Controlled chaos: New insights into genetically programmed cell cycle asynchrony
Bibliographic record
Abstract
Entry into and progression through mitosis critically depends on the activity of Cdk1 in complex with its non-catalytic subunit cyclin B. Conversely, in order to exit from mitosis the cyclin B-Cdk1 complex needs to be inactivated, which occurs through APC/Cdependent proteasomal degradation of cyclin B. This model is attractive in its simplicity and builds a foundation that explains multiple aspects of chromosome segregation.On first sight, it appears that the mitotic activity of Cdk1-cyclin B is constantly high until the metaphase-anaphase transition.Recent careful re-examination of Cdk1-cyclin B activity, however, revealed that even after entry into mitosis, the activity of Cdk1-cyclin B continues to rise. 1 More importantly, it appears that some events during mitosis require higher levels of Cdk1-cyclin B than others.Specifically, lowering Cdk1-cyclin B levels to an extent that just allows mitotic entry, causes defects in APC/C activation and spindle organization, two aspects of mitosis that are apparently dependent on high Cdk1-cyclin B activity. 1 These results indicated that maintaining and elevating Cdk1-cyclin B levels during mitosis is of critical importance to ensure genomic stability.One of the recently emerging proteins that is required to establish high levels of Cdk1-cyclin B activity during mitosis is the Greatwall kinase (GWL), as originally identified in Drosophila. 2 GWL mutant cells were initially described to display chromosome condensation defects as well as delayed progression through mitosis. 2 Subsequent analysis in Xenopus revealed that Greatwall kinase functions in a positive feedback loop with the maturation-promoting factor (MPF, which consists of CDK1 in complex with cyclin B) to promote mitotic entry. 3How exactly Greatwall exerts its effects is unclear, but biochemical Cell Cycle News & ViewsBuilding a great wall around mitosis: Evolutionary conserved roles for the Greatwall/MASTL kinases in securing chromosome stability
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.001 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.001 | 0.000 |
| Research integrity | 0.003 | 0.003 |
| Insufficient payload (model declined to judge) | 0.003 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".