Importantly, pseudopod activity, defined as the product of pseudopod size and frequency, is similar in sgc/pla2-null cells (20.8+/−1.7 µm/min) and wild type cells (21.6+/−2.0 µm/min), indicating that sgc/pla2-null mutant cells actively extend pseudopodia.
Although cells extend pseudopodia at a similar frequency as wild type cells, mutant cells change direction so often that the centroid of the cell follows the pseudopodia only for a short distance, resulting in the observed low speed of the cells.
Many eukaryotic cells extend pseudopodia.
Eukaryotic cells extend pseudopodia for movement.
Interestingly, in inx-14 ag17 inx-14 ag17he sheath coverage of germutants extheded disheath in the gonad arm sucoverageit bofdered the DTC.
In the mac1 mutant, the L2-d cells are unable to produce EN and SPL daughters but continue to generate supernumerary AR cells, extending the period of L2-d pluripotency (Wang et al. 2012b).
The scrib- mosaic clones, however, deviate significantly from previous studies in homozygous animals: instead of displaying grossly neoplastic overproliferation, the mutant cells form small disordered foci that never extend beyond original clonal region of expression.
Two daughter nuclei that were asymmetrical in size or lagging chromosomes were often observed in the dis3-54 Δmutantouble mutant cells, suggesting that although the spindle was extending normally, chromosome segregation was unequal.
Accordingly, removal of Fob1 failed to extend the lifespan of the gcn5∆ mutant cells (median lifespan of gcn5∆ fob1∆ double mutant cells = 27 generations, N = 150 cells; Figure 11B) and spt20∆ mutant cells (spt20∆ fob1∆ = 16 generations, N = 75 cells; Figure 11C).
To further test whether rapamycin and caffeine extend lifespan through TORC1 inhibition, we examined the CLS of tco89Δ mutant cells that lack a nonessential core component of TORC1 (Ikai et al., 2011).
