|Institution:||Washington University in St. Louis|
|Full text PDF:||http://openscholarship.wustl.edu/art_sci_etds/378
In this thesis, I studied the cell-size control in Chlamydomonas and contributed to the below two projects. First, preliminary results show that cdkg1 mutants reduce cell division and show large-cell phenotype. CDKG1 interacts with cyclinD3, and phosphorylates MAT3/RB. CDKG1 concentration peaks at S/M, and scales with mother cell size. CDKG1 concentration per nucleus decreases as cells divide. My data show that CDKG1 mis-expression has a small-cell phenotype that may be due to the inability of cells to eliminate the protein at the end of S/M phase. By measuring the N/C ratio during cell division I ruled out the dilution model for CDKG1 elimination and was able to show that CDKG1 must be actively degraded with each round of cell division. We were able to conclude that CDKG1 functions as a titratable regulator that couples cell size to cell-cycle progression. Second, with an in vivo nuclei marker ble-GFP, I measured N/C in wild-type, cell-size mutants, and vegetative diploids of Chlamydomonas. I concluded that N/C is constant over most of the cell-size range. In combination with previous data from a different eukaryotic phylum, yeast, my data suggest that a constant N/C may be a conserved property of eukaryotic cells. I also found evidence for a lower limit of the nuclear size, which might be a pure physical constraint of the nuclear DNA.