In addition to the genetic and environmental control of endoreduplication described above, increasing evidence points to an intriguing link between the maintenance of genome integrity and endoreduplication. FASCIATA1 (FAS1), FAS2 and MICROSATELLITE INSTABILITY1 (MSI1) are subunits of chromatin assembly factor CAF1 that is involved in the nucleosome assembly on newly replicated DNA (Kaya et al. 2001). Loss of this protein complex in fas1, fas2, and msi1 mutants leads to pleiotropic developmental phenotypes including fasciation, disorganized apical meristems and dwarfism (Kaya et al. 2001; Kirik et al. 2006; Exner 2006). These defects are associated with various cellular and subcellular abnormalities such as delayed progression of the mi-totic cell cycle, impaired heterochromatic and euchromatic conformation and stimulation of homologous recombination and other DNA repair response (Schonrock et al. 2006; Exner et al. 2006; Kirik et al. 2006). Interestingly, fas1, fas2, and msi1 mutants also have higher ploidy than wild type, suggesting that the endocycle is promoted in these mutant backgrounds (Schonrock et al. 2006; Exner et al. 2006; Kirik et al. 2006). Because of the complex pheno-types observed in these mutants, how ploidy is increased in these mutants is not clear. However, one interesting possibility is that the suboptimal genome integrity and/or resulting arrest of the mitotic cell cycle somehow triggers the endocycle as an alternative mechanism to protect genetic information and thus to sustain the life of cells. Another example that links DNA repair and endocycle control is the brushy1/tonsoku/mgoun3 (bru1/tsk/mgo3) mutants in Arabidopsis that exhibit the faciation phenotype similar to fas mutants (Takeda et al. 2004). The bru1/tsk/mgo3 mutants also display increased homologous recombination and elevated DNA damage response as well as stochastic release of transcriptional gene silencing and abnormal het-erochromatin structure (Takeda et al. 2004). Furthermore, these phenotypes also associate with the delayed progression of mitotic cell cycle from G2 to M-phase and an increased level of ploidy (Suzuki et al. 2005), further supporting the functional link between chromosome replication, DNA repair and endocycle control. The BRU1/TSK/MGO3 gene encodes a novel nuclear protein that contains TPR and LRR repeats (Takeda et al. 2004), and its homolog in Nicotiana tobaccum is expressed specifically at the S-phase (Suzuki et al. 2005). Thus, it is likely that BRU1/TSK/MGO3 has a role during and/or just after DNA replication.
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