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Netto et al (2008) analysed global methylation status by immunohistochemistry and concluded that SEs cells generally retain the lack of methylation that occurs due to normal developmental erasure of methylation marks, whereas NSEs do not, thus showing more methylation.
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Hence, the optimal performance is generally achieved in the ZnO/Zn x Cd1-x Se cells with nonzero x.
However, total time spent pausing by cMTs was lower in SE cells than in WT cells, while time spent shrinking was augmented in SE cells (Figure 5D).
Hence, cMTs in pre-anaphase SE cells are more dynamic than cMTs in WT cells.
Furthermore, deletion of BIK1, BIM1 or KAR3 in SA or SE cells is lethal.
Also, catastrophe and rescue frequencies were enhanced in SE cells (Figure 5A).
Therefore, we examined cell growth of WT, SA and SE cells at 30°C, 37°C or 10°C (Figure 1C).
We found that SA and SE cells were synthetic sick with the deletion of MAD2 (Table 2).
This feature for SA and SE cells could reflect a delay in anaphase onset due to abnormal nucleus positioning.
This number was dramatically reduced in SA cells whereas it was greatly enhanced in SE cells as compared to WT cells (3.2±0.6 and 21.2±3.7 vs. 8.9±1.2 cMTs, respectively).
To observe these oscillations, WT, SA and SE cells were transformed with a GFP-TUB1 construct, to label the pre-anaphase intra-nuclear spindle in live cells (Figure 3A).
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