DAVID M. EISENMANN

Associate Professor
Ph.D., Harvard University, 1992
Postdoctoral, Stanford University

eisenman@umbc.edu; FAX (410) 455-3875; Voice (410) 455-2256 

Research Interests

My laboratory studies the process of signal transduction during animal development. A basic question in developmental biology is how do undifferentiated cells respond to signals from other cells in order to differentiate correctly? We are addressing this question by studying the development of the vulva of the nematode worm, Caenorhabditis elegans. During development, six cells in the worm choose one of four different cell fates based on external signals they recieve. Three of the cells divide and form the vulva, while the other three become part of the skin. These cells respond to the signals by using a Ras signaling pathway, a cascade of proteins that has been conserved across species from C. elegans to mammals. Mutations in some components of this pathway cause tumors in humans. We have isolated mutations in several new genes which perturb the normal pattern of vulval development in interesting ways. The main focus of my lab is cloning and understanding the genes identified by these mutations. The first of these genes, called bar-1, encodes a C. elegans b-catenin/armadillo-related protein. Proteins of this type function in a different type of evolutionarily-conserved signal transduction pathway, the Wnt pathway. We are investigating how BAR-1 protein functions during vulval induction, how BAR-1 interacts with the Ras signaling pathway, and whether BAR-1 controls the expression of C. elegans HOX genes (transcription factors that regulate cell fate).

Selected Publications:

Natarajan L, B.M. Jackson, E. Szyleyko and D.M. Eisenmann. 2004. Identification of evolutionarily conserved promoter elements and amino acids required for function of the C. elegans beta-catenin homolog BAR-1. Dev Biol. 272:536-57. (Abstract)

Joshi P. and D.M. Eisenmann. 2004. The Caenorhabditis elegans pvl-5 gene protects hypodermal cells from ced-3-dependent, ced-4-independent cell death. Genetics. 167:673-85. (Abstract)

Koh K., S.M. Peyrot, C.G. Wood, J.A.Wagmaister, M.F. Maduro, D.M. Eisenmann and J.H. Rothman.  2002. Cell fates and fusion in the C. elegans vulval primordium are regulated by the EGL-18 and ELT-6 GATA factors -- apparent direct targets of the LIN-39 Hox protein.
Development. 129:5171-5180. (Abstract)

Gleason J.E., H.C. Korswagen and D.M. Eisenmann. 2002. Activation of Wnt signaling bypasses the requirement for RTK/Ras signaling during C. elegans vulval induction.  Genes Dev. 16:1281-1290. (Abstract)

Natarajan, L., N. Witwer and D. M. Eisenmann. 2001. The divergent C. elegans beta-catenin proteins BAR-1, WRM-1 and HMP-2 make distinct protein interactions but retain functional redundancy in vivo. Genetics 159:159-172. (Abstract)

D. M. Eisenmann and S. K. Kim. 2000 Protruding vulva mutants identify novel loci and Wnt signaling factors that function during C. elegans vulva development. Genetics 156: 1097-1116.  (Abstract)

Eisenmann, D. M., Maloof, J. N., Simske, J. S., Kenyon, C. and S. K. Kim. 1998. The beta-catenin homolog BAR-1 and LET-60 Ras coordinately regulate the Hox gene lin-39 during Caenorhabditis elegans vulval development. Development  125: 3667-3680. (Abstract)

Eisenmann, D.M. and S.K. Kim. 1997. Mechanism of activation of the C. elegans ras homolog let-60 by a novel, temperature-sensitive, gain-of-function mutation. Genetics  146 (2): 553-565. (Abstract)

Eisenmann, D.M. and S.K. Kim. 1994. Signal transduction and cell fate specification during Caenorhabditis elegans vulval development. Current Opinion in Genetics and Development  4: 508-516. (Abstract)