Ase1/Prc1-dependent spindle elongation corrects merotely during anaphase in fission yeast
Faithful segregation of sister chromatids requires the attachment of each kinetochore (Kt) to microtubules (MTs) that extend from opposite spindle poles. Merotelic Kt orientation is a Kt-MT misattachment in which a single Kt binds MTs from both spindle poles rather than just one. Genetic induction of merotelic Kt attachment during anaphase in fission yeast resulted in intra-Kt stretching followed by either correction or Kt disruption. Laser ablation of spindle MTs revealed that intra-Kt stretching and merotelic correction were dependent on MT forces. The presence of multiple merotelic chromosomes linearly antagonized the spindle elongation rate, and this phenomenon could be solved numerically using a simple force balance model. Based on the predictions of our mechanical model, we provide in vivo evidence that correction of merotelic attachment in anaphase is tension dependent and requires an Ase1/Prc1-dependent mechanism that prevents spindle collapse and thus asymmetric division and/or the appearance of the cut phenotype.
Results
Fig. 1
[x] rad21-K1 AT THE PERMISIVE TEMP:
[x] 22% merotelic attachment vs none wild-type
[ ] 75% of those are resolved
[ ] The 25% reamining one are splitted in two
[ ] Max distance before disruption is 1.56
Fig. 3
[x] rad21-K1
[x] decreased elongation speed? output_of the attachments since it is linearly correlated
Fig. 4
[ ] ase1D rad21-k1
[x] dies at semi-permissive temperature 31
[x] genetic interaction: synth lethal
[x] spindle collapse + uniform shrinkage
[ ] cut phenotype / diploidisation
GO
Anaphase B spindle elongation -> stretch of merotelic attachment (direct evidence) -> correction of merotelic attachment (inferred)
Mechanistic evidence through laser ablation (Fig. 2)
At the same time linear correlation with number of merotelic attachments -> slower elongation
When the attachment is resolved -> increase in speed again.
Ase1 (weak midzone) -> collapse + active shrinkage.
PMID:19948483
Ase1/Prc1-dependent spindle elongation corrects merotely during anaphase in fission yeast
Faithful segregation of sister chromatids requires the attachment of each kinetochore (Kt) to microtubules (MTs) that extend from opposite spindle poles. Merotelic Kt orientation is a Kt-MT misattachment in which a single Kt binds MTs from both spindle poles rather than just one. Genetic induction of merotelic Kt attachment during anaphase in fission yeast resulted in intra-Kt stretching followed by either correction or Kt disruption. Laser ablation of spindle MTs revealed that intra-Kt stretching and merotelic correction were dependent on MT forces. The presence of multiple merotelic chromosomes linearly antagonized the spindle elongation rate, and this phenomenon could be solved numerically using a simple force balance model. Based on the predictions of our mechanical model, we provide in vivo evidence that correction of merotelic attachment in anaphase is tension dependent and requires an Ase1/Prc1-dependent mechanism that prevents spindle collapse and thus asymmetric division and/or the appearance of the cut phenotype.
Results
Fig. 1
75% of those are resolvedThe 25% reamining one are splitted in twoMax distance before disruption is 1.56Fig. 3
Fig. 4
GO
Anaphase B spindle elongation -> stretch of merotelic attachment (direct evidence) -> correction of merotelic attachment (inferred)
At the same time linear correlation with number of merotelic attachments -> slower elongation
Ase1 (weak midzone) -> collapse + active shrinkage.