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> College of Agriculture > VMB > Faculty & Research > Dr. Schmidt
Department of Veterinary Molecular Biology

Ed Schmidt, Associate Professor

Veterinary Molecular Biology
P.O. Box 173610
Montana State University
Bozeman, MT 59717
(406) 994-6375
eschmidt@montana.edu

          Ed Schmidt

Research Interests

The Schmidt Lab studies intricate gene regulatory mechanisms that function in the development and maintenance of complex organisms like ourselves. Most of our work is based on analyses of mouse lines we produce that bear targeted mutations (e.g., "knockouts"); however, our approaches to understanding the roles of the mutated genes are broad, including phylogenetics, genetics, biochemistry, molecular biology, histology, biophysics, genomics, proteomics, and other techniques. The biological processes we are studying include early embryonic patterning and development, placental development, germ cell maturation, immune cell functions, and the maternal/fetal immune interaction.

Schmidt Laboratory Home Page

Education

  • B.S., B.A. University of Montana, Missoula, MT 1981-1985 Biology, Microbiol, Zoology
  • Ph.D. Oregon State University, Corvallis, OR 1986-1990 Biochemistry & Biophysics
  • Postdoc University of Geneva, Geneva, Switzerland 1991-1995 Molecular Biology
  • Postdoc University of Utah, Salt Lake City, UT 1996-1999 Molecular Genetics

Professional Experience

  • 1986-1990 Ph.D. Student, Oregon State University, Dept. Biochemistry and Biophysics
  • 1991-1995 Postdoctoral Assistant, University of Geneva, Dept. Mol. Biol. (group: Ueli Schibler)
  • 1996-1999 Postdoctoral Assistant, University of Utah, Dept. Hu. Genet. (group: Mario Capecchi)
  • 1999-pres. Assistant Professor, Montana State University, Dept. Veterinary Molecular Biology

Honors and Awards

  • 1984-1985 Watkins Honorary Undergraduate Research Scholarship, University of Montana
  • 1985 Graduated with Honors, University of Montana
  • 1986-1987 NIH Pre-Doctoral Training Grant, Oregon State University
  • 1987-1988 N.L. Tartar Pre-Doctoral Research Fellowship, Oregon State University
  • 1991-1993 N.I.H.-Fogarty/Swiss National Science Foundataion Post-Doctoral Fellowship
  • 1993-1996 State of Geneva (Switzerland) Post-Doctoral Fellowship, University of Geneva
  • 1996 Post-Doctoral Fellow supported by the Mather's Charitable Foundation
  • 1997-1999 Howard Hughes Medical Institute Fellow of the Life Sciences Research Foundation
  • 2001 Received personal letter of commendation from US Senator Conrad Burns
  • 2001-2003 Named Basil O'Connor New Investigator of the March of Dimes Foundation
  • 2002 Elected member of American Society for Biochemistry and Molecular Biology

Extramural Grant Activity

Ongoing Research Support.

  • NSF, 0090884, 2/01 - 1/05 "Vertebrate specific transcriptional signaling". Role: P.I. This project investigates evolution of the vertebrate-specific TBP N-terminus and takes a whole-genome approach to evaluating signaling through this protein domain in cells and in animals.
  • March of Dimes, 6-FY03-61, 6/03 - 5/06, "Regulation of the maternal/fetal immune interaction". Role: P.I. This project uses a mouse model system to look at maternal tolerance.

Completed Research Support

  • USDA-NRI, Seed Grant, 12/01 - 11/03, "Parameters affecting the efficiency of targeted mutagenesis in bovine cells. Role: P.I This project investigates the relationship between targeting vector design and targeting efficiency in bovine cells.
  • March of Dimes, Basil O'Connor New Investigator Award, 5-FY00-520, "Regulation of midgestation". Role: P.I. This project investigated defects in gene regulation leading to spontaneous miscarriages in a mouse model system that we developed.
  • NIH NICHD, R03-HD35824 7/98 - 6/00, "Disruption of spermatid-specific TBP expression in mice". Role: P.I. This project used targeted mutagenesis to create lines of mice bearing specific mutations in the tbp gene.
  • NSF, MONTS Award, 1/00 - 12/00, "Identification of the primary defect causing embryonic lethality in a mutant mouse line. Role: P.I. This project identified the reason that the mice which form the basis for the current proposal die of an interaction defect between the mother's immune system and the placenta.
  • NIH NICHHD, R03-HD39242 8/00 - 7/02, "Purifying homogeneous spermatid sub-populations". Role: P.I. This project developed transgenic mice with fluorescent markers that are expressed at different stages of spermiogenesis and developed technology for separating sub-populations of these spermatid by FACS.

Selected Publications

  1. Tucker, T.A., Kundert, J.A., Bondareva, A.A. and Schmidt, E.E. (2005) Reproductive and neurological Quaking(viable) phenotypes in a severe combined immune deficient mouse background. Immunogenetics 57, 226-231. [Paper, .pdf]
  2. Bondareva, A.A. and Schmidt, E.E. (2003). Early vertebrate evolution of the TATA-binding protein. Mol. Biol. Evol. 20, 1932-1939. [PUBMED-Abstract]
  3. Schmidt, E.E., Bondareva, A.A., Radke, J.R., and Capecchi, M.R. (2003) Fundamental cellular processes do not require verterbrate-specific sequences within the TATA-binding protein, TBP. J. Biol. Chem. 278, 6168-6174. [PUBMED-Abstract]
  4. Hobbs, N.K., A.A. Bondareva, S. Barnett, M.R. Capecchi, and E.E. Schmidt (2002) Removing the vertebrate-specific TBP N terminus disrupts placental b2m-dependent interactions with the maternal immune system. Cell 110, 43-54. [PUBMED-Abstract]
  5. Sealey, A.L., N.K. Hobbs, and E.E. Schmidt (2002) Molecular genotyping of the mouse scid allele. J. Imm. Meth. 260;303-304. [PUBMED-Abstract]
  6. Schmidt, E. E., D. S. Taylor, J. R. Prigge, S. Barnett, and M. R. Capecchi (2000) Illegitimate Cre-dependent chromosome rearrangements in transgenic mouse spermatids. Proc. Natl. Acad. Sci USA, 97;13702-13707. [PUBMED-Abstract]
  7. Schmidt, E. E., E. S. Hanson, and M. R. Capecchi (1999) Sequence-independent assembly of mRNAs into mRNP particles in spermatids. Mol. Cell. Biol. 19;3904-3915. [PUBMED-Abstract]
  8. Schmidt, E. E., Ohbayashi, T., Makino, Y., Tamura, T.-a., and U. Schibler (1997) Spermatid-specific overexpression of the TATA-binding protein gene involves recruitment of two potent testis specific promoters. J. Biol. Chem. 272;5326-5334. [PUBMED-Abstract]
  9. Schmidt, E. E., and U. Schibler (1997) Developmental testis-specific regulation of mRNA levels and mRNA translational efficiencies for TATA-binding protein mRNA isoforms. Dev. Biol. 184;138-149. [PUBMED-Abstract]
  10. Schmidt, E. E. (1996) Transcriptional promiscuity in testis. Curr. Biol. 6;768-769. [no abstract available-first paragraph on BioMednet]
  11. Ohbayashi, T., Schmidt, E. E., Makino, Y., Kishimoto, T., Nabeshima, Y.-i., Muramatsu, M., and Tamura, T.-a. (1996) Promoter structure of the mouse TATA-binding protein (TBP) gene. Biochem. Biophys. Res. Comm. 225;275-280. [PUBMED-Abstract]
  12. Schmidt, E. E., and U. Schibler (1995) Cell size regulation, a mechanism that controls cellular RNA accumulation: Consequences on regulation of the ubiquitous transcription factors Oct1 and NF-Y, and the liver-enriched transcription factor DBP. J. Cell Biol. 128;467-483. [PUBMED-Abstract]
  13. Schmidt, E. E., and U. Schibler (1995) High accumulation of components of the RNA polymerase II machinery in rodent spermatids. Development 121;2373-2383.

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