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Our lab is interested in understanding the molecular mechanisms
that control cell fate decisions following asymmetric cell division.
Asymmetric cell division is a common strategy to achieve different
cell fates during development, and dysregulation of asymmetric cell
division in stem and progenitor cells likely contributes to a variety
of human diseases, including cancer. In the fruit fly, Drosophila,
neural stem and progenitor cells divide asymmetrically and segregate
a cell fate determinant, Numb, to one daughter cell during mitosis.
Numb protein functions as an inhibitor of the Notch signaling pathway.
We currently use a combination of genetic, biochemical, molecular
modeling, and live cell imaging approaches to study how cell fate
determinants such as Numb are polarized during mitosis, and how,
following asymmetric cell division, Notch signaling is activated
in one daughter cell, and inhibited in the other daughter cell.
Our studies have shown that a tumor suppressor gene lethal giant
larvae and a novel transmembrane protein, Sanpodo, are critical
for the correct cell fate assignments in the adult peripheral nervous
system in flies. As many of the genetic programs used by organisms
are evolutionarily conserved, understanding how the genes we've
identified establish a context to control Notch signaling in asymmetrically
dividing cells will help guide future studies addressing mechanisms
of stem and progenitor cell regulation in development and disease.
Epigenetics
and Progenitor Cell Keystone program
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