k. a. HEC1 in mammalian species), SPC (spindle pole component) 24, SPC25, and NUF2, and mediates attachment of chromosomes to microtubules, were differentially expressed showing up-regulation of NDC80 and SPC25 and down-regulation of NUF2.
With regard to Plo1 localisation to the mitotic SPB, to our knowledge, this is the first study in any organisms to identify genetically a spindle pole component that plays a critical role in polo kinase recruitment to the SPB/centrosome.
In fucoid zygotes, one or more of these putative functions may be needed to hold pole components together.
To identify exactly how imp2 C) cells fail during cytokinesis, we imaged cells producing Sid4-GFP (a spindle pole body component) and Rlc1-GFP (a CR component) to visualize mitotic and cytokinetic progression, respectively.
In budding yeast genetic screens identified SPC97 (spindle pole body component of 97 kDa) and SPC98 as interacting partners of the γ-tubulin TUB4 [6], [7], [7].
The Dam1 kinetochore complex acts as a barrier and does not allow SAC proteins to interact with the spindle pole body component (Spc105) required for SAC activation.
The time evolution of this pole-force component was responsible for the periodic variations of cell length and strain energy that the cells underwent during migration.
As the reviewer correctly points out, the de novo localization, that resembles for instance nanos mRNA localization, could indeed be posterior recruitment by the pole plasm components.
Finally, the FK2 signal at the posterior of the oocyte is not due to the accumulation of ubiquitylated pole plasm components, because it persists in the vas PD mutant, which abolishes pole plasm formation downstream of Osk.
Finally, we examined whether two pole plasm components, Osk and Vas protein, localized normally to the posterior of the stage-10 oocyte in the knockdown lines where pole cell formation was compromised.
However, many genes, such as Aurora kinases, BUB1 and BUB1B, centromere proteins, kinesins, Max interacting protein 1 (minichromosomalmaintenancentenance deficient proteins (MCMs), and spindle pole body components were not previously recognized to be regulated by SB.
