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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1991-2-20
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pubmed:databankReference |
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pubmed:abstractText |
Several highly inducible enzyme activities are required for the degradation of allantoin in Saccharomyces cerevisiae. Induction of these pathway enzymes has been shown to be regulated at transcription, and response to inducer is lost in dal81 and dal82/durM mutants. The similar phenotypes generated by dal81 and dal82 mutations prompted the question of whether they were allelic. We demonstrated that the DAL81 and DAL82 loci are distinct, unlinked genes situated on chromosomes IX and XIV. DAL82 gene expression did not respond to induction by the allantoin pathway inducer or to nitrogen catabolite repression. Expression was also not significantly affected by mutation of the dal80 locus. From the nucleotide sequence of the DAL82 gene, we deduced that it encodes a protein with a mass of 29,079 Da that may possess the structural motifs expected of a regulatory protein. This protein was shown to be required for the function mediated by the cis-acting upstream induction sequence situated in the 5'-flanking regions of the inducible allantoin pathway genes.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-14582193,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-16561177,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2153652,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2493990,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2511434,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2552287,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2651902,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2660461,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2674683,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2686840,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2725678,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2776214,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2820939,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2830478,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2892826,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2911489,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2951591,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-2956925,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3025621,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3123916,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3301804,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3319781,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3327750,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-347451,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3561414,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3600658,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3762694,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3915539,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3916727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-3931077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-4580053,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-4591950,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-6152012,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-6236744,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-6336730,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-6392015,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-7039847,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1898922-7050082
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0021-9193
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
173
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pubmed:geneSymbol |
dal81,
dal82
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
255-61
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:1898922-Allantoin,
pubmed-meshheading:1898922-Alleles,
pubmed-meshheading:1898922-Base Sequence,
pubmed-meshheading:1898922-Escherichia coli,
pubmed-meshheading:1898922-Gene Expression,
pubmed-meshheading:1898922-Gene Expression Regulation, Fungal,
pubmed-meshheading:1898922-Genes, Fungal,
pubmed-meshheading:1898922-Genetic Complementation Test,
pubmed-meshheading:1898922-Genotype,
pubmed-meshheading:1898922-Molecular Sequence Data,
pubmed-meshheading:1898922-Mutagenesis, Site-Directed,
pubmed-meshheading:1898922-Restriction Mapping,
pubmed-meshheading:1898922-Saccharomyces cerevisiae,
pubmed-meshheading:1898922-Transcription, Genetic,
pubmed-meshheading:1898922-beta-Galactosidase
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pubmed:year |
1991
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pubmed:articleTitle |
DAL82, a second gene required for induction of allantoin system gene transcription in Saccharomyces cerevisiae.
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pubmed:affiliation |
Department of Microbiology and Immunology, University of Tennessee, Memphis 38163.
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pubmed:publicationType |
Journal Article
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