Links
Objectives
- Identify the major controlling input for each cell cycle checkpoint
- Discuss the role of cyclin-dependent kinases
Key Points
Regulation
- certain cell factors promote transition to division
- some proteins found to vary in level with cell cycle = cyclins
- genetic mutants found that regulate progression = cdc’s (cell div cycle)
- many found to encode kinases, interact with cyclins = cdk’s
- CDK’s
- cyclin-dependent kinases, partner with cyclins
- regulated by phosphorylation, in turn phosphorylate targets
- enzymes required for cellular processes
- checkpoints
- G1/S is primary
- external factors can influence
- links cell division to growth and nutritional status
- accumulation of G1 cyclins activate Cdc2 kinase, activates targets
- G2/M
- M-phase promoting factors involved in this check
- Mitotic cyclin + Cdc2 kinase
- integrity of DNA after replication critical
- M-phase promoting factors involved in this check
- Spindle
- tension on MT, chromosomes aligned at metaphase plate
- unclear how mechanical signaling occurs
- anaphase-promoting complex (APC) result in cohesin breakdown
- marks securin for degradation, releases inhibition on separase
- tension on MT, chromosomes aligned at metaphase plate
- G1/S is primary
- Growth factors
- proteins with specific cell surface receptors
- often trigger MAP kinase cascades that lead to G1 cyclin expression
- not all cells affected by all growth factors
- p53 is a tumor suppressor
- monitors DNA integrity, induces repair enzymes or cell death
- proto-oncogenes: normal genes that cancer-causing when mutated
- involved in signaling, either receptors or part of transduction
In-class Activities
Describe some features and characteristics of cells deficient in each of the cell cycle checkpoints. For example, what would a cell deficient in G1/S regulation be like? What would it have or lack?
Questions for Practice
- Which cell cycle checkpoint is most influenced by external factors? Why is this adaptive?
- Predict the consequences of a mutation in mitotic cyclin OR p53 OR a proto-oncogene.