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David Eisenmann, Ph.D.

Associate Professor

David Eisenmann

Office: BS 316
Phone: 410-455-2256
Lab: BS 307-308/317-319
Lab Phone: 410-455-1334

Research Group


Postdoctoral, Stanford University, 1997
Ph.D., Harvard University, 1992

Professional Interests

My laboratory studies animal developmental biology, in particular we are interested in the process of cell fate specification – how newly born cells know what fate to adopt during development. We focus on development of the skin in the invertebrate model system, the nematode worm C. elegans. Previously we have studied the regulation of gene expression downstream of the Wnt signaling pathway in the lateral seam cells and ventral vulval precursor cells in this animal, as well as regulation of expression of the Hox gene lin-39. More recently we have been examining 1) pax-3, a gene that regulates the choice between these two cell types during embryogenesis, and 2) the temporal co-regulation of a large set of genes in these hypodermal cells during larval life.


Gorrepati, L., Krause M. W., Chen W., Brodigan T. M., Correa-Mendez M. and D. M. Eisenmann (2015) Identification of Wnt pathway target genes regulating the division and differentiation of larval seam cells and vulval precursor cells in C. elegans. G3 Genes Genomes Genetics 5:551-1566. doi: 10.1534/g3.115.017715

Gorrepati L. and Eisenmann, D.M. (2015). The C. elegans embryonic fate specification factor EGL-18 (GATA) is reutilized downstream of Wnt signaling to maintain a population of larval progenitor cells. Worm 4(1): e996419. (Review)

Jackson, B. M. J., Abete-Luzi, P., Krause, M. W. and D. M. Eisenmann (2014) Use of an activated beta-catenin to identify Wnt pathway target genes in C. elegans, including a subset of collagen genes expressed in late larval development. G3 Genes Genomes Genetics 4: 733-747. mdoi: 10.1534/g3.113.009522

Liu, W. J., Reece-Hoyes, J. S., Walhout, A. J. M. and D. M. Eisenmann (2014) Multiple transcription factors directly regulate Hox gene lin-39 expression in ventral hypodermal cells of the C. elegans embryo and larva, including the hypodermal fate regulators LIN-26 and ELT-6. BMC Developmental Biology 14:17 (13 May 2014)

Gorrepati, L., K. W. Thompson and D. M. Eisenmann (2013).  C. elegans GATA factors EGL-18 and ELT-6 function downstream of Wnt signaling to maintain the progenitor fate during larval asymmetric divisions of the seam cells.  Development 140:2093-102.

Jackson, B.J. and Eisenmann, D. M. 2012. Beta-catenin dependent Wnt signaling in C. elegans: Teaching an old dog a new trick. Cold Spring Harbor Perspectives in Biology. doi: 10.1101/cshperspect.a007948.
[Abstract] (Review)

D. M. Eisenmann. (2011) C. elegans seam cells as stem cells: Wnt signaling and casein kinase Iα regulate asymmetric cell divisions in an epidermal progenitor cell type. Cell Cycle 10: pg 21. (Comment on: Banerjee D, et al. Cell Cycle 2010; 9:4748-65)

J. E. Gleason, and D. M. Eisenmann (2010) Wnt signaling controls the stem cell-like asymmetric division of the epithelial seam cells during C. elegans larval development. Developmental Biology 348, pages 58-66.

Gleason, J. E., E. A. Szyleyko and D. M. Eisenmann (2006) Multiple redundant Wnt signaling components function in two processes during C. elegans vulval development. Developmental Biology 298:442-457.

J. B. Weidhaas, D. M. Eisenmann, J.M. Holub and S. Nallur (2006). A C. elegans tissue model of radiation-induced reproductive cell death. Proceedings National Academy of Sciences 103: 9946-9951.

J. B. Weidhaas, D. M. Eisenmann, J.M. Holub and S. Nallur (2006). A Conserved EGFR/Ras/MAPK Pathway Regulates DNA Damage-Induced Cell Death Post-irradiation in Radelegans. Cancer Research 66: 10434-10438.

Wagmaister, J.A., Miley, G.R., Morris, C.A., Gleason, J. E., Miller, L.M., Kornfeld, K., and D. M. Eisenmann. (2006). Identification of cis-regulatory elements from the C. elegans Hox gene lin-39 required for embryonic expression and for regulation by the transcription factors LIN-1, LIN-31 and LIN-39. Developmental Biology 297: 550-565.

Wagmaister, J.A., Gleason, J. E., and D. M. Eisenmann. 2006. Transcriptional upregulation of the C. elegans Hox gene lin-39 during vulval cell fate specification. Mechanism of Development 123: 135-150.

Eisenmann, D. M. 2005. Signal Transduction: Wnt Signaling. Chapter in WormBook, ed. The C. elegans Research Community, WormBook, doi/10.1895/wormbook.1.7.1,

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. Developmental Biology 272: 536-557.

Joshi, P. and D. M. Eisenmann. 2004. The C. elegans pvl-5 gene protects hypodermal cells from ced-3-dependent, ced-4-independent cell death. Genetics 167: 673-685.

Koh, K., Peyrot, S. M.**, Wood, C. G., Wagmaister, J. A., Eisenmann, D. M., 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.

Gleason, J, H. C. Korswagen, and D. M. Eisenmann. 2002. Activation of Wnt signaling can bypass the requirement for Ras signaling during C. elegans vulval induction. Genes and Development 16: 1281-1290.

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 maintain functional redundancy in vivo. Genetics 159: 159 –172.

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

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

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

Stolinski, L.A., Eisenmann, D.M., and Arndt, K.M. 1997. Identification of RTF1, a novel gene important for TATA site selection by TATA box-binding protein in Saccharomyces cerevisiae. Molecular and Cellular Biology 17: 4490-4500

Eisenmann, D.M., C. Chapon, S.M. Roberts, C. Dollard, and F. Winston. 1994. The Saccharomyces cerevisiae SPT8 gene encodes a very acidic protein that is functionally related to SPT3 and TATA-binding protein. Genetics 137: 647-657.

Eisenmann, D.M., K.A. Arndt, S.L. Ricupero, J.W. Rooney, and F. Winston. 1992. SPT3 interacts with TFIID to allow normal transcription in Saccharomyces cerevisiae. Genes and Development 6: 1319-1331.

Arndt, K.M., S.L. Ricupero, D.M. Eisenmann, and F. Winston. 1992. Biochemical and genetic characterization of a yeast TFIID mutant that alters transcription in vivo and DNA-binding in vitro. Molecular and Cellular Biology 12: 2372-2382.

Eisenmann, D.M., C. Dollard, and F. Winston. 1989. SPT15, the gene encoding the yeast TATA-binding factor TFIID, is required for normal transcription initiation in vivo. Cell 58: 1183-1191.

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.

Courses Taught

BIOL 302: Molecular and General Genetics
BIOL 414: Eukaryotic Genetics and Molecular Biology
BIOL 442: Developmental Biology
BIOL 443: Advanced Topics in Developmental Biology
BIOL 445: Signal Transduction
BIOL 642: Introduction to Developmental Biology
BIOL 643: Topics in Advanced Developmental Biology
BIOL 645: Signal Transduction
BIOL 740: Graduate Seminar: Analysis of Development
BIOL 745: Research Seminar in Developmental Biology