Jeremy F. Nance

Associate Professor, Skirball Institute of Biomolecular Medicine, Developmental Genetics. Department of Cell Biology

Ph.D., 1999 University of Arizona

Keywords: C. elegans, Gastrulation, Cell Polarity, Adhesion, Germ Cells



Contact Information: 

Skirball Institute of Biomolecular Medicine
540 First Avenue 4th floor, Lab 17
New York, N.Y. 10016
Office Tel: (212) 263-3156
Lab Tel: (212) 263-3127
Fax: (212) 263-7760

Administrative Contact:

Theresa Walton
Tel: (212)263-7595

Gastrulation and Cell Polarity

During the morphogenetic movements of gastrulation, cells that will form internal tissues move into the interior of the developing embryo. We use the nematode C. elegans as a simple model tounderstand some of the basic cellular processes that control gastrulation movements. C. elegans is ideally suited for the study of gastrulation, since individual cell movements can be followed in the optically clear embryo and the genes involved can be found in genetic screens. Gastrulation movements begin when the contractile cytoskeletal protein non-muscle myosin accumulates at the contact-free surfaces (those facing the exterior of the embryo) of specific cells, causing this surface to constrict and driving the cells into the interior of the embryo. We have identified a cell-contact-induced signaling pathway that regulates gastrulation movements by polarizing earlyembryonic cells. In worm embryos, contact-induced polarity is required for gastrulating cells to properly position myosin at their apical surfaces. A mechanistically similar polarization occurs in mammals, and is thought to help drive the first lineage divergence – separation of inner and outer cells into embryonic and extra-embryonic populations, respectively.

Projects in the lab include understanding how cell contacts induce polarity and translate polarity information into cytoskeletal asymmetries that drive directional cell movement; investigating the triggers that induce gastrulation movements in specific cells; and learning how cells that are internalized during gastrulation polarize again during organogenesis, as they become epithelial cells and assemble cell-cell junctions.

Selected Publications:

R. Totong*, A. Achilleos*, and J. Nance. PAR-6 is required for junction formation but not apicobasal polarization in C. elegans embryonic epithelial cells. Development 2007: 134: 1259-1268. PMID: 17314130

D. C. Anderson, J. S. Gill*, R. M. Cinalli*, and J. Nance. Polarization of the C. elegans embryo by RhoGAP-mediated exclusion of PAR-6 from cell contacts. Science 2008: 320: 1771-1774. PMID: 18583611

A. Achilleos, A. M. Wehman and J. Nance. PAR-3 mediates the initial clustering and apical localization of junction and polarity proteins during C. elegans intestinal epithelial cell polarization. Development 2010: 137: 1833-1842. PMID: 20431121

A. M. Wehman, C. Poggioli, P. Schweinsberg, B. D. Grant, and J. Nance. The P4 ATPase TAT-5 inhibits the budding of extracellular vesicles in C. elegans embryos. Current Biology 2011: 21: 1951-1959. PMID: 22100064

D. Chihara and J. Nance. An E-cadherin-mediated hitchhiking mechanism for C. elegans germ cell internalization during gastrulation. Development 2012: 139: 2547-2556. PMID: 22675206

Click here to see all publications in PubMed