[
1989]
Classical embryological studies of nematodes, primarily by Van Beneden and Boveri near the turn of the century, have made lasting contributions to our understanding of embryonic development (1). However, during most of this century, nematodes have been eclipsed as a model system for embryology by organisms with more tractable embryos such as sea urchins, insects, amphibians, birds, and mice. Two features of the free-living soil nematode Caenorhabditis elegans have returned nematodes to a prominent place in embryological investigations: its suitability for genetic analysis and its invariant and completely described cell lineage. These two features, combined with technological advances in microscopy and molecular biology, are providing the opportunity to combine experimental embryology with genetic and molecular analyses of embryonic development at the level of individual cells in a single organism. This chapter focuses on efforts to understand the molecular and cellular events of early development in C. elegans with particular emphasis on events relating to the determination of embryonic cell fates. Extensive coverage of the various contributions that the study of Caenorhabditis has made to our knowledge of developmental biology can be found in ref. 2.
[
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.
[
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.