Formation of the skeletal neuromuscular junction is a multi-step proce
ss that requires communication between the nerve and muscle. Studies i
n many laboratories have led to identification of factors that seem li
kely to mediate these interactions. 'Knock-out' mice have now been gen
erated with mutations in several genes that encode candidate transsyna
ptic messengers and components of their effector mechanisms. Using the
se mice, it is possible to test hypotheses about the control of synapt
ogenesis. Here, we review our studies on neuromuscular development in
mutant mice lacking agrin alpha CGRP, rapsyn, MuSK, dystrophin, dystro
brevin, utrophin, laminin alpha 5, laminin beta 2, collagen alpha 3 (I
V), the acetylcholine receptor epsilon subunit, the collagenous tail o
f acetylcholinesterase, fibroblast growth factor-5, the neural cell ad
hesion molecule, and tenascin-C. ((C)Elsevier, Paris).