2 product in a developmental process, such as conidiation. In contrast, the mutant ccb-1 showed a threefold overinduction of carotenoid biosynthesis genes in response to light. This effect was not observed for the conidiation genes examined. The recessive nature of the ccb-1 mutation, together with its specific effect on light induction of the carotenoid biosynthesis genes, indicate that the gene product of ccb-1 acts as a repressor of transcription in some light-regulated processes, but not others.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0030934714&origin=inward; http://dx.doi.org/10.1007/s004380050398; http://www.ncbi.nlm.nih.gov/pubmed/9108272; http://link.springer.com/10.1007/s004380050398; http://www.springerlink.com/index/10.1007/s004380050398; http://www.springerlink.com/index/pdf/10.1007/s004380050398; https://dx.doi.org/10.1007/s004380050398; https://link.springer.com/article/10.1007/s004380050398
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