PbrBZR1 interacts with PbrARI2.3 to mediate brassinosteroid-regulated pollen tube growth during self-incompatibility signaling in pear

Abstract

S-RNase-mediated self-incompatibility (SI) prevents self-fertilization and promotes outbreeding to ensure genetic diversity in many flowering plants, including pear (Pyrus sp.). Brassinosteroids (BRs) have well-documented functions in cell elongation, but their molecular mechanisms in pollen tube growth, especially in the SI response, remain elusive. Here, exogenously applied brassinolide (BL), an active BR, countered incompatible pollen tube growth inhibition during the SI response in pear. Antisense repression of BRASSINAZOLE-RESISTANT1 (PbrBZR1), a critical component of BR signaling, blocked the positive effect of BL on pollen tube elongation. Further analyses revealed that PbrBZR1 binds to the promoter of EXPANSIN-LIKE A3 (PbrEXLA3) to activate its expression. PbrEXLA3 encodes an expansin that promotes pollen tube elongation in pear. The stability of dephosphorylated PbrBZR1 was substantially reduced in incompatible pollen tubes, where it is targeted by ARIADNE2.3 (PbrARI2.3), an E3 ubiquitin ligase that is strongly expressed in pollen. Our results show that during the SI response, PbrARI2.3 accumulates and negatively regulates pollen tube growth by accelerating the degradation of PbrBZR1 via the 26S proteasome pathway. Together, our results show that a ubiquitin-mediated modification participates in BR signaling in pollen and reveal the molecular mechanism by which BRs regulate S-RNase-based SI.

CPK1‐HSP90 phosphorylation and effector XopC2–HSP90 interaction underpin the antagonism during cassava defense‐pathogen infection

“…The recombinant plasmids (MeHSP90.9‐nYFP, MeCPK1‐cYFP and XopC2‐cYFP) were transformed into Agrobacterium tumefaciens strain GV3101, and then, the nYFP‐fused plasmids and cYFP‐fused plasmids were co‐transformed into N. benthamiana leaves by infiltration. Two days after infection, the yellow fluorescent protein (YFP) and 4′, 6‐diamidino‐2‐phenylindole (DAPI)‐stained fluorescence were detected under a confocal laser‐scanning microscope as described previously (Wei et al ., 2021b; Y. Wang et al ., 2023).…”

Molecular insights into self-incompatibility systems: From evolution to breeding

“…S -RNase also mediates actin cytoskeleton depolymerization by increasing pollen phosphatidic acid levels, repressing ABF–LRX signaling, and disrupting the interaction between MdMVG and F-actin ( Chen et al., 2018 ; Yang et al., 2018 ; Wu et al., 2023 ). Two phytohormone signaling pathways, the jasmonic acid (JA)–MdMYC2–MdD1 pathway and the BZR1-mediated brassinosteroid (BR) pathway, have been shown to be directly and indirectly induced, respectively, by S -RNase to inhibit PT growth ( Gu et al., 2019 ; Wang et al., 2023 ). Other cellular processes, such as alterations in cytoplasmic Ca 2+ concentration and reactive oxygen species (ROS) levels, are also likely to be involved in the SI response ( Jiang et al., 2014 ).…”

Localization of S-Locus-Related Self-Incompatibility in Lycium barbarum Based on BSA Analysis

“…Non-S factors implicated in the self-incompatibility response are primarily proteins that play critical roles at various stages of the reaction. Non-S factors identified as contributing to self-incompatibility include calcium-binding proteins (CaBP), ubiquitin-binding proteins, SKP1-like proteins, S-RNasebinding proteins (SBP1), S-locus F-box-interacting proteins, and actin depolymerizing factors (ADF) [11][12][13][14].…”