The fruiting body development of Myxococcus xanthus consists of two separat
e but interacting pathways: one for aggregation of many cells to form raise
d mounds and the other for sporulation of individual cells into myxospores.
Sporulation of individual cells normally occurs after mound formation, and
is delayed at least 30 h after starvation under our laboratory conditions.
This suggests that M. xanthus has a mechanism that monitors progress towar
ds aggregation prior to triggering sporulation. A null mutation in a newly
identified gene, espA (early sporulation), causes sporulation to occur much
earlier compared with the wild type (16 h earlier). In contrast, a null mu
tation in an adjacent gene, espB, delays sporulation by about 16 h compared
with the wild type. Interestingly, it appears that the espA mutant does no
t require raised mounds for sporulation. Many mutant cells sporulate outsid
e the fruiting bodies. In addition, the mutant can sporulate, without aggre
gation into raised mounds, under some conditions in which cells normally do
not form fruiting bodies. Based on these observations, it is hypothesized
that EspA functions as an inhibitor of sporulation during early fruiting bo
dy development while cells are aggregating into raised mounds. The aggregat
ion-independent sporulation of the espA mutant still requires starvation an
d high cell density. The espA and espB genes are expressed as an operon and
their translations appear to be coupled. Expression occurs only under deve
lopmental conditions and does not occur during vegetative growth or during
glycerol-induced sporulation. Sequence analysis of EspA indicates that it i
s a histidine protein kinase with a fork head-associated (FHA) domain at th
e N-terminus and a receiver domain at the C-terminus. This suggests that Es
pA is part of a two-component signal transduction system that regulates the
timing of sporulation initiation.