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Anne E. Griep

Associate Professor of Anatomy

Anne E. Griep
Address:
353 Bardeen Labs
Telephone:
262-8988
Email:
aegriep@wisc.edu
Research Fields:
Developmental Genetics
Mouse Genetics

Ph.D., University of Wisconsin-Madison

Postdoctoral Research: Developmental Biology, National Institutes of Health

Research Interests

Genetic and molecular regulation of mouse eye development and disease

Research Description

We are investigating the genetic pathways and molecular mechanisms through which cell proliferation and differentiation are regulated during normal mouse eye development. We use a variety of genetic, molecular, cell biological and embryological techniques, transgenic and knockout mice and associated tissue culture systems in our studies. In recent years we’ve identified several gene families that are critical regulators of different aspects of lens cell proliferation and differentiation. These include the pRb family of cell cycle regulators, the caspase family of proapoptotic enzymes, and the FGF growth factor signaling pathway. Presently, our studies are aimed at extending these findings. We are identifying the molecular mechanisms and genetic pathways through which the pRb family regulates cell proliferation in both the undifferentiated and differentiating cells. We are determing how the very limited subset of caspases can control the loss of specific cellular organelles like the nucleus without destroying the entire cell. Finally, we are determining the specific pathways through which FGF signaling controls lens cell differentiation and if a newly discovered form of FGF-2 ligand is involved. Ultimately, we hope to understand how these various pathways leads to ocular disease.

Representative Publications

  • Stolen, C.M. and A.E. Griep. 2000. Disruption of lens fiber cell differentiation and survival at multiple stages by region-specific expression of truncated FGF receptors. Dev. Biol., 217:205-22.
  • McCaffrey, J., L. Yamasaki, N. Dyson, E. Harlow, and A.E. Griep. 1999. Disruption of retinoblastoma protein family function by HPV-16 E7 alters lens development in part through E2F-1. Mol. Cell Biol. 19:6458-6468.
  • Pan, H. and A.E. Griep. 1995. Temporally distinct patterns of p53-dependent and p53-independent apoptosis during mouse lens development. Genes Dev. 9:2157-2169.