AtPEPTIDE RECEPTOR_2 mediates the AtPEPTIDE1‐induced cytosolic Ca^(2+) trise, which is required for the suppression of Glutamine Dumper gene expression in Arabidopsis roots

AtPEPTIDE RECEPTOR2 （AtPEPR2） is a member of leucine-rich repeat receptor-like kinase family and binds to a group of AtPROPEP gene-encoded endogenous peptides, AtPeps. Previously, we found that AtPEPR2 plays a moderate role in the AtPep1-mediated innate immunity responses in Arabidopsis leaf. In this study, we found that AtPEPR2 promoter has strong activity in the vascular tissues of the roots and the atpepr2 mutants showed a moderate but significantly shorter root phenotype. AtPEPR2 partial y mediated AtPep1-induced root elongation inhibition. AtPep1-triggered cytosolic Ca2t transient rise in roots showed partial dependence on AtPEPR2 and ful y on extracellular Ca2t （[Ca2t]ext）. Transcriptional profiling analysis found that expression of 75% of AtPep1-modulated genes in roots was ful y dependent on AtPEPR2, of which two dramatical y induced genes showed partial dependence on the [Ca2t]ext. Arabidopsis genome contains seven Glutamine Dumpers genes （AtGDUs）, encoding amino acid exporters. Three of them （AtGDU2, 3, 5） were among the top 10 genes that were＆amp;nbsp;downregulated by AtPep1 through AtPEPR2 ful y dependent pathway. Treatment with AtPep1 strongly suppressed pro-moter activity of AtGDU3 in roots, which was relieved by chelating [Ca2t]ext. Arabidopsis overexpressing AtGDU3 showed a shorter root phenotype and decreased sensitivity to the AtPep1-mediated inhibition of root elongation. Taken together, this study demonstrated a significant role of AtPEPR2 in the AtPep1-mediated signaling in the roots.

Arabidopsis ROOT HAIR DEFECTIVE3 is involved in nitrogen starvation-induced anthocyanin accumulation

Anthocyanin accumulation is a common phenomenon seen in plants under environmental stress. In this study,we identified a new allele of ROOT HAIR DEFECTIVE3（RHD3）showing an anthocyanin overaccumulation phenotype under nitrogen starvation conditions. It is known that ethylene negatively regulates light- and sucrose-induced anthocyanin biosynthesis. We hypothesized that RHD3 achieves its negative effect on anthocyanin biosynthesis via an ethylene-regulating pathway. In support of this, similar to rhd3 mutants, the Arabidopsis ethylene signaling mutants etr1, ein2, and ein3/eil1 showed an anthocyanin overaccumulation phenotype under nitrogen starvation conditions. The ethylene precursor ACC strongly suppressed anthocyanin accumulation, dependent on ETR1, EIN2, EIN3/EIL1, and, partially, RHD3. In addition,inactivating RHD3 partially reversed the suppressive effect of ETO1 inactivation-evoked endogenous ethylene production on anthocyanin accumulation. The expression of nitrogen starvation-induced anthocyanin biosynthesis genes was negatively regulated by RHD3, but ethylene response genes were Researchpositively regulated by RHD3. Wild-type seedlings overexpressing RHD3 showed similar phenotypes to rhd3 mutants,indicating the existence of a fine-tuned relationship between gene expression and function. RHD3 was initially identified as a gene involved in root hair development. This study uncovered a new physiological function of RHD3 in nitrogen starvationinduced anthocyanin accumulation and ethylene homeostasis.