Previous Article | Next Article ![]()
J. Bacteriol., 12 1995, 6910-6918, Vol 177, No. 23
JA Coffman, R Rai and TG Cooper
The expression of many nitrogen catabolic genes decreases to low levels
when readily used nitrogen sources (e.g., asparagine and glutamine) are
provided in the growth medium; this physiological response is termed
nitrogen catabolite repression (NCR). Transcriptional activation of these
genes is mediated by the cis-acting element UASNTR and the trans- acting
factor Gln3p. A second protein encoded by URE2 possesses the genetic
characteristics of a negative regulator of nitrogen catabolic gene
expression. A third locus, DAL80, encodes a repressor that binds to
sequences required for Gln3p-dependent transcription and may compete with
Gln3p for binding to them. These observations are consistent with an NCR
regulatory pathway with the structure environmental signal--
>Ure2p-->(Gln3p/Dal80p)-->UASNTR operation-->NCR-sensitive gene
expression. If NCR-sensitive gene expression occurs exclusively by this
pathway, as has been thought to be the case, then the NCR sensitivity of a
gene's expression should be abolished by a ure2 delta mutation. This
expectation was not realized experimentally; the responses of highly
NCR-sensitive genes to ure2 delta mutations varied widely. This suggested
that NCR was not mediated exclusively through Ure2p and Gln3p. We tested
this idea by assaying GAP1, CAN1, DAL5, PUT1, UGA1, and GLN1 expression in
single, double, and triple mutants lacking Gln3p, Dal80p, and/or Ure2p. All
of these genes were expressed in the triple mutant, and this expression was
NCR sensitive for four of the six genes. These results indicate that the
NCR regulatory network consists of multiple branches, with the
Ure2p-Gln3p-UASNTR pathway representing only one of them.
Copyright © 1995, American Society for Microbiology
Genetic evidence for Gln3p-independent, nitrogen catabolite repression- sensitive gene expression in Saccharomyces cerevisiae [published erratum appears in J Bacteriol 1996 Apr;178(7):2159]
Department of Microbiology and Immunology, University of Tennessee, Memphis 38163, USA.
This article has been cited by other articles:
| Appl. Environ. Microbiol. | Infect. Immun. | Eukaryot. Cell |
|---|---|---|
| Mol. Cell. Biol. | J. Virol. | Microbiol. Mol. Biol. Rev. |
| ALL ASM JOURNALS |