tified that involve sensory input coupled to motor 
output: 1) attraction to hermaphrodites, 2) recogni- 
tion of the hermaphrodite, 3) maintaining contact 
with hermaphrodites, 4) location of the vulva, 5) 
insertion of spicules, 6) transfer of sperm, and 7) 
retraction of spicules. The roles of the male-specific 
neurons and muscle cells in mediating mating be- 
havior are being examined by killing individual 
cells or classes of cells and observing the conse- 
quences for the behavior. For example, continued 
backward movement during vulval location re- 
quires the PVY interneuron. Vulval location is me- 
diated by the HOA and HOB sensory neurons. Inser- 
tion of spicules is mediated by the SPD sensory 
neuron and SPC motoneurons of the spicule. The 
SPV spicule sensory neurons are required to prevent 
sperm transfer until after spicule insertion. 
Mutant strains defective in male mating have been 
isolated. Some of these mutant males have obvious 
defects in the development of the spicules. Other 
mutants, called "Cod" (for copulation defective), 
are anatomically normal yet defective in mating be- 
havior. By studying Cod mutants, the genetic con- 
trol of each step in this complex behavior can be 
elucidated. 
Most of the initial Cod mutants analyzed are de- 
fective at only a single step in the mating process. 
For example, a mutant male defective in step 5 will 
locate the vulva, but fail to insert his spicules. This 
defect is similar to that of males whose spicule neu- 
rons have been ablated. Having mutants blocked at 
defined steps will allow the definition of genes nec- 
essary to specify this innate behavior. Based on map- 
ping and complementation studies, most Cod muta- 
tions of this first set define separate genes. 
The expression of four genes that encode a sub- 
units of heterotrimeric G proteins have been exam- 
ined. Two of these are expressed in cells required 
for male mating: gpa-1, in either the SPD or SPV 
spicule sensory neurons; and goa l, which encodes 
a nematode homologue of mammalian G„a, in the 
male diagonal muscles as well as a number of male- 
specific neurons. 
Cell-Type-Specific Functions 
During Vulval Development 
The anchor cell induces two distinct types of vul- 
val precursor cells (VPCs). The 1° VPC generates 
progeny that attach to the anchor cell during vulval 
morphogenesis. The 2° VPC generates progeny cells 
in a fixed anterior-posterior orientation. Genes spe- 
cific to the 1° or 2° VPC lineage are being studied 
by genetic and molecular techniques. The vex-1 
gene is involved in the divisions of the 1 ° but not the 
2° VPC lineage and is a candidate 1 " specific gene. 
The lin- 18 gene is necessary for the orientation and 
asymmetry of the 2° VPC and is a candidate 2°- 
specific gene. The "ground state" of a 2° VPC is to 
orient posteriorly, but in the presence of a signal 
from the developing gonad it reorients anteriorly. 
This signal is distinct from the inductive signal from 
the anchor cell, since mutations defective in induc- 
tive signaling do not affect the correct orientation of 
the 2° VPCs. 
Vulval Induction 
An inductive signal from the anchor cell stimu- 
lates vulval differentiation from nonspecialized epi- 
dermis. This inductive signal is encoded, at least in 
part, by the lin-3 gene, and is an EGF-like growth 
factor. The gene is expressed in the anchor cell at 
the time of vulval induction. The candidate receptor 
for lin-3 is the EGF receptor homologue encoded by 
the let- 2 3 gene. A number of let- 2 3 mutant alleles 
have been sequenced. Two that cause tissue- 
specific defects in let-23 function truncate the car- 
boxyl terminus of the protein. The inductive signal 
is transduced by a number of genes including let- 60 
ras and lin-45 raf. Several negative regulators of 
this pathway have been identified, including a 
clathrin adaptor protein that is the product of the 
unc-101 gene. (This project was supported by a 
grant from the National Institutes of Health.) 
A negative signal, possibly from nearby epider- 
mis, prevents vulval differentiation in the absence 
of the inductive signal. This signal was defined by 
mutations in the lin- 15 locus, which result in vulval 
differentiation in the absence of an inductive signal. 
The lin- 1 5 locus has been cloned and found to en- 
code two products required to prevent inappropri- 
ate vulval differentiation. (This project was sup- 
ported by a grant from the March of Dimes Birth 
Defects Foundation.) 
Dr. Sternberg is also Associate Professor of Biol- 
ogy at the California Institute of Technology and 
Adjunct Assistant Professor of Anatomy and Cell 
Biology at the University of Southern California 
School of Medicine, Los Angeles. 
Books and Chapters of Books 
Sternberg, P.W., Hill, R.J., and Chamberlin, H.M. 
1992. Inductive signalling in C. elegans. In Evo- 
lutionary Conservation of Developmental Mech- 
anisms (Spradling, A.C., Ed.). New York: Wiley- 
Liss, pp 141-158. 
Sternberg, P.W., Liu, K., and Chamberlin, H. 
1992. Specification of neuronal identity in C. ele- 
gans. In Determinants of Neuronal Identity 
GENETICS 267 
