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Mutant cells exhibited reduced sensitivity to glycogen synthase kinase 3 inhibition during self-renewal.
When codon-optimized PbSEY1 was expressed in ATL-deleted COS-7 cells, a majority of the mutant cells exhibited normal tubular ER network (Fig. 2H).
The mutant cells exhibited enhanced glucose uptake and glycolysis and survived in low-glucose conditions, phenotypes that all required GLUT1 expression.
At best, ctf7 mutant cells exhibited a very modest growth defect in response to MMS.
Quantification revealed that more than 17% of the ssn8 mutant cells exhibited this atypical morphology (Table 1).
As previously reported, atg1 mutant cells exhibited decreased viability after two days of starvation, and almost completely atg1Δ cells died after five days (3.0% of survival cells).
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In response to MMS, both rad24 and elg1 exhibited decreased growth with rad24 single mutant cells exhibiting the more dramatic adverse effect.
At restrictive condition, the rna14-11 mutant cells exhibit defects in cell cycle progression with high level of septation.
5A mutant cells exhibit both abnormal accumulation of excess DNA and larger cell size.
Nor did pol30 smc3Q double mutant cells exhibit additional growth defects beyond those evident in pol30 single mutant cells.
Subsequent studies revealed that both ctf18 and pol30 mutant cells exhibit precocious sister chromatid separation [10], [11], [24].
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