One major characteristic of how plants respond to various abiotic stresses is the production of reactive oxygen species (ROS), which include superoxide anions, hydrogen peroxide, hydroxyl radicals, and singlet oxygen. When the levels of ROS exceed the cellular detoxification capacity, they can be harmful to biomolecules. However, ROS also play crucial roles in stress signaling. For example, high light stress-induced retrograde signaling (starting in chloroplasts and inducing stress responses in the nucleus) and ABA signaling involve ROS. Although the accumulation of ROS under osmotic stress can occur independently of stress-induced ABA accumulation, the production of hydrogen peroxide through SnRK2-mediated activation of the NADPH oxidases RbohD and RbohF is clearly regulated by the ABA signaling pathway.
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In Arabidopsis, extracellular hydrogen peroxide can be sensed by the leucine-rich repeat receptor kinases HPCA1 (throughout the plant) and GHR1 (especially in guard cells), generating Ca2+ signals by activating Ca2+ channels. In guard cells, this Ca2+ signal is transmitted to downstream components such as Ca2+-dependent protein kinases (CPKs, also known as CDPKs), which can phosphorylate ABA-responsive effectors like SLAC1. Therefore, in addition to the ABA-PYL-PP2C-SnRK2 module, osmotic stress-induced regulation of stomatal closure can also be mediated by the H2O2–HPCA1/GHR1–Ca2+–CPK module. Moreover, these two signaling modules are connected: ABA induces hydrogen peroxide, which inactivates ABI1 and ABI2, thereby relieving the inhibition of GHR1 mediated by ABI2.