Cell Cycle Mutants

C. reinhardtii is a powerful genetic model and during the past few decades a number of cell cycle mutants have been recovered (for review see Harper 1999). Only a small portion of these mutations have been mapped; this number will undoubtedly increase with the completion of the C. reinhardtii genome sequence.

Recently, two groups of mutants in cell cycle related genes have been mapped. Both show an alteration in daughter cell size. The founding member of the first group is the mat3-4 mutant described by Umen and Goodenough (2001); mat3-4 cells are tiny compared to wild-type cells. This size phenotype is due to defects in cell size perception and/or regulation; mat3-4 cells attain commitment at a smaller cell size, and for a given mother cell size, mat3-4 cells undergo more rounds of cell division than would wild-type cells (that is, their division number n is larger). The mat3-4 phenotype is caused by a deletion in the C. reinhardtii homolog of the retinoblastoma protein. Mutations in E2F and DP protein, downstream of the retinoblastoma protein in other systems, were isolated as suppressors of the mat3-4 phenotype. Both DP and E2F mutants showed cell size alterations; DP1 null mutants show bigger commitment cell size than wild type (Fang et al. 2006).

The second group of size mutants arose from two members of the NIMA kinase family, FA2 and CNK2 (Mahjoub et al. 2002; Bradley and Quarmby 2005; Quarmby and Parker 2005). The fa2 mutant was isolated in a genetic screen for mutants defective in deflagellation; fa2 cells are bigger than wildtype cells. The commitment size is the same as that of wild type; the cells divide into more cells (the division number is higher) but that is in line with bigger mother cells (Mahjoub et al. 2002). Therefore, it seems that the length of the postcommitment period, rather than cell size perception, leads to cell division later at bigger cell size. CNK2, another member of the NIMA kinase family, is probably involved in the regulation of both the cell size and flagellar length. An increase in the amount of Cnk2p results in small cells and short flagella. Cells with less Cnk2p are larger and have longer flagella than wild type (Bradley and Quarmby 2005).

C. reinhardtii is powerful genetic model. It is also a remarkable model for the study of cell size because it allows one to discriminate between cell size change due to growth and/or alteration of cell cycle progression and changes due to alterations of the sizing mechanism (Umen 2005). Its set of cell cycle genes is complete yet without unnecessary duplications providing for a simple cell cycle model. However, its cell cycle organization differs from the classical G1-S-G2-M pattern. It would therefore be useful to have an organism with cell cycle organization in between the common cell cycle pattern and that of C. reinhardtii. Also, C. reinhardtii is a very close relative of land plants and it would be interesting to see which of the cell cycle regulators have been conserved in more distant algal species. The other model organisms described below therefore complement C. reinhardtii as a model organism.

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