Characterization of nitrogen metabolite signalling in Aspergillus via the regulated degradation of areA mRNA

Citation
Iy. Morozov et al., Characterization of nitrogen metabolite signalling in Aspergillus via the regulated degradation of areA mRNA, MOL MICROB, 42(1), 2001, pp. 269-277
Citations number
46
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Microbiology
Journal title
MOLECULAR MICROBIOLOGY
ISSN journal
0950-382X → ACNP
Volume
42
Issue
1
Year of publication
2001
Pages
269 - 277
Database
ISI
SICI code
0950-382X(200110)42:1<269:CONMSI>2.0.ZU;2-5
Abstract
AreA is the principal transcription factor involved in determining nitrogen utilization in Aspergillus nidulans. NH4+ and Gin are utilized preferentia lly but in their absence, AreA acts to facilitate the expression of genes i nvolved in metabolizing alternative nitrogen sources. It is crucial to the function of AreA that its expression is tightly modulated by the quality an d availability of nitrogen sources. One signalling mechanism involves regul ated degradation of the areA transcript in response to NH4+ and Gin, which provides the first direct means of monitoring nitrogen signalling in this f ungus. Here we assess the specificity of the transcript degradation respons e, determining that it responds qualitatively to a variety of additional ni trogen sources including Asn. Furthermore, the response to Gin and NH4+ req uires the same discrete region of the areA 3'-UTR but both NH4+ and Asn nee d to be metabolized to Gin before they are effective as a signal. However, NH4+ signalling is independent of AreA activity, unlike Gin and Asn signall ing. A mutation in the structural gene for NADP-linked glutamate dehydrogen ase, gdhA, which disrupts metabolism of NH4+ to Glu, is additive with mutat ions in two distinct regions of areA that disrupt the previously identified signalling mechanisms. The triple mutant is both strongly derepressed and expresses very high levels of nitrate reductase activity. These data sugges t nitrogen metabolism in A. nidulans is in part regulated in response to th e intracellular levels of Gln via the regulated degradation of areA mRNA, b ut the intracellular Gln level is not the sole determinant of nitrogen meta bolite repression.