Shoot Maturation Strengthens FLS2-Mediated Resistance to .

Temporospatial regulation of immunity components is essential for properly activating plant defense response. Flagellin-sensing 2 (FLS2) is a surface-localized receptor that recognizes bacterial flagellin. The immune function of FLS2 is compromised in early stages of shoot development. However, the underlying mechanism for the age-dependent FLS2 signaling is not clear. Here, we show that the reduced basal immunity of juvenile leaves against pv. DC3000 is independent of FLS2. The flg22-induced marker gene expression and reactive oxygen species activation were comparable in juvenile and adult stages, but callose deposition was more evident in the adult stage than the juvenile stage. We further demonstrated that microRNA156, a master regulator of plant aging, does not influence the expression of and () but mildly suppresses callose deposition in juvenile leaves. Our experiments revealed an intrinsic mechanism that regulates the amplitude of FLS2-mediated resistance during aging. [Formula: see text] Copyright © 2023 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.