Caenorhabditis Elegans is among the most highly studied and well
characterized organisms in biology. Additionally, the development of
the vulva in the C.elegans hermaphrodite is one of the most thoroughly
described morphogenic processes in this nematode. Despite this, there
are lingering questions regarding vulval formation, many related to
intercellular signaling and cell fate specification.
Two cells essential for proper vulva and uterus development are the
Ventral Uterine Precursor Cell (VU) and the Anchor Cell (AC). The
AC,
through a secreted EGF type ligand, induces cell fate patterning among
the Vulval Precursor Cells while the VU is the progenitor of a portion
of the mature uterus. In the absence of either cell, a functional
egg-bearing apparatus does not develop.
Recently, a conceptual model for the interaction of the AC/VU
precursors has been proposed based on a hypothetical transcription
factor inhibitor. I will discuss how I've translated this proposed
theoretical model into a mathematical model. The theoretical model is
found to make critically wrong predictions as seen through
mathematical analysis and in silico experiments. I propose an
alteration to the theoretical model, leading to its rescue. Both the
alteration to the theoretical model and the predictions of the
resulting mathematical model are consistent with in vivo results.
I'll contrast this to another theoretical model currently under
construction in the Sternberg Lab.
This work was done under the guidance of Professor Donald S. Cohen
(Applied and Computational Math) and Professor Paul W. Sternberg
(Biology).