Characterization of G1sA, Hsp70, and other Asymmetric Division Factors in Volvox

University Of Maryland Baltimore County, Baltimore MD

Investigators

Abstract

0077535 Miller Cell division is a fundamental process executed by all living things, yet surprisingly little is known about how cells decide where to place their division planes. Precise positioning of cell division planes plays a crucial role in the development of many plants and animals, by determining the relative sizes, shapes, and spatial relationships of the two cells formed by the division. Cell-division geometry is particularly consequential in cases in which important cytoplasmic components ("developmental determinants") are unequally distributed in the predivisional cell. This study will use the spherical green alga Volvox carteri is to explore mechanisms that regulate cell division symmetry. V. carteri is especially well suited for this purpose because it consists of just two cell types, large reproductive cells called gonidia and small nonreproductive cells called somatic cells, that are generated by a set of visibly unequal, or asymmetric, cell divisions. At least two different genes, called gls (for gonidialess), are required for the proper execution of these unequal cell divisions. In previous work one gls gene, glsA, was isolated and shown to encode a protein (GlsA) that is closely related to proteins found in yeast, worms, flies, plants, mice, and humans. GlsA protein appears to associate with the cell division machinery, and several lines of evidence suggest the hypothesis that it acts, together with at least two additional proteins (one of them a member of the well-studied Hsp70 family of molecular chaperones), as an adaptor-like molecule that targets the cell division machinery to an off-center location during asymmetric division. The long term goal of this work is to test this hypothesis, and to identify the other factor(s) that are essential for asymmetric division. The investigator will use cell biological, biochemical, and molecular genetic methods to further characterize the mode of action of GlsA and Hsp70 and to identify and study the additional asymmetric division factor(s) with which they are hypothesized to act.