| Summary: | Plant <i>glutamate-like receptor</i> genes (<i>GLRs</i>) are homologous to mammalian <i>ionotropic glutamate receptors</i> genes (<i>iGluRs</i>). Although GLRs have been implicated in plant defenses to biotic stress, the relationship between GLR-mediated plant immunity against fungal pathogens and electrical signals remains poorly understood. Here, we found that pretreatment with a GLR inhibitor, 6,7-dinitriquinoxaline-2,3-dione (DNQX), increased the susceptibility of tomato plants to the necrotrophic fungal pathogen <i>Botrytis cinerea</i>. Assessment of the <i>glr3.3</i>, <i>glr3.5</i> and <i>glr3.3/glr3.5</i> double-mutants upon <i>B. cinerea</i> infection showed that tomato GLR3.3 and GLR3.5 are essential for plant immunity against <i>B. cinerea</i>, wherein GLR3.3 plays the main role. Analysis of the membrane potential changes induced by glutamate (Glu) or glycine (Gly) revealed that amplitude was significantly reduced by knocking out <i>GLR3.3</i> in tomato. While treatment with Glu or Gly significantly increased immunity against <i>B. cinerea</i> in wild-type plants, this effect was significantly attenuated in <i>glr3.3</i> mutants. Thus, our data demonstrate that GLR3.3- and GLR3.5-mediated plant immunity against <i>B. cinerea</i> is associated with electrical signals in tomato plants.
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