Moreover, Δrho3 cells exhibited defects in vacuolar fusion induced by osmotic stress in a similar fashion to Δapm1 cells.
Animals with mutant acs-20 exhibited defects in the cuticle barrier, which normally prevents the penetration of small molecules.
These mice were viable and fertile but exhibited defects in hormone secretion from pancreatic islets, which were paralleled by slight glucose intolerance.
The Δsec22 mutant exhibited defects in sporulation and budding, and the mutant cells were also less resistant to stress despite an increase in cell sizes [5], [24], [25].
The BJ cells expressing hTERT Q169A exhibited defects in telomere length maintenance, exhausted their replicative potential after 25 mpd, and did not surmount replicative senescence (Figures 8B D).
However, UTI89 ΔhofQ and a CFT073 ΔhofQ ΔyheF double mutant both exhibited defects in colonizing the kidneys by day seven post-infection.
We thus tested whether fresh NFAT5−/− T cells exhibited defects in the expression of different cell cycle regulators when induced to proliferate in moderately hypertonic medium (380 420 mOsm/kg).
However, when we included a combination of EAF1-MO1 (4 ng) and EAF2-MO1 (4 ng), only about 10% of the embryos exhibited defects (Fig. 3Ba and 3Bc), while the majority of the embryos appeared morphologically normal (Fig. 3Bb), similar to the wild-type embryos.
In contrast, embryos that were heat shocked at 22 hpf expressed dnPDGFRβ-YFP throughout the tail and maintained dnPDGFRβ-YFP expression to 48 hpf and exhibited defects in ISV formation (Figure 6C and E, n = 23, p<0.0001) as shown by fli1a:eGFP.
The plx-1 mutants exhibited defects (9%; n = 180) similar to those of smp-1 smp-2 double mutants.
Yeast strains expressing mutant Myo1 exhibited defects in growth and endocytosis similar to those observed in the myo1 deletion strain.
