Fig. 4

Fine-tuning of plant development through antagonistic peptides. A model of pollen PCP-B peptides repression of stigma RALF23/33 peptide during pollen-stigma interaction. Before pollination, RALF23/33 induces ROS production in the stigmatic papillary cells through a FER/ANJ-controlled signaling pathway. Upon pollination, the competitive binding of pollen PCP-Bs to the stigma ANJ–FER receptor complex displaces stigmatic RALF23/33, repressing ROS production and thus stimulating pollen hydration. B Autocrine peptides RALF4/19 in the pollen tube activate the BUPS1/2–ANX1/2–LLG2/3 receptor complexes, ensuring the maintenance of cell wall integrity and promoting pollen tube growth within the transmitting tract. Upon reaching the micropyle, the ovule-secreted RALF34 competes with RALF4/19 for binding to BUPs/ANXs receptors, leading to pollen tube bursting and successful fertilization. C the competitive binding of STOMAGEN and EPF2 to the ER receptor kinase, along with its coreceptor TMM, finely tunes the initiation of stomatal development. The ER receptor kinase perceives the EPF2 peptide, leading to the inhibition of stomatal formation. Concurrently, STOMAGEN competes with EPF1/2 for the binding sites on the ER–TMM complex, positively regulating stomatal development. D the antagonistic regulation of leaf senescence by SCOOP10 and SCOOP12 peptides occurs via the MIK2 receptor-like kinase. MIK2 functions as a negative regulator of leaf senescence, with SCOOP10 promoting senescence by inhibiting MIK2 phosphorylation during the early stages. Conversely, SCOOP12 competes with SCOOP10 for binding to the MIK2 receptor, activating its phosphorylation during later stages of senescence, thereby suppressing senescence