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David Eisenmann


Biological Sciences
Biological Sciences Bldg, Room 316
Ph D, Harvard University (1992)
BS, University of Pennsylvania (1985)

I received my training in the fields of Genetics and Developmental Biology and I am fascinated by the process of development. I teach in both of these areas and have a lab studying development in the invertebrate model organism C. elegans. I also serve as Undergraduate Program Director for the Department of Biological Sciences.

Research 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 two types of skin cells that arise during development in the invertebrate model system, the nematode worm C. elegans. 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. 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.

Teaching Interests

BIOL 302 Molecular and General Genetics BIOL 442 Developmental Biology BIOL 443 Advanced Topics in Developmental Biology BIOL 445 Signal Transduction

Intellectual Contributions

The Paired-box protein PAX-3 regulates the choice between lateral and ventral epidermal cell fates in C. elegans. 2 vol. 412 191-207 Developmental biology

Identification of Wnt Pathway Target Genes Regulating the Division and Differentiation of Larval Seam Cells and Vulval Precursor Cells in Caenorhabditis elegans. 8 vol. 5 1551-66 G3 (Bethesda, Md.)

The C. elegans embryonic fate specification factor EGL-18 (GATA) is reutilized downstream of Wnt signaling to maintain a population of larval progenitor cells. 1 vol. 4 e996419 Worm

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. vol. 14 17 BMC developmental biology

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. 4 vol. 4 733-47 G3 (Bethesda, Md.)

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. 10 vol. 140 2093-102 Development (Cambridge, England)

β-catenin-dependent Wnt signaling in C. elegans: teaching an old dog a new trick. 8 vol. 4 a007948 Cold Spring Harbor perspectives in biology

C. elegans seam cells as stem cells: Wnt signaling and casein kinase Iα regulate asymmetric cell divisions in an epidermal progenitor cell type. 1 vol. 10 20-1 Cell cycle (Georgetown, Tex.)

Wnt signaling controls the stem cell-like asymmetric division of the epithelial seam cells during C. elegans larval development. 1 vol. 348 58-66 Developmental biology

A conserved RAS/mitogen-activated protein kinase pathway regulates DNA damage-induced cell death postirradiation in Radelegans. 21 vol. 66 10434-8 Cancer research

Multiple redundant Wnt signaling components function in two processes during C. elegans vulval development. 2 vol. 298 442-57 Developmental biology

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. 2 vol. 297 550-65 Developmental biology

A Caenorhabditis elegans tissue model of radiation-induced reproductive cell death. 26 vol. 103 9946-51 Proceedings of the National Academy of Sciences of the United States of America

Transcriptional upregulation of the C. elegans Hox gene lin-39 during vulval cell fate specification. 2 vol. 123 135-50 Mechanisms of development

Wnt signaling. 1-17 WormBook : the online review of C. elegans biology

Identification of evolutionarily conserved promoter elements and amino acids required for function of the C. elegans beta-catenin homolog BAR-1. 2 vol. 272 536-57 Developmental biology

The Caenorhabditis elegans pvl-5 gene protects hypodermal cells from ced-3-dependent, ced-4-independent cell death. 2 vol. 167 673-85 Genetics

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. 22 vol. 129 5171-80 Development (Cambridge, England)

Activation of Wnt signaling bypasses the requirement for RTK/Ras signaling during C. elegans vulval induction. 10 vol. 16 1281-90 Genes & development

The divergent Caenorhabditis elegans beta-catenin proteins BAR-1, WRM-1 and HMP-2 make distinct protein interactions but retain functional redundancy in vivo. 1 vol. 159 159-72 Genetics

Protruding vulva mutants identify novel loci and Wnt signaling factors that function during Caenorhabditis elegans vulva development. 3 vol. 156 1097-116 Genetics

Identification of RTF1, a novel gene important for TATA site selection by TATA box-binding protein in Saccharomyces cerevisiae. 8 vol. 17 4490-500 Molecular and cellular biology

Mechanism of activation of the Caenorhabditis elegans ras homologue let-60 by a novel, temperature-sensitive, gain-of-function mutation. 2 vol. 146 553-65 Genetics

Signal transduction and cell fate specification during Caenorhabditis elegans vulval development. 4 vol. 4 508-16 Current opinion in genetics & development

The Saccharomyces cerevisiae SPT8 gene encodes a very acidic protein that is functionally related to SPT3 and TATA-binding protein. 3 vol. 137 647-57 Genetics

SPT3 interacts with TFIID to allow normal transcription in Saccharomyces cerevisiae. 7 vol. 6 1319-31 Genes & development

Biochemical and genetic characterization of a yeast TFIID mutant that alters transcription in vivo and DNA binding in vitro. 5 vol. 12 2372-82 Molecular and cellular biology

SPT15, the gene encoding the yeast TATA binding factor TFIID, is required for normal transcription initiation in vivo. 6 vol. 58 1183-91 Cell