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At a cellular level, this suppression by stat92E heterozygosity correlates with restoration of more normal G1/S cell cycle phasing in mutant discs and a partial reversion of an ept enlarged-cell phenotype.
Thus a diploid dose of the stat92E gene is required for the effect of ept loss on G1/S cell cycle phasing and to a somewhat lesser degree for the enlarged size of ept mutant imaginal disc cells.
The cell cycle shift induced by the DN-DaPKC transgene only partially restored cell cycle phasing and had no discernable effect on the enlarged size of ept cells, suggesting that additional factors contribute to each of these phenotypes.
Consistent with this hypothesis, a reduction in the dose of the stat92E gene affects both cell cycle phasing and cell size in ept/M 3) tumors (see accompanying paper by Gilbert et al).
We have taken a dual approach to examine cell division control in ept mutant eye-antennal tumors: we have sought to identify genetic manipulations that suppress ept tumor growth, and in parallel we have characterized the effect of ept loss on cell cycle phasing and expression of core cell cycle regulatory factors.
To assess whether the proliferation defect observed in Slbp mutant cells corresponds with impaired progression through S-phase, we utilized FACS to profile cell cycle phasing in wing imaginal disc cells of 3rd instar wt and Slbp15 mutant larvae (Figure 6C).
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Thus, the cell cycle phase distribution per cycling cells would reflect the biology of cancers.
A short summary of the sequence of cell cycle phases can be found in Figure 1.
The sensitivity and consequent biological effects of radiation exposure are dependent on the cell cycle phase.
Cell cycle phase was detected using a flow cytometer (FACS420, BD Biosciences, San Jose, CA).
In live cells, Scm3-GFP is enriched at centromeres in all cell cycle phases.
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