Zebrafish embryos and larvae have stage-specific patterns of motility
or locomotion, Two embryonic structures accomplish this behavior: the
central nervous system (CNS) and skeletal muscles. To identify genes t
hat are functionally involved in mediating and controlling different p
atterns of embryonic and larval motility, we included a simple touch r
esponse test in our zebrafish large-scale genetic screen, In total we
identified 166 mutants with specific defects in embryonic motility. Th
ese mutants fall into 14 phenotypically distinct groups comprising at
least 48 genes, Here we describe the various phenotypic groups includi
ng mutants with no or reduced motility, mechanosensory defective mutan
ts, 'spastic' mutants, circling mutants and motor circuit defective mu
tants, In 63 mutants, defining 18 genes, striation of semitic muscles
is reduced, Phenotypic analysis provides evidence that these 18 genes
have distinct and consecutive functions during semitic muscle developm
ent. The genes sloth (slo) and frozen (fro) already act during myoblas
t differentiation, while 13 genes appear to function later, in the for
mation of myofibers and the organization of sarcomeres, Mutations in f
our other genes result in muscle-specific degeneration,103 mutations,
defining at least 30 genes, cause no obvious defects in muscle formati
on and may instead affect neuronal development. Analysis of the behavi
oral defects suggests that these genes participate in the diverse loco
motion patterns observed, such as touch response, rhythmic tail moveme
nts, equilibrium control, or that they simply confer general motility
to the animal, In some of these mutants specific defects in the develo
ping nervous system are detected, Mutations in two genes, nevermind (n
ev) and macho (mao), affect axonal projection in the optic tectum, whe
reas axon formation and elongation of motorneurons are disrupted by mu
tations in the diwanka (diw) and the unplugged (unp) genes.