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Disruption of the high-affinity nitrate transporter  NRT2.1  activates the priming defense against  Pseudomonas syringae , resulting in enhanced resistance. In this study, it is demonstrated that the high-affinity ammonium transporter  AMT1.1  is a negative regulator of  Arabidopsis  defense responses. The T-DNA knockout mutant  amt1.1  displays enhanced resistance against  Plectosphaerella cucumerina  and reduced susceptibility to  P. syringae . The impairment of  AMT1.1  induces significant metabolic changes in the absence of challenge, suggesting that  amt1.1  retains constitutive defense responses. Interestingly,  amt1.1  combats pathogens differently depending on the lifestyle of the pathogen. In addition, N starvation enhances the susceptibility of wild type plants and the mutant  amt1.1  to  P. syringae  whereas it has no effect on  P. cucumerina  resistance. The metabolic changes of  amt1.1  against  P. syringae  are subtler and are restricted to the phenylpropanoid pathway, which correlates with its reduced susceptibility. By contrast, the  amt1.1  mutant responds by activating higher levels of camalexin and callose against  P. cucumerina . In addition,  amt1.1  shows altered levels of aliphatic and indolic glucosinolates and other Trp-related compounds following infection by the necrotroph. These observations indicate that  AMT1.1  may play additional roles that affect N uptake and plant immune responses.

Disruption of the ammonium transporter AMT1.1 alters basal defenses generating resistance against Pseudomonas syringae and Plectosphaerella cucumerina