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Some of those mutant strains display tradeoffs between growth parameters and changed metabolic strategies, for example, a shift from respiration to fermentation.
However, it is not clear why the ptp mutant strains display higher mtDNA background than the pog1Δ.
As Cse4 is required for centromere function, it might be anticipated that snf2 mutant strains display a chromosome segregation defect.
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The pmt1D and pmt4D mutant strains displayed a similar but less severe temperature-dependent growth defect.
About 20 such mutant strains displayed low survival (<20%) in our initial screen and were retested.
The double mutant strains displayed synthetic slow growth phenotypes when compared to the single mutants (Fig. S1).
Interestingly, while the cap▵ mutant strains displayed an overall growth defect, they did not display increased sensitivity to copper-starvation (Figure 4A).
In contrast, both wild-type and pre-senescent tlc1 mutant strains displayed indistinguishable bindings of Rad proteins at VII-L before and after bleomycin treatment.
Both the wild type and ΔNirBD mutant strains displayed comparable viabilities (Fig. 6A), indicating that the NirBD complex is not required for nitrate-dependent protection from acid-induced death under hypoxia.
The 93 selected yeast mutant strains displayed significantly different survival rates (Table 4), ranging from drastic lifespan shortening to lifespan extension relative to wild-type cells.
Both steC-null and kinase-deficient mutant strains displayed enhanced replication in infected cells, suggesting that SteC manipulates the actin cytoskeleton to restrain bacterial growth, thereby regulating virulence.
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