High impact information on ASE1

• In addition, loss of ASE1 function destabilized telophase spindles, and expression of a nondegradable Ase1 mutant delayed spindle disassembly [1].
• Ase1 was degraded when cells exited from mitosis and entered G1 [1].
• A component of the Saccharomyces cerevisiae spindle, Ase1, was observed to undergo cell cycle-specific degradation mediated by the cyclosome, or anaphase promoting complex (APC) [1].
• APC-mediated proteolysis of Ase1 and the morphogenesis of the mitotic spindle [1].
• Kin4 is active in cells with mispositioned nuclei and predominantly localizes to mother cells, where it is ideally situated to inhibit MEN signaling at spindle pole bodies (SPBs) when anaphase spindle elongation occurs within the mother cell [2].

Biological context of ASE1

• The steady-state levels of Ase1p are regulated in a manner that is consistent with a function during anaphase: they are low in G1, accumulate to maximal levels after S phase and then drop as cells exit mitosis [3].
• Execution point experiments indicate that Dam1p has a role in formation of a metaphase spindle and in anaphase spindle elongation [4].
• PRC1 has sequence homology to the budding yeast anaphase spindle elongation factor Ase1p [5].
• Sumoylation of the budding yeast kinetochore protein Ndc10 is required for Ndc10 spindle localization and regulation of anaphase spindle elongation [6].

Anatomical context of ASE1

• In cells whose microtubule cytoskeleton has been perturbed, anaphase spindle elongation often occurs entirely within the mother cell, and the post-anaphase nuclear migration checkpoint introduces a compensatory delay of cytokinesis until one pole of the anaphase nucleus enters the bud [7].
• Since ectopic expression of proteolysis-resistant Cin8, Kip1 or Ase1 is sufficient for SPB separation even in the absence of Cdc28-Clb activity, we suggest that stabilization of these mechanical force-generating proteins is the predominant role of Cdc28-Clb in centrosome separation [8].

Regulatory relationships of ASE1

• Here, we show that Esp1 has a novel role in promoting anaphase spindle elongation [9].
• Excess Kar3p has a stronger inhibitory effect on the growth of cin8 kip1 mutants and can completely block anaphase spindle elongation in these cells [10].
• Consistent with the possibility that Ipl1 regulates Ase1, an ase1 mutant lacking the Ipl1 consensus phosphorylation sites cannot assemble spindles in the absence of Cin8 [11].

Other interactions of ASE1

• Strains lacking both ASE1 and BIK1, which encodes an S. cerevisiae microtubule-associated protein, are inviable [3].
• MIF2 is required for mitotic spindle integrity during anaphase spindle elongation in Saccharomyces cerevisiae [12].
• The kinesin-related Cin8p and cytoplasmic dynein are microtubule-associated motor proteins required for anaphase spindle elongation in the yeast Saccharomyces cerevisiae [13].

Analytical, diagnostic and therapeutic context of ASE1

• By size exclusion chromatography and velocity sedimentation, both Ase1p in extracts and purified Ase1p behaved as a homodimer [14].

References