In this paper, the effect of temperature (30, 10, 7, 4 and 2 °C) and pH (7.4, 6.1, 5.5, 5.0, 4.7 and 4.4) on the individual cell lag phase of Listeria monocytogenes was examined in a factorial design, using OD measurements.
The physiological state of the cells is affected by their previous growth environment and by exposure to stress conditions, which can extend the lag time considerably and also increase individual cell lag time variability [ 16– 16].
Cell-cell variability within an isogenic population has been observed in the stress survival of individual cells [1], [2], [8], [17] and in the single-cell lag times when resuming growth after stress [1], [2], [4], [17], [29], [32].
While iPS cells lag a little way behind, these too are showing great potential both as donor sources and as systems for disease modeling.
While the ventral expansion of the SIV and ICVs takes place, some cells lag back slightly and migrate dorsally to generate the arterial component of the plexus (Fig. 5C, purple arrows; Movie 3).
Furthermore, in Noc washout experiments with HeLa cells expressing MGRN1, MGRN1ΔR or C316DMGRN1 to study the MT network, the interphase cells showed that catalytic inactivation of MGRN1 distinctly compromised formation of a polymerized mesh – the MGRN1ΔR- or C316DMGRN1-expressing celag lag behind the MGRN1 cells by ∼30 min.
Although significant progress has been achieved in uncovering the molecular barriers to direct reprogramming in mice, research in reprogramming human cells lags far behind.
The quantified differences between infectious particles produced by dengue-infected control and NF90 knockdown cells was statistically significant at the 36 and 48-hour time points post-infection, with the NF90-depleted cells lagging the control cells by approximately 39% and 70%, respectively.
Comparing developmental experiments revealed that gene expression in filter developed cells lagged behind those treated with exogenous cAMP in suspension.
In a wound healing migration assay, vehicle-treated ALDH + cells exhibited complete wound recovery after 18 h, whereas vehicle-treated ALDH− cells lagged behind at the 18 h time point.
Live movies confirmed that in both pcs1Δ and clr4Δ mutant cells lagging kinetochores often displayed stretching or splitting, when they were in between the spindle poles but frequently rounded up when they were reaching one of the poles.
