The Questions of Developmental Biology

A series of mutations has been found that blocks some of the steps of this induction
cascade. Mutations in the sevenless (sev) gene or in the bride of sevenless (boss) gene can each
prevent the R7 cell from differentiating into a photoreceptor. (It becomes a lens cell instead.)
Analysis of these mutations has shown that they affect the inductive process. The sev gene is
required in the R7 cell itself. If mosaic embryos are made such that some of the cells of the eye
imaginal disc are heterozygous (normal) and some are homozygous for the sevenless mutation,
the R7 photoreceptor develops only if the R7 precursor cell has the wild-type sev allele (Basler
and Hafen 1989; Bowtell et al. 1989). Antibodies to the Sevenless protein have found it in the cell
membrane, and the sequence of the sev gene suggests that it encodes a transmembrane protein
with a tyrosine kinase site in its cytoplasmic domain (Banerjee et al. 1987; Hafen et al. 1987).
This finding is consistent with the protein's being a receptor for some signal an RTK.
The signal that tells the R7 precursor to differentiate into an R7 photoreceptor comes
from a protein encoded by the wild-type bride-of-sevenless gene. Flies homozygous for the boss
mutation also lack R7 photoreceptors. Genetic mosaic studies wherein some of the cells of the
eye imaginal disc are normal and some are homozygous for the boss mutation show that the wildtype
boss gene is not needed in the R7 precursor cell itself. Rather, the R7 photoreceptor
differentiates only if the wild-type boss gene is expressed in the R8 cell. Thus, the boss gene
encodes some protein whose existence in the R8 cell is necessary for the differentiation of the R7
cell. In fact, the Boss protein is the ligand for the Sev RTK. The Boss protein probably works in a
juxtacrine fashion, and its extracellular domain binds to the the extracellular domain of the Sev
protein (Reinke and Zipursky 1988; Hart et al. 1993). In Drosophila eyes, the RTK cascade
initiated by the binding of Boss to Sev activates the Sevenless-in-Absentia (Sina) transcription
factor, whose activity is necessary for the differentiation of photoreceptor R7 (Carthew and Rubin
1990; Dickson et al. 1992). Once R7 is induced, it reciprocally induces the expression of opsin
proteins in the R8 cell (Chou et al. 1999). A summary of the some of the cell-to-cell inductions in
the Drosophila retina (Figure 6.18) shows that individual cells are able
to induce other individual cells to create the precise arrangement of
cells in particular tissues.
Vulval Induction in Caenorhabditis elegans
Most C. elegans individuals are hermaphrodites. In their early
development, they are male, and the gonad produces sperm, which is stored for later use. As they
grow older, they develop ovaries. The eggs "roll" through the region of sperm storage, are
fertilized inside the nematode, and then pass out of the body through the vulva.
The vulva of Caenorhabditis elegans represents a case in which one inductive signal
generates a variety of cell types. This organ forms during the larval stage from six cells called the
vulval precursor cells (VPCs). The cell connecting the overlying gonad to the vulval precursor
cells is called the anchor cell. The anchor cell secretes the LIN-3 protein, a relative of epidermal
growth factor (EGF) and the Boss protein (Hill and Sternberg 1992). If the anchor cell is
destroyed (or if the lin-3 gene is mutated), the VPCs will not form a vulva; they will instead
become part of the hypodermis (skin) (Kimble 1981). The six VPCs influenced by the anchor cell
form an equivalence group. Each member of this group is competent to become induced by the
anchor cell and can assume any of three fates, depending on its proximity to the anchor cell
(Figure 6.19). The cell directly beneath the anchor cell divides to form the central vulval cells.
The two cells flanking that central cell divide to become the lateral vulval cells, while the three
cells farther away from the anchor cell generate hypodermal cells. If the anchor cell is destroyed,