A hormone balance theory has been invoked
in which ABA and GA act antagonistically to control both dormancy breakage and
germination (Karssen and Lacka, 1986; Karssen, 1995 and references therein).
Generally GAs are viewed as important for the promotion and maintenance of
germination, while ABA controls seed developmental events including the
inception of dormancy (Bewley, 1997). However, GA also appears to act as an
antagonistic to ABA function during seed development (White et al., 2000).
When
an ABA-deficient mutant of maize (vp5) is manipulated either genetically or via
biosynthesis inhibitors to induce GA-deficiency during early seed development,
vivipary is suppressed in developing kernels and the seeds acquire desiccation
tolerance and storage longevity. In cultured immature maize embryos, GA
deficiency induced by inhibiting biosynthesis enhances many ABA-responsive
developmental events including the accumulation of anthocyanins and transcripts
encoding storage proteins and LEAs (White and Riven, 2000). In situ, the major
accumulation of GA1 and GA3 occurs in wildtype maize kernels, just prior to a
peak in ABA content during development. It is speculated that these GAs induce
a developmental programme that leads to vivipary in the absence of normal
amounts of ABA, and that a reduction of GAs re-establishes an ABA/GA ratio
appropriate for suppression of germination and induction of maturation.
Induction of GA deficiency does not suppress vivipary in vp1 mutant kernels,
suggesting that VP1 (see above) acts downstream of both GA and ABA in
programming seed development.
Other mutants exhibiting reduced seed
dormancy include the rdo1 and rdo2 mutants of Arabidopsis (Leon-Kloosterziel et
al., 1996). Neither mutant is deficient in ABA biosynthesis, nor do the mutants
exhibit any differences in their responsiveness to auxin, ethylene, or
cytokinin as compared to wild-type Arabidopsis seed. However, the rdo2 mutant
is less sensitive to the inhibition of germination by the GA-biosynthesis
inhibitor tetcyclasis; thus a mutation in this gene somehow causes a reduced
requirement for GA biosynthesis to terminate dormancy.
As noted above, it is widely accepted that
GA promotes germination and in support of this, mutations in loci that control
GA biosynthesis and signal transduction can also affect germination potential.
However the mutants disrupted in GA response (e.g. gai, sleepy1, spindly, rga
and pickle), are generally not seed-specific, with respect to GA insensitivity
(Peng et al., 1997; Steber et al., 1998; Jacobsen et al., 1996; Silverstone et
al., 1998; Ogas et al., 1997). The spindly gene product is a negative regulator
of GA responses; interestingly it has high homology to N-acetylglucosamine
transferases, but the putative roles of this specific protein modification in
GA signalling remain elusive (Jacobsen et al., 1996). The Arabidopsis mutant
sleepy1 (sly1) was recovered as a suppressor of the abi1 mutation (Steber et
al., 1998); this mutant displays characteristics of a GA-response mutant
(severe dwarfing at the vegetative stage, dark green foliage, and
underdeveloped petals and stamens), yet it cannot be rescued by exogenous GA.
Mutation of the GA1 locus decreases germination and reduces the sensitivity of
plant growth to GA (Derxk et al., 1994).
The antagonistic effects of GA and ABA are
well known in isolated barley aleurone layers in relation to control of the
synthesis of αα-amylase. GAMYB is a GA-regulated transcriptional activator of
αα-amylase gene expression in aleurone layer cells of germinating barley grains
(see earlier discussion). SLN1 (a product of the SLENDER or SLN1 gene locus and
a negative regulator of GA signalling) is necessary for repression of GAMYB in
barley aleurone cells (Gubler et al., 2002). Interestingly, the activity of
SNL1 in aleurone layer cells is regulated posttranslationally and the level of
this protein declines rapidly in response to GA prior to any increase in GAMYB.
GA stimulates the degradation of SLN1; ABA down-regulates the expression of
GAMYB but has no effect on the stability of SLN1. The action of ABA in blocking
GA signalling then is downstream of SLN1 (Gubler et al., 2002). The barley
SLENDER gene appears to be the functional orthologue of GAI/RGA genes in
Arabidopsis (Richards et al., 2001). As components of the GA signalling
pathway, GAI and RGA genes mediate GA regulation of stem elongation (Lee et
al., 2002). RGL1 and RGL2 genes encode proteins that are closely related to GAI
and RGA. Of the four proteins, only RGL2 regulates seed germination in response
to GA and it acts as a negative regulator. In wild-type and mutant ga1-3 Arabidopsis
seeds, transcripts encoding this gene increase in amount during a moist
chilling period (4°C) and are maintained at high levels for as long as the
seeds are kept at 4°C. Wild-type seeds immediately imbibed in water at 23°C,
also show an increase in RGL2 transcripts, with expression restricted to the
elongating regions of pre-emergent and recently emerged radicles. Upon transfer
of wild-type seeds from moist chilling conditions to 23°C, the RGL2-related
transcripts decline, particularly upon completion of germination. In contrast,
in non-germinating mutant ga1-3 seeds maintained at 23°C, RGL2 transcript
levels remain high. It is speculated that RGL2 functions to prevent germination
upon imbibition; GA can overcome this inhibition and promote germination by
down-regulating RGL2 gene expression; it may further integrate environmental
and internal cues to control germination (Lee et al., 2002).
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