This topic has an obvious gene-environment interaction theme. The environmental signal is “stress of any kind”, the signal is transmitted via extracellular hydrogen peroxide (H2O2 or eH2O2), and the response by the cell’s genome is to survive the stress signal by all possible means. Chemically reactive, oxygen-containing molecules called reactive oxygen species (ROS) are central to cell function. Plant cells generate various ROS, including H2O2, which has a key role in cell
Signaling. Biosynthesis of eH2O2 by NADPH oxidases and superoxide dismutases — or possibly other mechanisms — is induced by various non-biological and biological stresses and internal cues in animals and plants; eH2O2 then initiates signaling pathways to regulate stress responses, as well as growth and development (e.g. eH2O2 plays a vital role throughout the plant life-cycle by regulating meiotic fate acquisition, pollen tube growth, root hair growth, root stem-cell niche maintenance and abscission, among others). It is known that eH2O2 enters the cytosol via aquaporins (water channels), and then oxidizes cytosolic proteins in both animals and plants. Several of these proteins with cysteine residues are modified by H2O2 function and then serve as “H2O2 sensors.”
H2O2 is produced in an extracellular space — between the plasma membrane and cell wall — called the apoplast, in response to a range of signals — including stressors, plant hormones such as abscisic acid, and physical or chemical
changes outside the cell. But how this eH2O2 is sensed at the cell surface has not been understood. Authors [see attached article and editorial] have now identified the first known cell-surface H2O2 receptor in plants. In this study, authors isolated mutants defective in eH2O2-induced increases in intracellular calcium ( [Ca2+]i ) levels, which led to identification of a cell-surface sensor for eH2O2.
Authors used forward genetics (i.e. going from a chosen phenotype to find the gene(s) that cause it; this is initially done by using naturally-occurring mutations in cells or mice, or inducing mutants with radiation, chemicals, or insertional mutagenesis) screening — based on Ca2+ imaging. They isolated H2O2-induced Ca2+ increases (hpca) mutants in Arabidopsis (a tiny mustard plant heavily used for plant genetics) and identified HPCA1 as a leucine-rich-repeat receptor kinase — belonging to a previously uncharacterized subfamily that features two extra pairs of cysteine residues in the extracellular domain.
HPCA1 is localized to the plasma membrane and is activated by H2O2 (via covalent modification of extracellular cysteine
residues), which leads to auto-phosphorylation of the HPCA1 protein. HPCA1 mediates H2O2-induced activation of Ca2+ channels in guard cells and this is required for stomatal closure (stoma is a tiny opening or pore, used for gas exchange, almost always found on under-surface of plant leaves). These data improve our understanding as to how the perception of extracellular H2O2 is integrated with responses to various external stresses and internal cues in plants. This study also has implications for future design of crops with enhanced fitness. 😊
Nature 127 Feb 2020; 578: 577-581 + editorial pp 518-519