Dr. David M Eisenmann
Professor · Tenured
Department of Biological Sciences
College of Natural and Mathematical Sciences
He/Him/His/Himself
About
I received my training in the fields of Genetics and Developmental Biology and I am fascinated by the process of development. I teach or have taught courses in the areas of genetics, biochemistry, molecular biology, developmental biology and cell signaling. I also serve as Undergraduate Program Director for the Department of Biological Sciences.
Research interests
For 25 years my laboratory studied animal developmental biology, in particular the process of cell fate specification - how newly born cells know what fate to adopt during development. We focused on two types of skin cells that arise during development in the invertebrate model system, the nematode worm C. elegans. In the past, we 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. More recently we examined: 1) the function of pax-3, a gene that regulates the choice between these two skin cell types during embryogenesis, and 2) the temporal co-regulation of a large set of genes in the worm's skin cells during larval life.
NOTE: The Eisenmann lab is no longer accepting students, graduate or undergraduate.
Teaching interests
BIOL 302 Molecular and General Genetics
BIOL 430 Biochemistry
BIOL 442 Developmental Biology
BIOL 443 Advanced Topics in Developmental Biology
BIOL 445 Signal Transduction
Education
- Ph D, Genetics — Harvard University (1992)
- BS, Biochemistry — University of Pennsylvania (1985)
Publications
- The Paired-box protein PAX-3 regulates the choice between lateral and ventral epidermal cell fates in C. elegans. 2016
- Identification of Wnt Pathway Target Genes Regulating the Division and Differentiation of Larval Seam Cells and Vulval Precursor Cells in Caenorhabditis elegans. 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. 2015
- 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. 2014
- Use of an activated beta-catenin to identify Wnt pathway target genes in caenorhabditis elegans, including a subset of collagen genes expressed in late larval development. 2014
- 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. 2013
- β-catenin-dependent Wnt signaling in C. elegans: teaching an old dog a new trick. 2012
- C. elegans seam cells as stem cells: Wnt signaling and casein kinase Iα regulate asymmetric cell divisions in an epidermal progenitor cell type. 2011
- Wnt signaling controls the stem cell-like asymmetric division of the epithelial seam cells during C. elegans larval development. 2010
- A conserved RAS/mitogen-activated protein kinase pathway regulates DNA damage-induced cell death postirradiation in Radelegans. 2006
- Multiple redundant Wnt signaling components function in two processes during C. elegans vulval development. 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. 2006
- A Caenorhabditis elegans tissue model of radiation-induced reproductive cell death. 2006
- Transcriptional upregulation of the C. elegans Hox gene lin-39 during vulval cell fate specification. 2006
- Wnt signaling. 2005
- Identification of evolutionarily conserved promoter elements and amino acids required for function of the C. elegans beta-catenin homolog BAR-1. 2004
- The Caenorhabditis elegans pvl-5 gene protects hypodermal cells from ced-3-dependent, ced-4-independent cell death. 2004
- 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. 2002
- Activation of Wnt signaling bypasses the requirement for RTK/Ras signaling during C. elegans vulval induction. 2002
- The divergent Caenorhabditis elegans beta-catenin proteins BAR-1, WRM-1 and HMP-2 make distinct protein interactions but retain functional redundancy in vivo. 2001
- Protruding vulva mutants identify novel loci and Wnt signaling factors that function during Caenorhabditis elegans vulva development. 2000
- Identification of RTF1, a novel gene important for TATA site selection by TATA box-binding protein in Saccharomyces cerevisiae. 1997
- Mechanism of activation of the Caenorhabditis elegans ras homologue let-60 by a novel, temperature-sensitive, gain-of-function mutation. 1997
- Signal transduction and cell fate specification during Caenorhabditis elegans vulval development. 1994
- The Saccharomyces cerevisiae SPT8 gene encodes a very acidic protein that is functionally related to SPT3 and TATA-binding protein. 1994
- SPT3 interacts with TFIID to allow normal transcription in Saccharomyces cerevisiae. 1992
- Biochemical and genetic characterization of a yeast TFIID mutant that alters transcription in vivo and DNA binding in vitro. 1992
- SPT15, the gene encoding the yeast TATA binding factor TFIID, is required for normal transcription initiation in vivo. 1989