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In addition to the melanin delay, the pmt1 and pmt4 mutant cells display aberrant cell morphology and pronounced cell aggregation.
Embryonic hrs mutant cells display more EGFR signalling activity and accumulate activated receptors and ubiquitinated proteins in enlarged endosomes [17], [18], [19], [20], [21].
Finally, the budding pattern of the newly budded cells could not be investigated since arp2-1 mutant cells display a random budding pattern even at permissive temperature [21].
cenp-metaΔ mutant cells display a mitotic delay.
These results suggest that WrnΔ hel /Δ hel mutant cells display an adaptive response to oxidative stress.
Drosophila Vps34 or Atg6 (Beclin) mutant cells display defects in PI3P formation and fail to endocytose a fluid phase marker [ 19, 39].
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The mutant cells displayed an increased length and multiple aberrant septa with incorrect placement.
These epigenetic deficiencies were coupled with defects in spermatogonia, with mutant cells displaying marked changes in gene expression and reactivation of retrotransposons.
As expected, NPC1 mutant cells displayed an inappropriate homeostatic response to accumulated intracellular cholesterol.
Heterozygous ΔT mutant cells displayed an intermediate level of receptor internalization (Fig. 5E), a phenotype previously seen in cells from some patients with WHIM syndrome [23].
hrs mutant and hrs, stam double mutant cells displayed a much reduced capacity to sprout since we observed 16.6±5.0 (p<0.001) and 15.7±4.9 (p<0.001) branching points, respectively (Fig. 4C D and table 2).
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