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13 The Arabidopsis thaliana Glutamate-like Receptor Family(AtGLR) 195<br />

injection of any AtGLRs. Additionally, ABA, BMAA, GABA, NMDA, and<br />

glutamine have not activated any currents in any heterologous system containing<br />

any AtGLRs as tested so far (Cheffings 2001; Lacombe et al. 2001b;<br />

Meyerhoff et al. 2005; M. Gilliham, unpublished), although incubation of<br />

the AtGLR3. 4 injected oocytes with DNQX did reduce the Na + -permeable<br />

“leak” current (M. Gilliham, unpublished).<br />

Although at least AtGLR3.4 is expressed at the plasma membrane in<br />

heterologous systems (D. Becker, unpublished), it is possible that AtGLRs<br />

may require plant-specific processing for proper function. It is possible that<br />

the activity of some AtGLRsismodifiedbyendogenoussubunitsinoocytes<br />

and other heterologous systems, resulting in activation of atypical currents<br />

or loss of AtGLR channel function (Green et al. 2002; Anantharam et al.<br />

2003). Other proteins or cofactors may also be needed for proper activity<br />

of AtGLR in heterologous systems, for instance, SOL-1, a CUB-like protein,<br />

colocalises at the neuron cell surface with GLR1 in Caenorhabditis elegans<br />

and is required for ligand-gated GLR1 activity (Zheng et al. 2004).<br />

In planta evidence for ion channel activity of glutamate receptors is limited.<br />

Kim et al. (2001) constitutively overexpressed AtGLR3. 2, which led to<br />

signs of Ca 2+ deficiency and a hypersensitivity to K + and Na + .Although<br />

total tissue Ca 2+ was the same in wild-type plants and plants overexpressing<br />

AtGLR3.2, medium supplemented with Ca 2+ could rescue the mutant phenotype.<br />

On the basis of these findings AtGLR3.2, which is most abundantly<br />

expressed in vascular tissues, has a proposed role in Ca 2+ distribution<br />

within the plant (Kim et al. 2001; Turano et al. 2002). Antisense AtGLR1.1<br />

plants did not show hypersensitivity to K + and Na + compared with wildtype<br />

plants, but root growth was more inhibited by high levels of Ca 2+ (Kang<br />

and Turano 2003). In unpublished work, Qi et al. (2004) have reported that<br />

AtGLR T-DNA insertional mutants have aberrant growth rate responses to<br />

glutamate or light. Knockouts of AtGLR3.3 also displayed reduced depolarisations<br />

in the root and hypocotyl associated with glutamate or glycine,<br />

whereas knockouts of AtGLR3.4 showed reduced response to glycine only<br />

(Qi et al. 2005).<br />

13.3.4<br />

C:N Signalling<br />

Phenotypic analysis of antisense AtGLR1.1 (antiAtGLR1.1) plantshasimplicated<br />

a role for AtGLR1.1 in C:N perception and signalling (Kang and Turano<br />

2003; Kang et al. 2004). antiAtGLR1.1 seed germination was inhibited<br />

by sucrose, but rescued by supplemental nitrate. Compared with wild-type,<br />

seed germination of antiAtGLR1.1 plants was also more susceptible to inhibition<br />

by DNQX, possibly because antiAtGLR1.1 suppressed AtGLR activity

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