Myxococcus xanthus is a gram-negative bacterium which has a complex life cy
cle that includes multicellular fruiting body formation. Frizzy mutants are
characterized by the formation of tangled filaments instead of hemispheric
al fruiting bodies on fruiting agar. Mutations in the frz genes have been s
hown to cause defects in directed motility, which is essential for both veg
etative swarming and fruiting body formation. In this paper, we report the
discovery of a new gene, called frgA (for frz-related gene), which confers
a subset of the frizzy phenotype when mutated. The frgA null mutant showed
reduced swarming and the formation of frizzy aggregates on fruiting agar. H
owever, this mutant still displayed directed motility in a spatial chemotax
is assay, whereas the majority of frz mutants fail to show directed movemen
ts in this assay. Furthermore, the frizzy phenotype of the frgA mutant coul
d be complemented extracellularly by wild-type cells or strains carrying no
n-frz mutations. The phenotype of the frgA mutant is similar to that of the
abcA mutant and suggests that both of these mutants could be defective in
the production or export of extracellular signals required for fruiting bod
y formation rather than in the sensing of such extracellular signals. The f
rgA gene encodes a large protein of 883 amino acids which lacks homologues
in the databases. The frgA gene is part of an operon which includes two add
itional genes, frgB and frgC. The frgB gene encodes a putative histidine pr
otein kinase, and the frgC gene encodes a putative response regulator. The
frgB and frgC null mutants, however, formed wild-type fruiting bodies.