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Gene Review

mutT  -  MutT/nudix family protein

Streptococcus pneumoniae R6

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Disease relevance of mutT


High impact information on mutT

  • The involvement of mismatch repair defects in microsatellite instability and tumorigenesis suggests that a generalized mutator phenotype is responsible for the large number of genetic alterations observed in tumors [3].
  • Site-directed mutagenesis and analysis of nitrosoguanidine-induced mutT mutants suggest that a small region of high homology between the two proteins (61% identity over 23 residues) is part of the catalytic site of the nucleoside triphosphatase [1].
  • Here we report that disrupting the pneumococcal mutY homologue abolishes the hyperrecombination induced by ami36 and leads to a mutator phenotype specifically enhancing AT-to-CG transversions [4].
  • In agreement with this hypothesis, an increase in mutS gene copy number abolished the hexA-induced mutator phenotype [5].
  • Fitness limitations of mutators may be overcome simply by the high bacterial cell densities that can be achieved during acute infection or by the adoption of transient mutator status [6].

Chemical compound and disease context of mutT


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