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THE CONTROL OF CELL POLARITY IN C. ELEGANS
Overview

From yeast cells to the embryonic blastomeres, neurons and skin cells of multicellular organisms, almost all cells exhibit some form of polarity. Interestingly, the mechanisms and event the molecules involved in these various forms of polarity are conserved, such that studies of cell polarity in genetically tractable organism such as C. elegans are informative for vertebrates, including humans.


We want to understand how cell polarity is generated and maintained during animal development. Proper cell polarity requires both the generation of cellular asymmetry and the orientation of the asymmetric cell to the body axis. Our approach is to identify and study genes involved in the control of cell polarity by identifying mutations that disrupt the polarities of individual cells. For example, mutations in the C. elegans Wnt gene lin-44, primarily cause the polarities of certain cells in the tail to be reversed with respect to the body axis, whereas mutations in the frizzled-related gene lin-17, primarily cause those same cells to loose their polarity. LIN-44/Wnt is made by the cells at the tip of the developing tail and functions to specify the polarity of more anterior tail cells called T and B. Wnt proteins act as short-range signaling molecules in many different species. We have identified several genes, including egl-27, tlp-1, tcl-1 and tcl-2 that are involved in the generation of cellular asymmetry and the orientation of that asymmetry to the body axis. We continue to analyze these genes as well as to identify others that are involved in Wnt signaling and the control of cell polarity.


In C. elegans, Wnt signaling controls cell fate decisions, cell migrations and cell polarity. As in most animals, C. elegans has both canonical Wnt pathways which function through a ß-catenin homolog, and noncanonical Wnt pathways, that do not. A C. elegans canonical Wnt pathway controls a neuroblast migration. We have shown that the Wnt pathways that control cell polarity in the tail are noncanonical. Furthermore, we have also recently determined that different noncanonical pathways control T cell and B cell polarities. We are currently determining the nature of these pathways.
Our current work aims to discover how signaling pathways interact with the centrosome to control cell polarity in developing tissues.

T cell polarity

POP-1/Tcf is asymmetrically localized during the T cell division:

B cell polarity

POP-1/Tcf is also asymmetrically localized during the B cell division:

Recent Wnt/cell polarity publications

Yu H, Seah A, Herman MA, Ferguson EL, Horvitz HR, Sternberg PW 2009. Wnt and EGF pathways act together to induce C. elegans male hook development. Dev Biol, 327: 419-432.(PDF)

Van Hoffelen, S. and Herman, M.A. 2009. Analysis of Wnt signaling during C. elegans postembryonic development. Methods Mol Biol., 469, 87-102.(PDF)

Wu, M. and Herman, M.A. 2007. Asymmetric localization of LIN-17/Fz and MIG-5/Dsh are required for the the asymmetric B cell division in C. elegans. Dev. Biol., 303:650-662. (PDF)

Walston, T., Guo, C., Proenca, R., Wu, M. Herman, M., Hardin, J., Hedgecock, E. 2006. mig-5/Dsh controls cell fate determination and cell migration in C. elegans. Dev. Biol, 298: 485-497.(PDF)

Arata, Y., Kouike, H. Zhang, Y., Herman, M.A., Okano, H, and Sawa, H. 2006. The Wnt signal and Hox cooperate to express PSA-3/Meis, which determines specific daughter fates after asymmetric division in C. elegans, Dev Cell, 11, 105-115.(PDF)

Wu, M. and Herman, M.A. 2006. A novel noncanonical Wnt pathway is involved in the regulation fo the asymmetric B cell division in C. elegans. Dev. Biol, 293:316-329.(PDF)

 



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