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Riddle DL, Blumenthal T, Meyer BJ, et al., editors. C. elegans II. 2nd edition. Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press; 1997.

Cover of C. elegans II

C. elegans II. 2nd edition.

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Section IIIVPC Generation and Identity

Twelve P cells are present at hatching. The VPCs are the posterior daughters of P3P8 (see Fig. 4). The nuclei of all of the P cells are initially present in a lateral position and migrate ventrally within the cells during the L1 stage (Sulston and Horvitz 1977). The migration appears to be an active process and requires the activity of the unc-83 and unc-84 genes (Sulston and Horvitz 1981; Fixsen 1985; W. Fixsen and H.R. Horvitz, pers. comm.). After nuclear migration is completed, the P cells divide in an anterior-posterior manner (Sulston and Horvitz 1977). The anterior daughters are neuroblasts that contribute descendants to the ventral nerve cord. The posterior daughters of P3P8 are the VPCs, whereas the posterior daughters of the other P cells fuse with hyp7, the major hypodermal syncytium encompassing the animal. P3.pP8.p are not specified to adopt vulval fates until the L3 stage.

A. Genes Required for the Identity of P3.p–P8.p as VPCs

Genes required for the identity of P3.pP8.p as VPCs have been identified by mutations that cause a Vulvaless phenotype. In lin-39 mutants, P3.pP8.p fuse with the hypodermis in the L1 stage and therefore behave like the posterior daughters of the other P cells (Clark et al. 1993; Wang et al. 1993). lin-39 is a member of the C. elegans Hox gene cluster and is generally involved in patterning cells of the mid-body region (Clark et al. 1993; Wang et al. 1993). Thus, VPC identity appears to depend on the position of posterior daughters of P cells within the animal.

In lin-26 partial loss-of-function mutants, P3.pP8.p become neurons or neuroblasts instead of VPCs; null mutants are inviable, with much hypodermal cell death (Ferguson et al. 1987; Labouesse et al. 1994). lin-26 encodes a predicted protein with a zinc finger, suggesting that it functions as a transcription factor to repress expression of neural target genes or activate expression of hypodermal target genes (Labouesse et al. 1994).

B. Heterochronic Genes and VPC Identity

Heterochronic genes are involved in cell identity by controlling the timing of stage-specific events. In retarded mutants, cells behave as if they belong to an earlier larval stage, and in precocious mutants, cells behave as if they belong to a later larval stage (Chalfie et al. 1981; Ambros and Horvitz 1984, 1987; see Ambros, this volume). The global heterochronic genes lin-4 , lin-14 , and lin-28 affect vulval development. They appear to affect the maturation of VPCs by controlling the length of their cell cycles (Euling and Ambros 1996a). lin(n300) also appears to have a vulva-specific heterochronic defect, and genetic epistasis tests suggest that it may be a target of the global heterochronic genes (Euling and Ambros 1996a).

C. Other Genes Involved in VPC Generation or Identity

Two genes, lin-25 and lin-31 , have been primarily studied for their roles in VPC specification, but they may also have roles in VPC generation or identity. Null alleles of lin-25 and lin-31 sometimes cause P3.pP8.p to divide precociously to generate two cells, each of which can be a VPC (i.e., has the potential to adopt vulval fates) or, in the case of lin-31 , a neuroblast (Ferguson et al. 1987; Miller et al. 1993; Tuck and Greenwald 1995). These genes are potential targets of the Ras-Raf-MEK-MAPK cascade of the inductive signaling pathway (see below), raising the possibility that this cascade is utilized in cell signaling events involved in VPC generation or identity.

Copyright © 1997, Cold Spring Harbor Laboratory Press.
Bookshelf ID: NBK20041


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