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Related Experiment Videos

Clustered alpha-amanitin resistance mutations in mouse

M S Bartolomei1, J L Corden

  • 1Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Molecular & General Genetics : MGG
|March 20, 1995
PubMed
Summary

Researchers identified three new mutations in mouse RNA polymerase II (RPII215) conferring alpha-amanitin resistance. These findings highlight a conserved region critical for transcription elongation and suggest a potential drug-binding site.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Alpha-amanitin is a potent toxin that inhibits RNA polymerase II (RPII215).
  • Mutations in RPII215 can confer resistance to alpha-amanitin.
  • Previous studies identified resistance mutations in Drosophila and Caenorhabditis elegans.

Purpose of the Study:

  • To identify new alpha-amanitin resistance mutations in the mouse RPII215 gene.
  • To investigate the functional significance of these mutations in transcription elongation.
  • To define a potential alpha-amanitin binding pocket within RPII215.

Main Methods:

  • Site-directed mutagenesis was used to introduce specific amino acid substitutions in mouse RPII215.
  • Alpha-amanitin resistance was assessed through phenotypic analysis.

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  • Sequence conservation analysis was performed across various species.

    • Main Results:

    • Three novel alpha-amanitin resistance mutations were identified: L745F, R749P, and I779F.
    • These mutations are clustered in a transcription elongation domain of RPII215.
    • This domain is highly conserved across species and shows conservation in naturally resistant organisms.

    Conclusions:

    • The identified mutations are located in a conserved region of RPII215 critical for transcription elongation.
    • This region likely plays a conserved catalytic role and is involved in alpha-amanitin binding.
    • The mutations, along with a previously reported substitution, define a potential alpha-amanitin binding pocket crucial for polymerase translocation during elongation.