CaMACPF1 and CaMACPF6 positively regulate hypoxia tolerance through modulating jasmonate and auxin metabolic pathways.
TL;DR
Findings suggest that CaMACPF proteins may act as molecular switches linking EPCS dynamics to phytohormone signaling during hypoxic adaptation.
Abstract
Submergence and flooding impose severe crop losses through hypoxic stress. The Membrane Attack Complex/Perforin (MACPF) superfamily proteins function as pore-forming effectors in development and immunity across eukaryotic organisms, yet their role in plant hypoxia responses remains largely unexplored. Here, we identify two MACPF proteins in pepper (Capsicum annuum), CaMACPF1 and CaMACPF6, as positive regulators of hypoxia tolerance. CaMACPF1 and CaMACPF6 localize to endoplasmic reticulum-plasma membrane contact sites (EPCS) and the Golgi apparatus, with CaMACPF1 additionally detected in the nucleus and plasma membrane. When either protein was overexpressed, plants showed markedly better endurance under hypoxic stress and submergence, with accumulating less reactive oxygen species (ROS). Both proteins triggered jasmonic acid (JA) biosynthesis under oxygen deprivation, yet only CaMACPF6 specifically redirected auxin metabolism by converting indole-3-pyruvic acid (IPA) to indole-3-lactic acid (ILA). Taken together, these findings suggest that CaMACPF proteins may act as molecular switches linking EPCS dynamics to phytohormone signaling during hypoxic adaptation.