Our group uses the multicellular green alga Volvox carteri to study mechanisms of cellular differentiation, and how they evolve. V. carteri possesses ~2000 cells but just two cell types: large reproductive cells called gonidia, and small, motile somatic cells. Gonidial and somatic cell precursors are set aside when a subset of blastomeres undergo visibly asymmetric cell divisions during embryogenesis. The larger progeny produced by these divisions become reproductive cells, or gonidia, which act as asexual stem cells that ultimately produce the next generation of gonidia and somatic cells, while the smaller cells ultimately differentiate into bi-flagellate somatic cells that provide the organism motility but never divide.

Most research in our lab aims to better understand two important aspects of V. carteri development. First, we want to know how asymmetric cell divisions are regulated—why certain cells undergo them while others do not, and how the division plane is shifted off center to produce cells that differ in size. Proper control of cell division symmetry is crucial for all plants and animals to develop normally, yet relatively little is known about the mechanisms that determine where division planes are placed.   We are using V. carteri mutants defective for asymmetric division (called Gonidialess, because they fail to make large cells that can become gonidia) to clone genes required for asymmetric division; analysis of these genes should yield important insights into how asymmetric division is controlled in V. carteri. So far we have cloned one gls gene, glsA, which encodes an embryo-specific, J-protein chaperone (GlsA) that localizes to the nucleus and is ~equally abundant in all blastomeres, those that divide symmetrically as well as asymmetrically. GlsA interacts with another chaperone, Hsp70A, which is enriched in the blastomeres that cleave asymmetrically. We hypothesize that GlsA and Hsp70A regulate the activities of transcription factors that control downstream genes required for asymmetric division, and we also hypothesize that relative Hsp70A abundance determines which cells will divide asymmetrically.  Current projects in the lab aim to reveal how Hsp70A becomes asymmetrically distributed in the embryo, to identify and characterize other proteins that GlsA interacts and functions with, to clone and characterize additional gls genes.

Our second major goal is to understand how the somatic cell fate is maintained in V. carteri, and how it evolved. The key to these studies is the somatic regenerator, or regA gene. regA mutants develop normally through the first day of the two-day life cycle, forming gonidia and somatic cells as in the wild type, but the somatic cells dedifferentiate, enlarge, and become gonidia. Thus regA is required to maintain the repression of growth and cell division in somatic cells. regA encodes a nuclear protein (RegA) that is enriched in the types of amino acids normally abundant in transcriptional repressors, and it also possess a ~110-aa VARL domain (Volvocine Algal RegA like) that resembles the DNA-binding SAND domain that has been identified in a number of plant and animal transcription factors. We are testing the idea that RegA can repress transcription, and we also aim to determine if it can bind DNA, and if so, what its direct targets are. In addition, we are analyzing several regA-related genes from V. carteri and the related unicellular alga, Chlamydomonas reinhardtii. Learning more about these genes, and about regA, should tell us how certain cells differentiate as, and remain as somatic cells, and how the somatic cell fate arose in the first place.