The aphid effector CathB6 suppresses EDS1-dependent immunity and rewires MORF2–GUN1–GLK signalling to sustain host cellular homeostasis in Arabidopsis

Aphids use stylet mouthparts to probe plant tissues and deliver oral secretions into host cells, modulating immunity to establish long-term phloem feeding sites in sieve elements. This feeding behaviour make aphids efficient vectors of plant pathogens. We previously showed that Myzus persicae cathepsin B (CathB) effectors promote aphid colonization, accumulate in dynamic cytoplasmic processing bodies (p-bodies), bind the key Arabidopsis thaliana immune regulator EDS1, and recruit EDS1 together with its signalling partners PAD4 and ADR1 to p-bodies. However, the extent to which CathB effectors suppress EDS1-regulated immunity remains unclear. Here, we show that CathB6-expressing Arabidopsis lines exhibit substantial transcriptomic overlap with the eds1-2 mutant, consistent with CathB6 suppression of EDS1-dependent immunity. However, CathB6 also induces broader transcriptional reprogramming beyond that explained by loss of EDS1 function. A yeast two-hybrid screen identified the transcription factors GLK1 and GLK2, as well as several MORF proteins, as CathB6 interactors. CathB6-expressing plants recapitulated GLK- and MORF-regulated transcriptional changes, suppressing GUN1-associated activity while maintaining GLK-mediated expression of photosynthesis-associated nuclear genes (PhANGs). We found that GLKs promotes CathB6 nuclear accumulation and reduces its p-body association. TurboID proximity labelling further linked CathB6 to PhANG-associated proteins, known MORF2- and GUN1-interacting factors, p-body components, and actin–tubulin/myosin machinery, the latter being consistent with the highly dynamic behaviour of CathB6-associated p-bodies. Together, these data indicate that, beyond suppressing EDS1-mediated defenses, CathB6 interferes with the MORF2–GUN1–GLK signalling pathway, modulating plant defense responses while sustaining GLK-mediated PhANG expression to maintain cellular homeostasis during aphid attack.