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Aberrant chromosome segregation defects can lead to aneuploidy, a common characteristic of human solid tumors. Aneuploidy is generated due to defects in the mitotic spindle or due to inefficient mitotic checkpoint response. We have isolated a novel mutant allele of  wat1 , a WD repeat containing protein that exhibits conditional synthetic lethality with  chk1  knock out. We observed only a marginal decrease in the level of α tubulin protein level in  wat1-17  mutants after prolong exposure at semi permissive temperature. Interestingly the protein level of α-tubulin was reduced in the  chk1 Δ  wat1-17  double mutant at 18°C with defective microtubule structure. Consistent with loss of microtubule structure in the c hk1  deletion background, the double mutant of  wat1-17 chk1 Δ was hypersensitive to the microtubule destabilizing agent TBZ suggesting severe defects in microtubule integrity in  wat1-17  mutant in the absence of Chk1. Combination of  wat1-17  with the  chk1  deletion also aggravates the defects in the maintenance of genome ploidy. The mutation in  wat1-17  was mapped to Cys 233 that was changed to tyrosine. Based on the molecular modeling studies, we hypothesize that the substitution of the bulky Tyr residue at Cys233 position in  wat1-17  mutant results in conformational changes. This in turn can affect its intercations with other interacting partners and perturb the overall functions of the Wat1 protein.

plos one

Wat1/pop3, a Conserved WD Repeat Containing Protein Acts Synergistically with Checkpoint Kinase Chk1 to Maintain Genome Ploidy in Fission Yeast S. pombe