Mitochondrial retrograde signaling (MRS) supports photosynthetic function under a variety of conditions. Induction of
mitochondrial dysfunction with
myxothiazol (a specific inhibitor of the mitochondrial bc1 complex) or
antimycin A (an inhibitor of the mitochondrial bc1 complex and cyclic electron transport in the chloroplast under light conditions) in the light and dark revealed diurnal control of MRS. This was evidenced by (1) significantly enhanced binding of ANAC017 to promoters in the light compared with the dark in Arabidopsis plants treated with
myxothiazol (but not
antimycin A), (2) overlap in the experimentally determined binding sites for ANAC017 and circadian clock regulators in the promoters of ANAC013 and AOX1a, (3) a diurnal expression pattern for ANAC017 and
transcription factors it regulates, (4) altered expression of ANAC017-regulated genes in circadian clock mutants with and without
myxothiazol treatment, and (5) a decrease in the magnitude of LHY and CCA1 expression in an ANAC017-overexpressing line and
protein-
protein interaction between ANAC017 and PIF4. This study also shows a large difference in transcriptome responses to
antimycin A and
myxothiazol in the dark: these responses are ANAC017 independent, observed in shoots and roots, similar to biotic challenge and
salicylic acid responses, and involve ERF and ZAT
transcription factors. This suggests that
antimycin A treatment stimulates a second MRS pathway that is mediated or converges with
salicylic acid signaling and provides a merging point with chloroplast retrograde signaling.