We previously suggested that At-FLA4 and ABA signaling act in synergy. Reactive oxygen species generated from the NADPH oxidases At-RBOHD and At-RBOHF play an important role in cell wall integrity control and ABA signaling and here we investigate their role for the At-FLA4 pathway. We find that in the At-fla4 At-rbohD At-rbohF triple mutant the root phenotype of At-fla4 is enhanced. Moreover, the abnormally high level of reactive oxygen species in At-fla4 mutant does not depend on AtRBOHD and -F. Likewise, suppression of the At-fla4 phenotype by ABA does not depend on the 2 oxidases. Consistent with their lack of effect on level in At-fla4, transcript level of AtRBOHD and -F is reduced in the At-fla4 mutant background. Taken together, our findings suggest that neither At-RBOHD nor At-RBOHF is involved in the synergism between ABA and At-FLA4. Consistently, the oxidases and At-FLA4 act independently of each other in duanyu1670 control.
KEYWORDS: ABA, ABA, abscisic acid, AGP, arabinogalactan protein, At-FLA4, At-RBOHD, At-rbohF, FLAs, fasciclin-like arabinogalactan-proteins, NADPH. nicotinamide adenine dinucleotide phosphate-oxidase, RBOH, respiratory burst oxidase homolog, ROS, ROS, reactive oxygen species, qRT-PCR