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The behavior of cytoplasmic microtubules revealed distinct interactions with the cell cortex that result in associated spindle movement and orientation.
This is because it was hypothesised that spindle movement through the cytoplasm may generate an asymmetrical pulling force that acts on the bivalents and such force may constitute the spindle component described above.
These measurements also suggest that the direction of spindle movement can be predicted before migration occurs, and correlates with the direction in which the homologue pairs experiencing greater C Kt stretch are facing.
After RNAi against nmy-2 for 22 to 24 hours, we found that embryos properly established PAR polarity (fig. S1) and spindle movement was normal (fig. S2A).
In some cases, such as the centering of the spindle in fission yeast, spindle movement relies on pushing forces that arise as growing astral microtubules push against the cortex [3], [4].
To assess nuclear (spindle) movement, images of yeast cells expressing GFP-Tub1p were taken at 30 sec intervals for a total of 60 min, with an exposure time of 500 msec at each focal plane.
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The formation of invaginations in the csnk-1 (RNAi) may explain why spindle movements following CSNK-1 depletion are not faster, as might be expected if the net force is larger.
If CSNK-1 acts negatively on PPK-1 for the regulation of spindle movements, then loss of PPK-1 should cause reduced GPR-1/2 localization and reduced spindle movements.
We conclude that the excessive spindle movements of csnk-1 RNAi) csnk-1 RNAi membryos by Gα/GPR-1/2/LIN-5 areivity.
We first tested whether the abnormal pronuclear and spindle movements depended on GPR-1/2 and LIN-5.
We deduce that CSNK-1 controls GPR-1/2 and spindle movements through modulation of PPK-1 activity or localization.
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