Dataset Information

CEPR2 perceives group II CEPs to regulate cell surface receptor-mediated immunity in Arabidopsis

ABSTRACT: Plant endogenous peptides are crucial for diverse aspects of plant physiology. Among them, C-TERMINALLY ENCODED PEPTIDEs (CEPs) have recently emerged as important regulators of plant growth and stress responses. CEPs are divided into two major subgroups: group I CEPs and the less studied group II CEPs. We recently demonstrated that group I CEPs coordinate cell surface receptor-mediated immunity with nitrogen status in Arabidopsis thaliana (hereafter Arabidopsis). To mount full group I CEP responsiveness, the three phylogenetically related CEP RECEPTOR 1 (CEPR1), CEPR2 and RECEPTOR-LIKE KINASE 7 (RLK7) are required. Here, we provide evidence that biotic stress induces expression of the group II CEP peptide CEP14. CEP14 and the related CEP13 and CEP15 trigger hallmark immune signalling outputs in a proline hydroxylation pattern-dependent manner in Arabidopsis. Genetic data indicate that group II CEP members contribute to cell surface receptor-mediated immunity against bacterial infection. We further show that group II CEP perception primarily depends on CEPR2. Our work provides new insights into CEP function during biotic stress and sheds new light on the complexity of sequence-divergent CEP signalling mediated by specific endogenous receptors.

ORGANISM(S): Arabidopsis Thaliana

SUBMITTER: Christina Ludwig

PROVIDER: PXD062482 | panorama | Tue Sep 16 00:00:00 BST 2025

REPOSITORIES: PanoramaPublic

ACCESS DATA

Similar Datasets

Project description:Kolodkin2013 - Nuclear receptor-mediated cortisol signalling network This model is described in the article: Optimization of stress response through the nuclear receptor-mediated cortisol signalling network. Kolodkin A, Sahin N, Phillips A, Hood SR, Bruggeman FJ, Westerhoff HV, Plant N. Nat Commun 2013; 4: 1792 Abstract: It is an accepted paradigm that extended stress predisposes an individual to pathophysiology. However, the biological adaptations to minimize this risk are poorly understood. Using a computational model based upon realistic kinetic parameters we are able to reproduce the interaction of the stress hormone cortisol with its two nuclear receptors, the high-affinity glucocorticoid receptor and the low-affinity pregnane X-receptor. We demonstrate that regulatory signals between these two nuclear receptors are necessary to optimize the body's response to stress episodes, attenuating both the magnitude and duration of the biological response. In addition, we predict that the activation of pregnane X-receptor by multiple, low-affinity endobiotic ligands is necessary for the significant pregnane X-receptor-mediated transcriptional response observed following stress episodes. This integration allows responses mediated through both the high and low-affinity nuclear receptors, which we predict is an important strategy to minimize the risk of disease from chronic stress. This model is hosted on BioModels Database and identified by: BIOMD0000000576. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

Dataset Information

CEPR2 perceives group II CEPs to regulate cell surface receptor-mediated immunity in Arabidopsis

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets