Evidence map›Paper›PMID 9258674›Full record

ArticleGenetics1997

Constitutive mutations of the Saccharomyces cerevisiae MAL-activator genes MAL23, MAL43, MAL63, and mal64.

A W Gibson, L A Wojciechowicz, S E Danzi, B Zhang, J H Kim, Z Hu, C A Michels

Abstract read
In one paragraph

Article in Genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

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16citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

16 citing papers in PubMed.

  1. Comprehensive deletion scan of anti-CRISPR AcrIIA4 reveals essential and dispensable domains for Cas9 inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  4. Predictive Modeling of Microbial Behavior in Food.Foods (Basel, Switzerland) · 2019
    Review
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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

7 authors.

A W GibsonDepartment of Biology, Queens College, Flushing, New York 11367, USA.
L A Wojciechowicz
S E Danzi
B Zhang
J H Kim
Z Hu
C A Michels

Funding

YEAST: AMODEL FOR STUDYING REGULATION IN CANCER CELLSR01GM028216 · NIGMS · QUEENS COLLEGE · PI MICHELS, CORINNE ANTHONY · 1985 to 2004
$1.2M
NIGMS NIH HHS GM-28216
6 · The paper itself

Abstract

We report the sequence of several MAL-activator genes, including inducible, constitutive, and noninducible alleles of MAL23, MAL43, MAL63, and mal64. Constitutive alleles of MAL23 and MAL43 vary considerably from inducible alleles in their C-terminal domain, with many of the alterations clustered and common to both alleles. The 27 alterations from residues 238-461 of Mal43-C protein are sufficient for constitutivity, but the minimal number of alterations needed for the constitutive phenotype could not be determined. The sequence of mal64, a nonfunctional homologue of MAL63, revealed that Mal64p is 85% identical to Mal63p. Two mutations that activate mal64 and cause constitutivity are nonsense mutations resulting in truncated proteins of 306 and 282 residues. We conclude that the C-terminal region of the MAL-activator, from residues 283-470, contains a maltose-responsive negative regulatory domain, and that extensive mutation or deletion of the entire region causes loss of the negative regulatory function. Additionally, certain sequence elements in the region appear to be necessary for efficient induction of the full-length Mal63 activator protein. These studies highlight the role of ectopic recombination as an important mechanism of mutagenesis of the telomere-associated family of MAL loci.

Indexed as

Genes, FungalMutationAllelesalpha-GlucosidasesBase SequenceDNA, FungalDNA PrimersEnzyme ActivationFermentationFungal ProteinsGene Expression Regulation, FungalMaltoseMolecular Sequence DataPolymerase Chain ReactionRecombination, GeneticRestriction Mappingalpha-GlucosidasesDNA, FungalDNA PrimersFungal ProteinsMaltose

Identifiers

PMID9258674
PMCPMC1208075

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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.