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Genetics at UW-Madison Faculty and Their Research

Photo of Philip Anderson

4302A Genetics/Biotech




  • Gene Expression
  • Molecular Genetics
  • C. elegans

Philip Anderson

Professor of Genetics

Ph.D., University of California at Berkeley, 1977
Postdoctoral Research: MRC Laboratory of Molecular Biology, Cambridge, England

Research Interests

Molecular genetics of C. elegans

Research Description

The steady-state levels of eukaryotic mRNAs are deteremined by their relative rates of synthesis and degradation. It is increasingly apparent that mRNAss stability plays an important role in gene expression. Turnover of many, if not all, mRNAs is intimately coupled to translation. The importance of translation in mRNA turnover is particuarly striking in the case of nonsense-mutant mRNA's, Messenger RNAs that contain contain premature stop codons are unstable in all eukaryotes. The Anderson lab investigates nonsense medicated mRNA decay in the nematode Caenorhabditis elegans. Mutations in any of seven different genes (smg-1 through smg-7) eliminate nonsense-mediated mRNA decay and cause nonsense mutant mRNAs to be stable, rather than unstable.

Our work is designed to answer four questions: What are the smg gene products? Where are smg proteins located in the cell, and with what do they associate? How are nonsense mutant mRNAs targeted for selective degradation? What are the natural substrates for nonsense-mediated mRNA decay in vivo? We combine genetic, molecular, and biochemical approaches to answer these questions.

The Anderson lab also studies regulation of muscle contraction in C. elegans. Muscle Contraction occurs following release of calcium ions from intracelluar stores through high conducatnce ion channels termed ryanodine receptors. The Anderson lab investigates functions of the C. elegans ryanodine receptor and its role in excitation-contraction coupling using a combination of genetic, molecular and biochemical methods.

Representative Publications