[
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.
[
2000]
There is growing interest in the use of bioindicators to assess metal toxicity in soil. The current ASTM Standard Guide for Conducting Laboratory Soil Toxicity Test with the lumbricid earthworm Eisenia fetida (E 1676-97) uses a common earthworm. The nematode Caenorhabditis elegans is a natural soil inhabitant with many characteristics that make an ideal alternate test organism. It has been used to assess metal toxicity in aquatic media, agar plates and in soil. Work is currently underway on the design of a C. elegans procedure for metals in soil. The objective of this study was to determine differences in LC50S between the chloride salt and the nitrate salt forms of cadmium, copper, lead, nickel, and zinc, in three types of soil: Cecil, Tifton, and ASTM artificial soil. Results indicated that the toxicological effect of the metallic salt varies and is dependent on the particular metal. For Cd and Pb the nitrate form is more toxic while Cu and Ni are more toxic in the chloride form. The composition of the soil also effected toxicity, with the metal being the least toxic in ASTM soil and more toxic in the Tifton soil. This strongly correlated with organic matter and clay content of the soil. It is important to determine the effects of carrier salt form and soil composition on metal toxicity, not only in order to standardize the protocol for C. elegans soil toxicity testing, but also in establishing acceptable exposure concentrations in the soil.
[
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.