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sufficiently to make plants more susceptible to DNQX. BMAA counteracted
the inhibitory effect of DNQX on
antiAtGLR1.1
seed germination despite
previous observations that DNQX and BMAA have superficially analogous
effects on plant growth and development (Brenner et al. 2000; Sect. 13.2.1),
suggesting one must be cautious in ascribing a precise mode of action
to either of these compounds in plants. Glutamate (and to a lesser extent
glutamine) rescued germination of
antiAtGLR1.1
seed by DNQX, but both
were less effective than BMAA. It was proposed that glutamate uptake or
distribution was poor compared with DNQX, or that glutamate is not the
natural ligand for
At
GLRs. However, as
AtGLR1.1
encodes the only subunit
predicted to bind glutamate (Dubos et al. 2003)
antiAtGLR1.1
plants would
be expected to be particularly impaired in glutamate perception.
The expression of genes and the accumulation of proteins related to
carbon and nitrogen metabolism, as well as ABA responses and metabolism,
were altered in
antiAtGLR1.1
plants (Kang and Turano 2003; Kang et al.
2004). For instance,
antiAtGLR1.1
plantshadelevatedABAlevels,increased
transcript abundance of ABA biosynthetic genes, enhanced ABA sensitivity,
reduced stomatal apertures, and increased drought resistance. Given that
ABA has been implicated in sugar signalling (Gibson 2005), the alteration
of ABA metabolism and response in
antiAtGLR1.1
plants provides another
link to carbon sensing in these plants.
A model has been proposed that places
At
GLR1.1 at the interface of
sucrose and amino acid signalling, suggesting
At
GLR1.1 is stimulated by
amino acids and suppresses ABA biosynthesis and sugar signalling, allow-
ing seed germination to occur (Kang and Turano 2003; Kang et al. 2004). The
model also suggests that
At
GLR1.1 is inhibited by sucrose, which, in turn,
allows sugar signalling and ABA biosynthesis to occur and results in inhi-
bition of seed germination. However, the strict involvement of
At
GLR1.1 in
C:N signalling needs to be confirmed. The segment of the
At
GLR1.1 gene
that was used to generate the antisense construct shares sequence identity
with several
At
GLR genes, including
AtGLR
1.2,
AtGLR
1.4, and
AtGLR
3.6. It
may be that these other members of the
AtGLR
family were also suppressed
by the antisense construct and therefore they may also contribute to the
phenomena observed in the
antiAtGLR1.1
lines.
13.3.5
Stress Responses
The GENEVESTIGATOR microarray toolbox suggests that, with respect to
abiotic stress, there is no single stress factor or plant hormone that induces
or represses expression of
At
GLR in general (Zimmermann et al. 2004).
For instance, while
AtGLR
2.5 and
AtGLR
3.2 were upregulated by ABA,
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