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The Center for Reproductive Sciences

Faculty

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Jay L. Vivian, Ph.D.
Pathology and Laboratory Medicine

Research Description

My research interests focus on the use of the mouse as a genetic and developmental system to study cell-cell communication during embryogenesis.  The focus of the Vivian lab is to understand the genes and signaling that direct embryonic vascular differentiation. The cardiovascular system is the first functional organ system of the developing embryo, and is required for the transport of nutrients from the maternal-fetal interface to the rapidly growing organism.   The embryonic vasculature is a critical component of the developing chorioallantoic and choriovitelline placentae; defects in embryonic vascular differentiation can result in impaired embryonic or fetal growth and loss of pregnancy.  My research utilizes the genetic manipulability of the mouse to understand the molecular mechanisms that control the differentiation of the embryonic vasculature, including functions of the components of the TGF-beta, Notch, and VEGF signaling pathways.  Using mouse embryonic stem cells, our laboratory is developing new genomic analysis methods, including homologous recombination and chemical mutagenesis, to generate novel reagents to study these signaling pathways.

 

Representative Publications

Kirn-Safran, CB, Oristian, DS, Focht, RJ, Parker, SG, Vivian, JL, and Carson, DD. (2007).  Global growth deficiencies in mice lacking the ribosomal protein, HIP/RPL29.  Dev. Dyn. 236, 447-460.

Vivian, JL, Chen, Y, and Magnuson, T. (2004). Gene-based screens of chemically mutagenized mouse embryonic stem cells.  In: Handbook of Stem Cells. Lanza, R. P., et al (Eds), Academic Press.

Chen, Y, Vivian, JL, and Magnuson, T. (2003).  Gene-based chemical mutagenesis in mouse embryonic stem cells. Methods Enzymol. 365, 406-415.

Vivian, JL, Chen, Y, Yee, D, Schneider, E, and Magnuson, T. (2002). An allelic series of mutations in Smad2 and Smad4 identified in a genotype-based screen of N-ethyl-N-nitrosourea-mutagenized mouse embryonic stem cells. Proc. Natl. Acad. Sci. USA, 99, 15542-15547.

Vivian, JL, Olson, EN, and Klein, WH. (2000). Thoracic Skeletal Defects in Myogenin- and MRF4-Deficient Mice Correlate with Early Defects in Myotome and Intercostal Musculature. Dev. Biol. 224, 29-41.

Vivian, JL, Klein, WH, and Hasty, P.  (1999).  Temporal, Spatial and Tissue-Specific Expression of a Myogenin-lacZ Transgene Targeted to the Hprt Locus in Mice.  BioTechniques, 27, 154-62.

Vivian, JL, Gan, L, Olson, EN, and Klein, WH.  (1999).  A Hypomorphic Myogenin Allele Reveals Distinct Myogenin Expression Levels Required for Viability, Skeletal Muscle Development, and Sternum Formation.  Dev. Biol. 208, 44-55.

Myer, A, Wagner, DS, Vivian, JL, Olson, EN, and Klein, WH. (1997).  Wild-Type Myoblasts Rescue the Ability of Myogenin-Null Myoblasts to Fuse in Vivo.  Dev. Biol. 185,127-138.

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