The Molecular
Characterization of GA1, a mutation that disrupts sexual
reproduction in Chlamydomonas reinhardtii
Allison Johnston Coble
Class of 1998
Mentor: A. Malcolm Campbell
Co-Mentor: John H. Williamson
Department of Biology
Davidson College
Davidson, NC 28036
The molecular mechanisms that regulate cell adhesiveness are important in understanding cell-cell interactions. Although there is not much known about these particular mechanisms, a mutant strain of the unicellular green algae, Chlamydomonas reinhardtii, called GA1, provides new hope for the analysis of the roles of adhesion molecules and signal transduction in cell-cell fusion. GA1 contains a mutated gene which disrupts the sexual reproduction of these cells. Dr. Virginia Armbrust of the University of Washington has shown that the gene is associated with a 4.4 kb segment of mRNA; however the sequence of the entire gene and its location within the chromosome have yet to be determined. The present study was designed to further characterize the gene and to continue the molecular dissection of cell-cell interactions within C. reinhardtii. Here we isolate and clone half of the putative GA1 gene. Sequence analysis of the GA1 cDNA reveals that the gene is similar to a H+-ATPase which is suggestive that the gene could be essential for the glycosylation of adhesion molecules located on the flagella. Experiments involving drugs that increase intracellular pH or inhibit H+ATPAases, however, failed to mimic the GA1 phenotype.