Display Settings:

Format

Send to:

Choose Destination
Genetics. 2009 Mar;181(3):861-74. doi: 10.1534/genetics.108.099051. Epub 2008 Dec 22.

Nitrogen catabolite repression-sensitive transcription as a readout of Tor pathway regulation: the genetic background, reporter gene and GATA factor assayed determine the outcomes.

Author information

  • 1Institut de Recherches Microbiologiques J.-M. Wiame, Laboratoire de Microbiologie, Université Libre de Bruxelles, Brussels, Belgium.

Erratum in

  • Genetics. 2009 Jul;182(3):927.

Abstract

Nitrogen catabolite repression (NCR)-sensitive genes, whose expression is highly repressed when provided with excess nitrogen and derepressed when nitrogen is limited or cells are treated with rapamycin, are routinely used as reporters in mechanistic studies of the Tor signal transduction pathway in Saccharomyces cerevisiae. Two GATA factors, Gln3 and Gat1, are responsible for NCR-sensitive transcription, but recent evidence demonstrates that Tor pathway regulation of NCR-sensitive transcription bifurcates at the level of GATA factor localization. Gln3 requires Sit4 phosphatase for nuclear localization and NCR-sensitive transcription while Gat1 does not. In this article, we demonstrate that the extent to which Sit4 plays a role in NCR-sensitive transcription depends upon whether or not (i) Gzf3, a GATA repressor homologous to Dal80, is active in the genetic background assayed; (ii) Gat1 is able to activate transcription of the assayed gene in the absence of Gln3 in that genetic background; and (iii) the gene chosen as a reporter is able to be transcribed by Gln3 or Gat1 in the absence of the other GATA factor. Together, the data indicate that in the absence of these three pieces of information, overall NCR-sensitive gene transcription data are unreliable as Tor pathway readouts.

PMID:
19104072
[PubMed - indexed for MEDLINE]
PMCID:
PMC2651060
Free PMC Article

Images from this publication.See all images (12)Free text

F igure  1.—
F igure  2.—
F igure  3.—
F igure  4.—
F igure  5.—
F igure  6.—
F igure  7.—
F igure  8.—
F igure  9.—
F igure  10.—
F igure  11.—
F igure  12.—
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Write to the Help Desk