is dormancy the result of a deficiency in some vital cellular
event of germination, or is there is some dormancy-imposed
event that must be negated before germination can be completed?
A broader issue is whether release from dormancy,
which can be triggered by a variety of environmental and
chemical stimuli, is mediated through a common signal
transduction chain that coordinates diverse cellular responses
but that may differ between the seeds of different species
and dormancy types. It has been suggested that there are
related or common receptors for dormancy-breaking agents
within the plasma membrane of the responsive embryonic
cells. When triggered, these receptors then initiate a signal
transduction cascade, perhaps involving synthesis of or sensitization
to germination-promoting gibberellins (GAs), that
leads to the completion of germination (Hilhorst, 1993;
Vleeshouwers et al., 1995). Changes in the phosphorylating
activity of membrane-associated, Caz+-dependent protein
kinases that lead to dormancy or germination have been
proposed as well (Trewavas, 1988). However, in the absence
of any corroborating evidence, these suggestions must be
regarded only as stimulating bases for future research.