Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.4.1.2 (glutamate dehydrogenase)
 4,380 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the further analysis of a cross in which the mis-sense allele, am3, of the Neurospora crassa am (glutamate dehydrogenase) gene was present in one parent together with two ectopic wild-type gene copies, one ascus was identified in which the two ectopic copies had been inactivated by the RIP process whereas the am3 allele continued to produce its characteristic enzyme variety in active, but heat-sensitive, form. The am3 allele had also acquired a new HindIII restriction site. It had no detectable methylation. The mutations responsible respectively for the new restriction site and the modified enzyme properties were separated from each other, and from the original am3 mutation, by selecting for intragenic recombination on either side of the am3 site. In this way two new effectively wild-type alleles were generated, one characterised by its heat-sensitive and kinetically modified enzyme product and the other by a new HindIII site. These results demonstrate that the RIP phenomenon can be a source of new functional alleles.
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PMID:Generation of new functional mutant alleles by premeiotic disruption of the Neurospora crassa am gene. 215 Mar 48

Premeiotic inactivation of duplicated sequences (the RIP phenomenon of Selker et al.) was studied by tetrad analysis using ectopic copies of am+ (coding for NADP-specific glutamate dehydrogenase) and a missense allele am3, coding for a distinctive form of the enzyme, at the normal locus. In duplication crosses either both gene copies were inactivated or neither. Two inactivated am3 derivatives were shown to have undergone methylation and numerous base-pair changes, reflected in losses and gains of restriction sites, but without sequence rearrangement. Cutting at restriction sites within the disrupted sequences was incomplete but became almost complete following growth in the presence of 5-azacytidine. In a triplication cross in which one parent carried two unlinked ectopic gene copies together with am3 at the normal locus, premeiotic inactivation, when it occurred, tended to affect two of the three copies in any one ascus, but there were a few asci in which all three were inactivated.
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PMID:Premeiotic disruption of duplicated and triplicated copies of the Neurospora crassa am (glutamate dehydrogenase) gene. 252 44