University of Wisconsin–Madison
College of Agriculture and Life Sciences | School of Medicine and Public Health

Phil Anderson

Emeritus

andersn@wisc.edu

608-263-8429

4302A Genetics/Biotech

Education
Ph.D., University of California at Berkeley, 1977, Postdoctoral Research: MRC Laboratory of Molecular Biology, Cambridge, England
Department
Genetics
Research Interests
Molecular genetics of C. elegans
Research Fields
Gene Expression, Molecular Genetics, C. elegans

Research Description:
The steady-state levels of eukaryotic mRNAs are determined by their relative rates of synthesis and degradation. It is increasingly apparent that mRNAs 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 mRNAs. 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 conductance 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:
Search PubMed for more publications by Philip Anderson

Grimson, A., O’Connor, S., Loushin Newman, C. and Anderson, P. 2004. SMG-1 is a phosphatidylinositol kinase-related protein kinase required for nonsense-mediated mRNA decay in C. elegans. Mol. Cell. Biol. 24:7483-749.

Anders, K., Grimson, A.W., and Anderson, P. 2003. SMG-5, required for C. elegans nonsense-mediated mRNA decay, associates with SMG-2 and protein phosphatase 2A. EMBO J. 22:641-65.

Mitrovich, Q.M. and Anderson, P. 2000. Unproductively spliced ribosomal protein mRNAs are natural targets of mRNA surveillance in C. elegans. Genes Dev. 14:2173-218.

Cali, B.M., Kuchma, S.L., Latham, J. and Anderson, P. 1999. smg-7 is required for mRNA surveillance in Caenorhabditis elegans. Genetics. 151:605-16.

Page, M.F, Carr, B., Anders, K.R., Grimson, A. and Anderson, P. 1999. SMG-2 is a phosphorylated protein required for mRNA surveillance in Caenorhabditis elegans and related to Upf1p of yeast. Mol. Cell. Biol. 19:5943-5951.