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We have shown that Coil −/− mice display significant viability defects.
Double mutant combinations showing synthetic growth or viability defects then identify loci that are buffered by expression of the test gene.
Deletion of both Peril and Mdgt also results in viability defects.
By contrast, expression of dilp6 in the brain (driven by dilp2-GAL4) wasufficientntoto rescue both the growth and viability defects, as well as sedation resistance.
This suggests that any viability defects associated with the marked chromosome are too small in magnitude to markedly affect recombination frequency as estimated by our backcrossing assay.
By contrast, hat1Δ single mutant cells retained full viability as compared to the wild-type control, indicating that the hat1Δ loss-of-function mutation specifically amplifies the viability defects associated with impaired ORC.
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Developing aprA - cells have abnormal fruiting bodies and a more severe spore viability defect than gα8 - cells [ 4].
It is clear that there is both a spore viability defect and an increase in meiosis I nondisjunction in nbs1-2.
Similar to hat1Δ and hat2Δ, sum1Δ null mutations also reduce the restrictive temperature of orc-ts mutations, while having no obvious viability defect on their own [ 11, 56].
We hypothesize that the viability defect found in msh4 ∆ mutants could be due to the presence of nonexchange events on large chromosomes.
Mutations in Ctp1 that prevent interaction with the FHA domain of S. pombe Nbs1 cause a spore viability defect as well (Dodson et al. 2010).
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