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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 IIntroduction and Overview

Formation of the hermaphrodite vulva has been particularly amenable to genetic and developmental studies. These studies have revealed that vulva formation is a microcosm of events important in the development of all animals and that these events utilize molecules that appear to be conserved in all animals. Indeed, some of these molecules or their involvement in development were first identified through studies of vulval development in Caenorhabditis elegans.

The vulva consists of 22 cells and serves as the passageway through which sperm enter and fertilized eggs leave the gonad (Fig. 1). Vulval development may be roughly divided into four stages. First, in the L1 stage, the vulval precursor cells (VPCs) are born. The VPCs are six hypodermal cells, consecutively numbered P3.p through P8.p, each of which has the potential to contribute cells to the vulva. Second, in the early L3 stage, cell-cell interactions specify the fates of the VPCs. In wild-type hermaphrodites, three discrete signaling events specify P5.p, P6.p, and P7.p to adopt vulval fates (i.e., to undergo lineages that result in the production of vulval cells) and P3.p, P4.p, and P8.p to adopt a nonvulval fate (i.e., to produce additional hypodermal cells). Third, the VPCs execute the fates that have been specified, generating the appropriate number and types of vulval cells. Fourth, the vulval cells undergo cell movements, cell fusion, and eversion to form the mature vulva.

Figure 1. Overview of vulval development.

Figure 1

Overview of vulval development. Left lateral view of nuclei, indicated by circles. (Open circles) Nuclei of P6.p and its descendants, produced by execution of the 1o fate; (closed (more...)

The somatic gonad influences vulval development. The most pervasive influence is provided by the anchor cell (AC), which has many important roles in vulval development, from VPC fate specification and patterning to morphogenesis. In addition, other somatic gonadal cells also influence vulval morphogenesis and eversion.

Genetic screens have exploited the fact that a functional vulva is not necessary for viability. In the absence of a vulva, eggs are produced by self-fertilization and mature internally, so that larvae hatch internally and ultimately devour their parent. This activity leads to the formation of a “bag of worms” (Fig. 2), which is essentially the parent's cuticle surrounding its progeny. The bag of worms phenotype of Vulvaless mutants is distinctive and easily viewed in the dissecting microscope (Fig. 2B), enabling rapid and powerful screens for mutations affecting vulval development. Moreover, the absence of eggs on a plate of Vulvaless mutants is also readily apparent in the dissecting microscope, enabling the identification of suppressor mutations, which may define additional genes with related functions. Genetic screens have also exploited another possible anomaly of vulval development: A Multivulva phenotype, in which P3.p, P4.p, and P8.p, which normally adopt a nonvulval fate, instead generate vulval cells. The Multivulva phenotype is readily visualized in the dissecting microscope by multiple pseudovulval protrusions (Fig. 2C) and is also easy to revert. Through genetic screens of these kinds, a large collection of genes involved in vulval development have been identified (Table 1).

Figure 2. Vulval mutants, viewed in the dissecting microscope.

Figure 2

Vulval mutants, viewed in the dissecting microscope. (A) N2 (wild-type); (B) let-23(sy97), Vulvaless; (C) lin-15(e1763), Multivulva. Large arrow-head indicates the vulva. Smaller (more...)

Table 1. Genes featured in this chapter.

Table 1

Genes featured in this chapter.

In this chapter, I first consider aspects of the development and function of the AC. I then consider the four stages of vulval development, with a focus on key genes that have been identified through mutations. Because more is known about VPC specification than any other stage, there will be considerable detail about the cell-cell interactions that specify VPC fates and the cell signaling and signal transduction pathways that mediate these interactions.

Copyright © 1997, Cold Spring Harbor Laboratory Press.
Bookshelf ID: NBK20095
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