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C ‐terminal truncation of the transcriptional activator encoded by areA in Aspergillus nidulans results in both loss‐of‐function and gain‐of‐function phenotypes
Author(s) -
Stankovich M.,
Platt A.,
Caddick M. X.,
Langdon T.,
Shaffer P. M.,
Arst H. N.
Publication year - 1993
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.1993.tb01099.x
Subject(s) - aspergillus nidulans , biology , gene , activator (genetics) , psychological repression , genetics , phenotype , gene product , function (biology) , gene expression , loss function , structural gene , repressor , microbiology and biotechnology , mutant
Summary Mutations truncating as many as 143 C ‐terminal residues from the transcriptional activator encoded by the areA gene, mediating nitrogen metabolite repression in Aspergillus nidulans , do not significantly reduce the ability of the areA product to activate expression of most genes under areA control. Such mutations can even have a gain‐of‐function, derepressed phenotype, consistent with a critical role for this region in modulating the activity of the areA protein. However, expression of a few genes under areA control is substantially impaired by such C ‐terminal truncations, indicating that regions of an activator protein can play differing roles in the control of different structural genes. This underlines the advantages of being able to monitor effects of areA mutations on expression of large numbers of structural genes. Additionally, it is shown that truncation of as many as 153 C ‐terminal residues, virtually all amino acids C ‐terminal to the DNA‐binding region, is compatible with retention of some areA function.