Evolutionary Dynamics of the Spindle Assembly Checkpoint in Eukaryotes

Kops, Geert J.P.L.; Snel, Berend; Tromer, Eelco C.

doi:10.1016/j.cub.2020.02.021

Cited by 62 publications

(61 citation statements)

References 170 publications

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“…S8 ). This contrasts with the RVSF SLiM, which binds PP1 to KNL1 and is present throughout the eukaryotic tree of life ( Kops et al, 2020 ; Tromer et al, 2015 ; van Hooff et al, 2017 ; Fig. S8 ).…”

Section: Resultsmentioning

confidence: 94%

“…The full list of annotated and excluded PBMs is included in Data S1 . The majority of KNL1 sequences used to determine presence/absence of the KNL1-RVSF were published previously ( Kops et al, 2020 ; Tromer et al, 2015 ; van Hooff et al, 2017 ). Any unannotated genomes were searched by blast using KNL1 orthologues from the closest species.…”

Section: Methodsmentioning

confidence: 99%

“…Data S2 shows the KNL1 orthologues from Fig. S8 that are not published in Kops et al (2020) , Tromer et al (2015) , and van Hooff et al (2017) .…”

Section: Methodsmentioning

confidence: 99%

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Kinetochore phosphatases suppress autonomous Polo-like kinase 1 activity to control the mitotic checkpoint

Cordeiro

Smith

Saurin

2020

Journal of Cell Biology

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Local phosphatase regulation is needed at kinetochores to silence the mitotic checkpoint (a.k.a. spindle assembly checkpoint [SAC]). A key event in this regard is the dephosphorylation of MELT repeats on KNL1, which removes SAC proteins from the kinetochore, including the BUB complex. We show here that PP1 and PP2A-B56 phosphatases are primarily required to remove Polo-like kinase 1 (PLK1) from the BUB complex, which can otherwise maintain MELT phosphorylation in an autocatalytic manner. This appears to be their principal role in the SAC because both phosphatases become redundant if PLK1 is inhibited or BUB–PLK1 interaction is prevented. Surprisingly, MELT dephosphorylation can occur normally under these conditions even when the levels or activities of PP1 and PP2A are strongly inhibited at kinetochores. Therefore, these data imply that kinetochore phosphatase regulation is critical for the SAC, but primarily to restrain and extinguish autonomous PLK1 activity. This is likely a conserved feature of the metazoan SAC, since the relevant PLK1 and PP2A-B56 binding motifs have coevolved in the same region on MADBUB homologues.

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Section: Resultsmentioning

confidence: 94%

Section: Methodsmentioning

confidence: 99%

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Kinetochore phosphatases suppress autonomous Polo-like kinase 1 activity to control the mitotic checkpoint

Cordeiro

Smith

Saurin

2020

Journal of Cell Biology

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“…[ 91 ] They could explain how the network is being shaped to the “needs” of different eukaryotes. [ 92 ]…”

Section: Discussionmentioning

confidence: 99%

SAC during early cell divisions: Sacrificing fidelity over timely division, regulated differently across organisms

Duro

Nilsson

2020

BioEssays

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Early embryogenesis is marked by a frail Spindle Assembly Checkpoint (SAC). The time of SAC acquisition varies depending on the species, cell size or a yet to be uncovered developmental timer. This means that for a specific number of divisions, biorientation of sister chromatids occurs unsupervised. When error‐prone segregation is an issue, an aneuploidy‐selective apoptosis system can come into play to eliminate chromosomally unbalanced cells resulting in healthy newborns. However, aneuploidy content can be too great to overcome, endangering viability. SAC generates a diffusible signal to lengthen time spent in mitosis if needed, ensuring correct chromosome segregation, a fundamental factor in the generation of euploid cells. Thus, it remains puzzling what benefit could come from delaying SAC acquisition till later in the development. In this review, we describe what is known on SAC acquisition in distinct species and highlight pending research as well as potential applications for such knowledge.

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“…[9,12,14,15,17,18] Collectively, these observations strongly support the notion that NPCs and the SAC have extensive and ancient shared functions. [86] Intriguingly, the SAC is regulated by Nups that are not recruited to kinetochores. Instead, the impact on SAC function stems from the ability of Mad1 to interact with NPCs.…”

Section: Co-evolution Of Nups and Sac Proteinsmentioning

confidence: 99%

From the Nuclear Pore to the Fibrous Corona: A MAD Journey to Preserve Genome Stability

Cunha-Silva

Conde

2020

BioEssays

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The relationship between kinetochores and nuclear pore complexes (NPCs) is intimate but poorly understood. Several NPC components and associated proteins are relocated to mitotic kinetochores to assist in different activities that ensure faithful chromosome segregation. Such is the case of the Mad1-c-Mad2 complex, the catalytic core of the spindle assembly checkpoint (SAC), a surveillance pathway that delays anaphase until all kinetochores are attached to spindle microtubules. Mad1-c-Mad2 is recruited to discrete domains of unattached kinetochores from where it promotes the rate-limiting step in the assembly of anaphase-inhibitory complexes. SAC proficiency further requires Mad1-c-Mad2 to be anchored at NPCs during interphase. However, the mechanistic relevance of this arrangement for SAC function remains ill-defined. Recent studies uncover the molecular underpinnings that coordinate the release of Mad1-c-Mad2 from NPCs with its prompt recruitment to kinetochores. Here, current knowledge on Mad1-c-Mad2 function and spatiotemporal regulation is reviewed and the critical questions that remain unanswered are highlighted.

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Evolutionary Dynamics of the Spindle Assembly Checkpoint in Eukaryotes

Cited by 62 publications

References 170 publications

Kinetochore phosphatases suppress autonomous Polo-like kinase 1 activity to control the mitotic checkpoint

Kinetochore phosphatases suppress autonomous Polo-like kinase 1 activity to control the mitotic checkpoint

SAC during early cell divisions: Sacrificing fidelity over timely division, regulated differently across organisms

From the Nuclear Pore to the Fibrous Corona: A MAD Journey to Preserve Genome Stability

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