Source:http://linkedlifedata.com/resource/pubmed/id/12770777
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3-4
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pubmed:dateCreated |
2003-5-28
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pubmed:abstractText |
UDP-GlcNAc: alpha-3-D-mannoside beta1,2-N-acetylglucosaminyltransferase I (GnT I) is a Golgi-resident enzyme which transfers a GlcNAc residue in beta1,2 linkage to the Manalpha1,3Manbeta-terminus of (Manalpha1,6(Manalpha1,3)Manalpha1,6)(Manalpha1,3)Manbeta1,4GlcNAcbeta1,4GlcNAc-Asn-protein, thereby initiating the synthesis of hybrid N-glycans. Three Caenorhabditis elegans genes homologous to mammalian GnT I (designated gly-12, gly-13 and gly-14) have been cloned. All three cDNAs encode proteins with GnT I enzyme activity. We report in this paper the preparation by ultra-violet (UV) light irradiation in the presence of trimethylpsoralen, of mutants lacking either gly-12, gly-13 or gly-14. A double null mutation in the gly-12 and gly-14 genes (gly-14; gly-12) has also been prepared. These mutations are intragene deletions, removing large portions of the GnT I catalytic domain, and are therefore, all molecular nulls. The gly-12 and gly-14 mutants as well as the gly-14; gly-12 double mutant all displayed wild-type phenotypes, indicating that neither gly-12 nor gly-14 is necessary for worm development under standard laboratory conditions. In contrast, about 60% of the mutants lacking the gly-13 gene arrested as L1 larvae at 20 degrees C and the remaining 40% homozygous worms grew to adulthood but displayed severe morphological and behavioral defects despite the presence of the other two GnT I genes, gly-12 and gly-14. Attempts to rescue the gly-13 null phenotype with the wild type transgene were not successful. However, lethality co-segregated with the gly-13 deletion within 0.02 map units (mu) in genetic mapping experiments, suggesting that the gly-13 mutation is responsible for the phenotype.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0300-9084
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
85
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
391-401
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12770777-Alleles,
pubmed-meshheading:12770777-Animals,
pubmed-meshheading:12770777-Base Sequence,
pubmed-meshheading:12770777-Caenorhabditis elegans,
pubmed-meshheading:12770777-Chromosome Mapping,
pubmed-meshheading:12770777-Crosses, Genetic,
pubmed-meshheading:12770777-DNA, Helminth,
pubmed-meshheading:12770777-Female,
pubmed-meshheading:12770777-Gene Deletion,
pubmed-meshheading:12770777-Genes, Helminth,
pubmed-meshheading:12770777-Genes, Lethal,
pubmed-meshheading:12770777-Male,
pubmed-meshheading:12770777-Mutation,
pubmed-meshheading:12770777-N-Acetylglucosaminyltransferases,
pubmed-meshheading:12770777-Phenotype
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pubmed:articleTitle |
Isolation of null alleles of the Caenorhabditis elegans gly-12, gly-13 and gly-14 genes, all of which encode UDP-GlcNAc: alpha-3-D-mannoside beta1,2-N-acetylglucosaminyltransferase I activity.
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pubmed:affiliation |
The Burnham Institute, La Jolla, CA 92037, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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