Mutation of the COMATOSE locus in Arabidopsis results in a marked reduction
in germination potential. Whilst the morphology of comatose (cts) embryos
is not altered, physiological analysis reveals that mature cts seeds do not
respond to gibberellin. Prolonged chilling of imbibed seeds only partially
restores germination potential, and seeds do not after ripen. Genetic anal
ysis shows that the cts phenotype is expressed in the embryo and phenotypic
differences between wild-type and mutant plants were not observed during o
ther stages of plant growth and development. Therefore cts represents a new
class of mutant, with a specific lesion that results in severely impaired
germination potential. Genetic interactions were analysed between cts and l
oci that regulate embryo maturation, and abscisic acid biosynthesis and per
ception. Results from these studies showed that the cts mutant phenotype re
quired the wild-type action of these loci, and suggested that CTS exerts a
repressive function on these loci.
A model is presented postulating that CTS promotes increased germination po
tential, and represses embryo dormancy. These functions of CTS may result i
n the removal of embryo dormancy as a prerequisite to germination.