Cell proliferation and cell death are two opposing sides of the same coin. The development and homeostasis of multicellular organisms requires the accurate control of both processes. The death that occurs normally as a process of development is called 'programmed cell death' or 'apoptosis'. The phenomenon of developmentally programmed cell death has been known for more than 100 years, but it is only in the last decade that its molecular mechanisms have begun to be uncovered. The nematode Caenorhabditis elegans is one of the few experimental systems in which a genetic approach is available to dissect the processes of programmed cell death, and in fact, findings from studies using C. elegans have already played a very important role in elucidating these mechanisms. Here, we summarise the progress to date in understanding how cell death is controlled in C. elegans, and review the main machinery of programmed cell death/apoptosis with respect to its evolutionary conservation between C. elegans and other species.
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WormBook,
2005]
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 G 1 into S phase, and from G 2 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.
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WormBook,
2006]
There are two sexes in C. elegans, hermaphrodite and male. While there are many sex-specific differences between males and hermaphrodites that affect most tissues, the basic body plan and many of its structures are identical. However, most structures required for mating or reproduction are sexually dimorphic and are generated by sex-specific cell lineages. Thus to understand cell fate specification in hermaphrodites, one must consider how the body plan, which is specified during embryogenesis, influences the fates individual cells. One possible mechanism may involve the asymmetric distribution of POP-1 /Tcf, the sole C. elegans Tcf homolog, to anterior-posterior sister cells. Another mechanism that functions to specify cell fates along the anterior-posterior body axis in both hermaphrodites and males are the Hox genes. Since most of the cell fate specifications that occur in hermaphrodites also occur in males, the focus of this chapter will be on those that only occur in hermaphrodites. This will include the cell fate decisions that affect the HSN neurons, ventral hypodermal P cells, lateral hypodermal cells V5 , V6 , and T ; as well as the mesodermal M, Z1 , and Z4 cells and the intestinal cells. Both cell lineage-based and cell-signaling mechanisms of cell fate specification will be discussed. Only two direct targets of the sex determination pathway that influence cell fate specification to produce hermaphrodite-specific cell fates have been identified. Thus a major challenge will be to learn additional mechanisms by which the sex determination pathway interacts with signaling pathways and other cell fate specification genes to generate hermaphrodite-specific cell fates.