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The csk1Δ rhp57Δ double mutants grew very slowly (Fig. 3C and data not shown), suggesting compromised genomic stability even in unchallenged cells.
We found that ess1 H164R swi4 Δ double mutants grew very slowly (synthetic sick) at the semipermissive temperature (34°).
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However, relative to a met3 mutant, the met6 mutant grew very slowly and was less heat-shock resistant.
Because ubx2Δ deletion mutant grew very slowly in our strain background, we conditionally controlled the expression of UBX2 with a galactose-inducible promoter that can be suppressed with glucose.
In contrast, the pmt1D mutant grows very poorly in the presence of sorbitol (Figure 6B), but its growth is unaffected by SDS (Figure 6C).
In contrast, the hupAB double mutant grows very slowly and is highly pleiotropic: a number of cell processes, such as cell division, initiation of DNA replication, transposition, and other biochemical functions, are altered and cause a slow-growth phenotype [9], [10].
At the non-permissive temperature, sec9-4 mutant cells grew very poorly and failed to form individual colonies, while sec9-4 vmutantouble mutant cells grew and formed colonies.
For the fabT deletion mutant though, no final conclusion regarding its sensitivity to carolacton treatment could be drawn since the mutant strain grew very poorly under the tested conditions and formed very thin biofilms.
Initially, the mutant cells grew very slowly, were abnormal in shape and likely to burst open.
This is supported by the fact that the AAMD, AAMA, AAAD mutants grew poorly but the NQMD and NQMN mutants, which have quite different substitutions at the 'DE' residues, grew very robustly at all temperatures.
Interestingly, the isoleucine to glutamine substituted mutant yeast cells showed severe growth phenotypes as they grew very slowly at 23°C (Fig. 3D).
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