ArticleJournal of bacteriology1997
The minimal transactivation region of Saccharomyces cerevisiae Gln3p is localized to 13 amino acids.
Article in Journal of bacteriology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Moonlighting transcriptional activation function of a fungal sulfur metabolism enzyme.Scientific reports · 2016Article
- Recent advances in nitrogen regulation: a comparison between Saccharomyces cerevisiae and filamentous fungi.Eukaryotic cell · 2008Review
- Transmitting the signal of excess nitrogen in Saccharomyces cerevisiae from the Tor proteins to the GATA factors: connecting the dots.FEMS microbiology reviews · 2002Review
- Gln3p nuclear localization and interaction with Ure2p in Saccharomyces cerevisiae.The Journal of biological chemistry · 2001Article
- Functional domain mapping and subcellular distribution of Dal82p in Saccharomyces cerevisiae.The Journal of biological chemistry · 2000Article
- Synergistic operation of the CAR2 (Ornithine transaminase) promoter elements in Saccharomyces cerevisiae.Journal of bacteriology · 1999Article
- Nitrogen catabolite repression in Saccharomyces cerevisiae.Molecular biotechnology · 1999Review
- Control of nitrogen catabolite repression is not affected by the tRNAGln-CUU mutation, which results in constitutive pseudohyphal growth of Saccharomyces cerevisiae.Journal of bacteriology · 1999Article
- The Saccharomyces cerevisiae GATA factors Dal80p and Deh1p can form homo- and heterodimeric complexes.Journal of bacteriology · 1998Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Regulated nitrogen catabolic gene transcription in Saccharomyces cerevisiae is mediated by four positive (Gln3p and Gat1p/Nil1p) and negative (Dal80p/Uga43p and Deh1p/Nil2p/GZF3p) regulators which function in opposition to one another. All four proteins contain GATA-type zinc finger domains, and three of them (Gln3p, Dal80p, and Deh1p) have been shown to bind to GATA sequences situated upstream of genes whose expression is sensitive to nitrogen catabolite repression (NCR). The positive regulators, Gln3p and Gat1p, are able to support transcriptional activation when tethered by LexAp to the promoter of a reporter gene whose upstream activation sequences have been replaced with one or more lexA operator sites. Existing data suggest that these four proteins regulate transcription by competing with one another for binding to the GATA sequences which mediate NCR-sensitive gene expression. We show that the minimal Gln3p domain mediating transcriptional activation consists of 13 amino acids with a predicted propensity to form an alpha-helix. Genetic analysis of this region (Gln3p residues 126 to 138, QQNGEIAQLWDFN) demonstrated that alanine may be substituted for the aromatic and acidic amino acids without destroying transcriptional activation potential. Similar substitution of alanine for the two hydrophobic amino acids, isoleucine and leucine, however, destroys activation, as does introduction of basic amino acids in place of the acidic residues or introduction of proline into the center of the sequence. A point mutation in the Gln3p activation region destroys its in vivo ability to support NCR-sensitive DAL5 expression. We find no convincing evidence that NCR regulates Gln3p function by modulating the functioning of its activation region.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.