Browse Articles

Article|04 Oct 2021|OPEN
PbrRALF2-elicited reactive oxygen species signaling is mediated by the PbrCrRLK1L13-PbrMPK18 module in pear pollen tubes
Xiaobing Kou1, Jiangmei Sun1, Peng Wang1, Danqi Wang1, Peng Cao1, Jing Lin2, Youhong Chang2, Shaoling Zhang1 & Juyou Wu1,2,
1Center of Pear Engineering Technology Research, State Key Laboratory of Crop Genetics and Germplasm Enhancement, College of Horticulture, Nanjing Agricultural University, 210095 Nanjing, China
2Jiangsu Key Laboratory for Horticultural Crop Genetic Improvement, 210014 Nanjing, China

Horticulture Research 8,
Article number: 222 (2021)
doi: 10.1038/hortres.2021.222
Views: 53

Received: 07 Apr 2021
Revised: 26 Jul 2021
Accepted: 04 Aug 2021
Published online: 04 Oct 2021

Abstract

Rapid alkalinization factors (RALFs) are cysteine-rich peptides that play important roles in a variety of biological processes, such as cell elongation and immune signaling. Recent studies in Arabidopsis have shown that RALFs regulate pollen tube growth via plasma membrane receptor-like kinases (RLKs). However, the downstream signal transduction mechanisms of RLKs in pollen tubes are unknown. Here, we identified PbrRALF2, a pear (Pyrus bretschneideri) pollen RALF peptide that inhibits pollen tube growth. We found that PbrRALF2 interacts with a malectin-like domain-containing RLK, PbrCrRLK1L13. The relative affinity between PbrRALF2 and PbrCrRLK1L13 was at the submicromolar level, which is consistent with the values of ligand–receptor kinase pairs and the physiological concentration for PbrRALF2-mediated inhibition of pollen tube growth. After binding to its extracellular domain, PbrRALF2 activated the phosphorylation of PbrCrRLK1L13 in a dose-dependent manner. We further showed that the MAP kinase PbrMPK18 is a downstream target of PbrCrRLK1L13 that mediates PbrRALF2-elicited reactive oxygen species (ROS) production. The excessive accumulation of ROS inhibits pollen tube growth. We show that MPK acts as a mediator for CrRLK1L to stimulate ROS production, which might represent a general mechanism by which RALF and CrRLK1L function in signaling pathways.