The avian retroviral v-myb gene and its cellular homologues throughout the
animal and plant kingdoms contain a conserved DNA binding domain. We have i
solated an insertional mutant of Dictyostelium unable to snitch from slug m
igration to fruiting body formation i.e. unable to culminate. The gene that
is disrupted, mybC, codes for a protein with a myb-like domain that is rec
ognized by an antibody against the v-myb repeat domain. During development
of myb(+) cells, mybC is expressed only in prestalk cells, When developed t
ogether with wild-type cells mybC(-) cells are able to farm both spores and
stalk cells very efficiently. Their developmental defect is also bypassed
by overexpressing cAMP-dependent protein kinase, However even when their de
fect is bypassed, mybC null slugs and culminates produce little if any of t
he intercellular signalling peptides SDF-1 and SDF-2 that are believed to b
e released by prestalk cells at culmination. We propose that the mybC gene
product is required for an intercellular signaling process controlling matu
ration of stalk cells and spores and that SDF-1 and/or SDF-2 may be implica
ted in this process.