Although Ago2-deficient oocytes can develop to morphologically normal mature oocytes, the spindle and the organization of the chromosomes are abnormal.
To address whether the capability to circumvent the SAC was restricted to multipolar cell divisions, we exposed normal fibroblasts and WiT49 cells to the spindle-disrupting agent Colcemid for 18 h, after which the cells were stained with antibodies to AURKA and CCNB1.
The commonly accepted view, therefore, is that spasticity is due to an abnormal processing in the spinal cord of a normal input from the spindles.
After the surface normal vector is calculated based on the laser sensors' feedback, the 2-EDNA concept is conceived specifically to address the deviation of the spindle from the surface normal at the drilling point.
Apparently, even in those cases where spindles appear normal during the metaphase in apoptin-expressing cells, cells are not able to easily progress past the spindle assembly checkpoint (SAC) into anaphase.
The existence of the latter mechanism is evidenced by otherwise normal spindles with one pole stretched and extended to the cortex, as if the spindle were being displaced, which we observed in both the klp10A RNAi knockdown and klp10A P mut heterozygous oocytes.
Their effectiveness in cancer chemotherapy is thought to be due to their ability to reduce the dynamics of microtubules in mitotic spindles, thus preventing spindle assembly and interrupting the normal movement of sister chromatids toward the spindle poles [ 3- 9].
Together, these data suggest that the two basal body proteins Wtip and Vangl2 interact and are required to establish the normal mitotic spindle angles in the anterior and middle pronephros.
If the spindle is normal, the bypass of the checkpoint has no consequence on cell viability.
In cells lacking PIASγ, normal metaphase plates form, but the spindle checkpoint is activated, leading to a prolonged metaphase block.
However, unlike wild-type Lgl-GFP, neither the myrLgl-GFP nor the LglASA-GFP construct was able to restore normal mitotic spindle orientation in lgl mutant clones in the follicle cell epithelium.
