scholarly journals miR-433 overexpression attenuates the spindle assembly checkpoint response to paclitaxel

2010 ◽  
Vol 12 (S1) ◽  
Author(s):  
F Furlong ◽  
M Prencipe ◽  
A McGoldrick ◽  
P McGettigan ◽  
D Carney ◽  
...  
Keyword(s):  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Checkpoint Response

scholarly journals The Spindle Assembly Checkpoint Functions during Early Development in Non-Chordate Embryos

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1087
Author(s):  
Janet Chenevert ◽  
Marianne Roca ◽  
Lydia Besnardeau ◽  
Antonella Ruggiero ◽  
Dalileh Nabi ◽  
...  
Keyword(s):  
Early Development ◽  
Spindle Assembly Checkpoint ◽  
Sea Urchins ◽  
Volume Ratio ◽  
Spindle Assembly ◽  
Mitotic Progression ◽  
Checkpoint Response ◽  
Ascidian Embryos ◽  
Spindle Microtubules ◽  
Prolonged Delay

In eukaryotic cells, a spindle assembly checkpoint (SAC) ensures accurate chromosome segregation, by monitoring proper attachment of chromosomes to spindle microtubules and delaying mitotic progression if connections are erroneous or absent. The SAC is thought to be relaxed during early embryonic development. Here, we evaluate the checkpoint response to lack of kinetochore-spindle microtubule interactions in early embryos of diverse animal species. Our analysis shows that there are two classes of embryos, either proficient or deficient for SAC activation during cleavage. Sea urchins, mussels, and jellyfish embryos show a prolonged delay in mitotic progression in the absence of spindle microtubules from the first cleavage division, while ascidian and amphioxus embryos, like those of Xenopus and zebrafish, continue mitotic cycling without delay. SAC competence during early development shows no correlation with cell size, chromosome number, or kinetochore to cell volume ratio. We show that SAC proteins Mad1, Mad2, and Mps1 lack the ability to recognize unattached kinetochores in ascidian embryos, indicating that SAC signaling is not diluted but rather actively silenced during early chordate development.

scholarly journals Sustained Spindle-Assembly Checkpoint Response Requires De Novo Transcription and Translation of Cyclin B1

PLoS ONE ◽  
2010 ◽  
Vol 5 (9) ◽  
pp. e13037 ◽  
Author(s):  
Ana Lúcia Mena ◽  
Eric W.-F. Lam ◽  
Sukalyan Chatterjee
Keyword(s):  
Spindle Assembly Checkpoint ◽  
De Novo ◽  
Spindle Assembly ◽  
Cyclin B1 ◽  
Checkpoint Response

scholarly journals Aurora Kinase-A Inactivates DNA Damage-Induced Apoptosis and Spindle Assembly Checkpoint Response Functions of p73

Cancer Cell ◽  
2012 ◽  
Vol 21 (2) ◽  
pp. 196-211 ◽  
Author(s):  
Hiroshi Katayama ◽  
Jin Wang ◽  
Warapen Treekitkarnmongkol ◽  
Hidehiko Kawai ◽  
Kaori Sasai ◽  
...  
Keyword(s):  
Dna Damage ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Aurora Kinase ◽  
Response Functions ◽  
Checkpoint Response ◽  
Aurora Kinase A ◽  
Induced Apoptosis ◽  
Kinase A

scholarly journals Spindle assembly checkpoint: the third decade

2011 ◽  
Vol 366 (1584) ◽  
pp. 3595-3604 ◽  
Author(s):  
Andrea Musacchio
Keyword(s):  
Cell Cycle Progression ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Mitotic Checkpoint ◽  
Anaphase Promoting Complex ◽  
Checkpoint Control ◽  
Checkpoint Response ◽  
The Third ◽  
Binding Interface ◽  
Mitotic Checkpoint Complex

The spindle assembly checkpoint controls cell cycle progression during mitosis, synchronizing it with the attachment of chromosomes to spindle microtubules. After the discovery of the mitotic arrest deficient ( MAD ) and budding uninhibited by benzymidazole ( BUB ) genes as crucial checkpoint components in 1991, the second decade of checkpoint studies (2001–2010) witnessed crucial advances in the elucidation of the mechanism through which the checkpoint effector, the mitotic checkpoint complex, targets the anaphase-promoting complex (APC/C) to prevent progression into anaphase. Concomitantly, the discovery that the Ndc80 complex and other components of the microtubule-binding interface of kinetochores are essential for the checkpoint response finally asserted that kinetochores are crucial for the checkpoint response. Nevertheless, the relationship between kinetochores and checkpoint control remains poorly understood. Crucial advances in this area in the third decade of checkpoint studies (2011–2020) are likely to be brought about by the characterization of the mechanism of kinetochore recruitment, activation and inactivation of checkpoint proteins, which remains elusive for the majority of checkpoint components. Here, we take a molecular view on the main challenges hampering this task.

scholarly journals Spindle assembly checkpoint proteins regulate and monitor meiotic synapsis in C. elegans

2015 ◽  
Vol 211 (2) ◽  
pp. 233-242 ◽  
Author(s):  
Tisha Bohr ◽  
Christian R. Nelson ◽  
Erin Klee ◽  
Needhi Bhalla
Keyword(s):  
Spindle Assembly Checkpoint ◽  
Meiotic Chromosome ◽  
Spindle Assembly ◽  
Anaphase Promoting Complex ◽  
Checkpoint Response ◽  
Checkpoint Proteins ◽  
Cis Acting ◽  
C Elegans ◽  
Meiotic Synapsis ◽  
The Stability

Homologue synapsis is required for meiotic chromosome segregation, but how synapsis is initiated between chromosomes is poorly understood. In Caenorhabditis elegans, synapsis and a checkpoint that monitors synapsis depend on pairing centers (PCs), cis-acting loci that interact with nuclear envelope proteins, such as SUN-1, to access cytoplasmic microtubules. Here, we report that spindle assembly checkpoint (SAC) components MAD-1, MAD-2, and BUB-3 are required to negatively regulate synapsis and promote the synapsis checkpoint response. Both of these roles are independent of a conserved component of the anaphase-promoting complex, indicating a unique role for these proteins in meiotic prophase. MAD-1 and MAD-2 localize to the periphery of meiotic nuclei and interact with SUN-1, suggesting a role at PCs. Consistent with this idea, MAD-1 and BUB-3 require full PC function to inhibit synapsis. We propose that SAC proteins monitor the stability of pairing, or tension, between homologues to regulate synapsis and elicit a checkpoint response.

scholarly journals The spindle assembly checkpoint functions during early development in non-chordate embryos

2019 ◽  
Author(s):  
Janet Chenevert ◽  
Marianne Roca ◽  
Lydia Besnardeau ◽  
Antonella Ruggiero ◽  
Dalileh Nabi ◽  
...  
Keyword(s):  
Early Development ◽  
Spindle Assembly Checkpoint ◽  
Sea Urchins ◽  
Volume Ratio ◽  
Spindle Assembly ◽  
Eukaryotic Cells ◽  
Embryonic Cells ◽  
Checkpoint Response ◽  
Early Embryos ◽  
Spindle Microtubules

In eukaryotic cells, a spindle assembly checkpoint (SAC) ensures accurate chromosome segregation. This control mechanism monitors proper attachment of chromosomes to spindle microtubules and delays mitotic progression if connections are erroneous or absent. The SAC operates in all eukaryotic cells tested so far, but is thought to be relaxed during early embryonic development in animals. Here, we evaluate the checkpoint response to lack of kinetochore-spindle microtubule interactions in early embryos of diverse animal species from the main metazoan groups. Our analysis shows that there are two classes of embryos, either proficient or deficient for SAC activation during cleavage. Sea urchins, mussels and jellyfish embryos show a prolonged mitotic block in the absence of spindle microtubules from the first cleavage division, while ascidian and amphioxus embryos, like those of Xenopus and zebrafish, continue mitotic cycling without delay. SAC competence during early development shows no correlation with cell size, chromosome number or kinetochore to cell volume ratio, ruling out the hypothesis that lack of checkpoint activity in early embryos is due to the large egg volume. Our results instead indicate that there is no inherent incompatibility between SAC activity and large fast-dividing embryonic cells. We suggest that SAC proficiency is the default situation of metazoan embryos, and that SAC activity is specifically silenced in chordate species with fast dividing embryos.

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