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00:54Interphase
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The cell cycle occurs over approximately 24 hours (in a typical human cell) and in two distinct stages: interphase, which includes three phases of the cell cycle (G1, S, and G2), and mitosis (M). During interphase, which takes up about 95 percent of the duration of the eukaryotic cell cycle, cells grow and replicate their DNA in preparation for mitosis.
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02:39Positive Regulator Molecules
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Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
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02:38S-Cdk Initiates DNA Replication
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The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
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00:56What is the Cell Cycle?
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The cell cycle refers to the sequence of events occurring throughout a typical cell’s life. In eukaryotic cells, the somatic cell cycle has two stages: the interphase and the mitotic phase. During interphase, the cell grows, performs its basic metabolic functions, copies its DNA, and prepares for mitotic cell division. Then, during mitosis and cytokinesis, the cell divides its nuclear and cytoplasmic materials, respectively. This generates two daughter cells that are identical to the...
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01:28The Cell Cycle Control System
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The cell cycle regulation directs how a cell proceeds from one phase to the next and begins mitosis. The cell cycle control system includes intracellular regulatory molecules and external triggers. They provide "stop" or "advance" signals and operate at specific cell cycle stages termed checkpoints to ensure that a particular process is completed before the cell advances to the next phase.
Cyclins and cyclin-dependent kinases (Cdks) are the primary cell cycle regulators and...
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01:27Molecular Factors Affecting Cell Division
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Several external and internal factors influence the initiation and inhibition of cell division. For instance, the death of nearby cells or the release of human growth hormone (hGH) promotes cell division. In contrast, lack of hGH or crowding of cells can inhibit cell division.
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Measuring Cell Cycle Progression Kinetics with Metabolic Labeling and Flow Cytometry
Published on: May 22, 2012
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Core control principles of the eukaryotic cell cycle.
Souradeep Basu1,2, Jessica Greenwood3, Andrew W Jones3
1Cell Cycle Laboratory, The Francis Crick Institute, London, UK. souradeepb@deepmind.com.
Nature
|June 8, 2022
Summary
Cyclin-dependent kinases (CDKs) control cell division. This study shows that increasing CDK activity, not just substrate specificity, drives cell cycle events, reconciling two major CDK models.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Cyclin-dependent kinases (CDKs) regulate the eukaryotic cell cycle, with distinct cyclin-CDK complexes initiating DNA replication (S-CDK) and mitosis (M-CDK).
- The precise mechanisms by which these complexes organize cell cycle progression remain debated, with two prominent models: functional specialization versus redundant CDK activity.
- One model emphasizes distinct substrate specificities for S-CDKs and M-CDKs, while the other posits that overall CDK activity levels, rather than specificity, dictate cell cycle order.
Purpose of the Study:
- To reconcile the opposing models of cell cycle control by investigating the functional specialization and substrate specificities of S-CDKs and M-CDKs.
- To determine whether CDK substrate specificity or overall CDK activity is the primary determinant of cell cycle event ordering.
- To elucidate the interplay between CDK activity levels and substrate specificity in driving key cell cycle transitions.
Main Methods:
- Utilized phosphoproteomic assays to measure in vivo CDK activity in fission yeast.
- Compared the substrate specificities of S-CDK and M-CDK complexes.
- Investigated the effect of altering CDK activity on the ability of S-CDK to perform M-CDK functions, including the role of protein phosphatase 1.
Main Results:
- Found that S-CDK and M-CDK exhibit remarkably similar substrate specificities, challenging the notion of complete functional specialization.
- Demonstrated that S-CDK can drive mitosis when protein phosphatase 1 is removed from the centrosome, indicating that increased S-CDK activity can overcome specificity differences.
- Showed that elevated S-CDK activity in vivo is sufficient to execute M-CDK functions, supporting the role of quantitative activity increases.
Conclusions:
- The core cell cycle engine relies primarily on a quantitative increase in CDK activity throughout the cell cycle.
- Minor, surmountable qualitative differences in catalytic specialization exist between S-CDKs and M-CDKs.
- This study unifies the functional specialization and redundant activity models, highlighting the importance of both quantitative activity and substrate specificity in cell cycle control.