Abolishing ANAC017-Mediated Mitochondria Retrograde Signalling Alleviates Ammonium Toxicity in  Arabidopsis thaliana.

Ammonium (NH(4) (+)), an important nitrogen source, often fails to stimulate plant growth as a sole nitrogen source, a phenomenon known as ammonium toxicity syndrome. NH(4) (+) is believed to disrupt cellular redox status by increasing chloroplast reducing capacity and exporting excess reducing equivalents, which trigger retrograde signalling. The precise role of mitochondria in this process remains unclear. Here, we demonstrate that the loss of ARABIDOPSIS NAC DOMAIN TRANSCRIPTION FACTOR17 (ANAC017, rao2-1), a master regulator of mitochondrial retrograde signalling, significantly increased shoot biomass under both nitrate (NO(3) (-)) and NH(4) (+), thus utilising NH(4) (+) more effectively than Col-0 wildtype. In contrast, loss of function of ALTERNATIVE OXIDASE1A (aox1a) improved recovery of nitrogen-starved seedlings with NO(3) (-) but had no effect with NH(4) (+). Metabolomic analysis revealed that the rao2-1 mutant assimilated NH(4) (+) more efficiently than the wild type, incorporating it into nitrogen-rich metabolites. Transcriptomic analyses showed that with NO(3) (-) resupply, ANAC017 acted to stimulate photosynthesis, carbon fixation, and NO(3) (-) reduction. Under NH(4) (+) resupply, however, ANAC017 suppressed plastid biogenesis and metabolism through classical retrograde signalling pathways. In rao2-1, a variety of chloroplast retrograde pathways were de-repressed. Unlike NO(3) (-), NH(4) (+) fails to generate the signals necessary to suppress ANAC017-dependent retrograde stress responses, thereby impairing nitrogen assimilation and growth.