Hawkins Lab

The Hawkins lab uses C. elegans to investigate the molecular mechanisms underlying asymmetric cell division.

Asymmetric cell division is the process by which a mother cell divides to produce two daughter cells that adopt distinct cell fates and is essential for the generation of cell diversity during development. Many outstanding questions include: How does cell signaling contribute to asymmetric cell division? Are asymmetrically localized determinants conserved between organisms or cell types? How does an asymmetrically localized factor ultimately lead to differential gene expression necessary for cell fate determination? C. elegans is ideally suited to investigate these questions. Since the entire cell lineage is known, the timing, location and polarity of cell divisions can be analyzed at the resolution of single cells. Both cell signaling and the asymmetric segregation of intracellular proteins are required to specify distinct daughter cell fates during asymmetric cell division. We are currently using molecular, genetic and cell biological approaches to understand the mechanisms by which the highly conserved Wnt signaling pathway and the asymmetrically localized HAM-1 protein contribute to asymmetric cell division.

For more information, visit our research lab website.

Email: 

NANCY HAWKINS
nhawkins@sfu.ca 

Lab Room: 

SSB 7179

Lab Phone: 

(778) 782-5931

Selected Publications: 

  • Leung et al., C. elegans HAM-1 functions in the nucleus to regulate asymmetric cell division. Dev Biol 2016
  • Hingwing et al. CWN-1 functions with DSH-2 to regulate C. elegans asymmetric neuroblast division in a ß-catenin independent Wnt pathway. Dev Biol 2009.
  • King et al. The N- or C-terminal domains of DSH-2 can activate the C. elegans Wnt/ß-catenin asymmetry pathway. Dev Biol 2009.
  • Hawkins, N., and Ronchi, E. (2008). Seeking a seat at the policy table: Engaging women in biotechnology research and in decision making. In F. Molfino and F. Zucco (eds.) Women in Biotechnology - Building Interfaces. Springer.

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