<i>Pratylenchus coffeae</i> Effector PcENG2 Targets the Maize Chitinase ZmCHI5 to Promote Parasitism

<i>Pratylenchus coffeae</i>, a damaging root-lesion nematode, secretes effectors to manipulate host processes and promote parasitism. Here, we characterize PcENG2, a β-1,4-endoglucanase localized in the nematode esophageal gland cells and secreted during infection. <i>PcENG2</i> expression is upregulated during the early parasitic stage of <i>P. coffeae</i>. PcENG2 promotes cell wall and callose degradation, as demonstrated by immunolocalization and immunoelectron microscopy. It also suppresses host reactive oxygen species (ROS) production and enhances susceptibility to <i>P. coffeae</i> when ectopically expressed in <i>Arabidopsis</i>. PcENG2 directly interacts with maize (<i>Zea mays</i> L.) chitinase, a key defense-related protein. This interaction suppresses chitinase enzymatic activity and protects nematode eggs from degradation. Virus-induced gene silencing (VIGS) demonstrated that ZmCHI5 is essential for broad-spectrum nematode resistance in maize. Collectively, these findings identify PcENG2 as a key effector that modulates host immunity to promote <i>P. coffeae</i> infection.