Abstract

Cell-division control affects many aspects of development. Caenorhabditis elegans cell-cycle genes have been identified over the past decade, including at least two distinct Cyclin-Dependent Kinases (CDKs), their cyclin partners, positive and negative regulators, and downstream targets. The balance between CDK activation and inactivation determines whether cells proceed through G1 into S phase, and from G2 to M, through regulatory mechanisms that are conserved in more complex eukaryotes. The challenge is to expand our understanding of the basic cell cycle into a comprehensive regulatory network that incorporates environmental factors and coordinates cell division with growth, differentiation and tissue formation during development. Results from several studies indicate a critical role for CKI-1, a CDK inhibitor of the Cip/Kip family, in the temporal control of cell division, potentially acting downstream of heterochronic genes and dauer regulatory pathways.

Highlights

  • Animal development from a single-cell zygote to fertile adult requires many rounds of cell division

  • The level of questions include: how is cell division temporally and spatially controlled during development, and how is progression through the cycle coordinated with cell growth, differentiation, migration, and death? C. elegans is well suited to study developmental control of cell division and to address how nutritional signals, differentiation factors, checkpoint controls, heterochronic genes, and dauer regulatory pathways act upon the cell-cycle machinery to affect cell-cycle entry and exit

  • The collective results from studies in various eukaryotes have demonstrated that progression through the cell-division cycle is driven by activation and inactivation of cyclin-dependent kinases (CDKs), which trigger the transition to subsequent phases of the cycle

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Summary

Overview

Animal development from a single-cell zygote to fertile adult requires many rounds of cell division. Cells complete an ordered series of events that collectively form the "cell cycle". Variations of this typical somatic division cycle are used to fulfill specific requirements (Figure 1B). These include rapid embryonic cell cycles that lack G and G phases, meiotic cell cycles that allow formation of haploid gametes, and endoreduplication (or: "endore1plicatio2n") cycles in which S phases are not followed by mitosis. These variant cell cycles form part of the stereotypical pattern of cell divisions during C. elegans development. Insights into the basic regulators of cell-cycle progression in C. elegans form the foundation for such studies and are the focus of this chapter

The paradigm of cell-cycle control
CDKs and cyclins
CDK inhibitory proteins
Cell-cycle variation
Embryonic cell cycles
Larval somatic cell cycles
Endoreduplication cycles
The meiotic cell cycle
Checkpoint control
DNA-damage induced checkpoint
DNA-replication induced checkpoint
Spindle-assembly checkpoint
Cell-cycle entry and arrest

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