Molecular mimicry and trafficking of peptide effectors in sedentary nematodes: emerging drivers of feeding site formation and host signaling hijack

Despite significant advances in understanding the biology of plant-parasitic nematodes, the emergence of peptide hormone mimicry as a virulence strategy presents a complex facet of nematode parasitism. This review integrates recent advances on how nematode effectors, such as CLEs, CEPs, RALFs, IDA, and PSYs, are processed, post-translationally modified, and trafficked to hijack host signaling and developmental programs. By linking structural mimicry with receptor engagement and subcellular targeting, we highlight how these effectors reprogram plant transcriptional and immune responses to drive the formation of nematode feeding sites. We further explore the evolutionary origins of these effectors, emphasizing how processes such as horizontal gene transfer, neofunctionalization, and convergent selection have shaped peptide effectors into lineage-specific virulence factors. Finally, we outline critical research gaps focusing on structural and computational analyses of effector-receptor interfaces, functional genomics of trafficking and activation and translational opportunities for engineering durable host resistance. Together, these insights underscore the influence of molecular mimicry on nematode virulence and position effector biology as a frontier for translational innovation in crop protection.