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The rectal epithelial cell Y produces the support cells (and neurons) of the PCS, which lies posterior to the hook. Divisions are anterior-posterior unless otherwise indicated. bm, body muscle; cc, coelomocyte; um1, type 1 uterine muscle; um2, type 2 uterine muscle; vm1 type 1 vulval muscle; vm2, type 2 vulval muscle. Aspects of many of these cell fate decisions are covered in more detail in other chapters, which will be referred to where appropriate. Green nuclei are ectodermal, red nuclei are mesodermal. The body plan must influence the fates of individual cells, however the mechanisms by which this occurs are not yet clear. POP-1 is asymmetrically distributed to anterior-posterior sister cells in many divisions during development (Herman, 2002; Herman and Wu, 2004; Lin et al., 1998).
In hermaphrodites, P cells in the mid-body make the vulval epithelium. Each of these structures is generated by sex-specific cell lineages. Individual nuclei of intestine are not shown, brown indicates endoderm. At most divisions, the nucleus of the anterior daughter has a higher level of POP-1 than does the posterior daughter.
In the male, cells of the posterior lateral seam generate the sensory rays, instead of alae.
hyp cells of the tail tip reorganize to form a blunt tail morphology.
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.
Ventrally, hypodermal P cells in the posterior generate the hook. Even the intestinal cells have sex-specific fates (Figure 5). Nuclear positions of sexually dimorphic hermaphrodite cells discussed in this chapter. Tcfs are transcription factors that function to activate or repress expression of specific genes in response to Wnt signals (see Wnt chapter).There are many sex-specific differences between males and hermaphrodites.Although these differences affect most tissues, the basic body plan and many of its structures are identical (Sulston et al., 1980; Sulston and Horvitz, 1977).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., hermaphrodite and male.
Hermaphrodites are basically females that produce a small number of sperm that can fertilize their own oocytes. Males are smaller than hermaphrodites and produce only sperm.Interestingly, almost all of these sexually dimorphic structures are made during larval development by the sex-specific divisions of just 16 blast cells (Figure 4). However, there must be other mechanisms at work as well, since not all cell fates are defective in mutants (Herman, 2001; Lin et al., 1998; Siegfried and Kimble, 2002).