To determine whether the same kinetics of CSIG and p33ING1 after UV treatment was due to cell-cycle arrest, expressions of cyclin A, cyclin B and cyclin D1, which indicated different cell-cycle phase, were also detected.
Furthermore, the leukemia cells exhibited maturation arrest (without expression of sIgm) as well as over-, under-, and asynchronous expression of antigens observed on normal B-cell precursors.
DOI: http://dx.doi.org/10.7554/eLife.09886.011 Interestingly, we found that while wild-type Rtt109 and Rtt109(T46D) were inducibly expressed to high levels upon release from HU arrest, Rtt109(T46A) expression was delayed and reached a lower level.
We were able to rescue the VSG221 RNAi induced cell-cycle arrest through expression of a second different VSG (VSG117 which is not recognised by the VSG221 RNAi) from the VSG221 expression site.
After the release from nocodazole arrest the expression of both SSEA-3 and SSEA-4 increased, probably reflecting the changes in cell surface glycolipids as the first event.
In the rad3Δ background, which lacks any cell-cycle arrest, constitutive expression of mik1 provides modest resistance to both treatments, accounting for about half of the resistance due to cdc10-2E-dependent G1/S transcript expression (Figure 4B,C).
To address the exact mechanism of Pep-7-induced G1 arrest, the expression of different proteins involved in regulating G1-to-S transition was monitored by qRT-PCR and Western blot.
Furthermore, the abnormal nuclear morphology was also seen in SW480 cells [18] which do not undergo a G2 arrest following expression of either M2- or M3-APC (Figure 5).
In contrast, in cells with a G1 arrest, p21WAF1/CIP1 expression was enhanced at different times postirradiation.
BLM assembles at stalled replication forks [ 4, 6], which supports the notion of DNA replication arrest inducible expression of OsRecQl4 (Additional file 1: Figure S5).
