Study uncovers plant sensing mechanism to guard against pests

A new study has identified a previously unknown mechanism by which plants sense insect attack and activate defense responses.

Published in Nature on November 12, the study was conducted by researchers at the Center for Excellence in Molecular Plant Sciences (CEMPS) of the Chinese Academy of Sciences (CAS) led by CHEN Xiaoya, in collaboration with WAN Li’s team.

Insect pests threaten crop production and cause substantial damage to vegetation. During feeding, herbivorous insects release oral secretions containing digestive enzymes that hydrolyze plant macromolecules to facilitate nutrient acquisition. The products of this digestive process may also act as host-derived signaling molecules.

However, how plants perceive these molecules and activate downstream defense responses had largely been a mystery.

In this study, the researchers discovered that, during feeding, the rice green stink bug secretes the T2 ribonuclease NVR1 into plant tissues, where it generates 2′,3′-cyclic nucleotides (2′,3′-cNMPs), which are perceived by NIB1, a glycine-rich RNA-binding protein in rice.

Binding of these products promotes liquid–liquid phase separation of NIB1 and the formation of nuclear condensates that recruit the core immune regulator EDS1, thereby activating downstream defense responses.

While T2 ribonucleases are commonly present in herbivorous insects, including the rice leaf folder, green mirid, and cotton bollworm, NIB1-homologous RNA-binding proteins are widely distributed across land plants. This signaling mechanism may be a broadly deployed strategy in plant–insect interactions.

Exogenous application of these RNA degradation products elicits plant defense responses, highlighting their potential as immune activators for crop protection.

More broadly, this study provides a conceptual advance, opens the door to further exploring the involvement of RNA-centered networks in plant immunity and adaptation, and offers potential applications in plant protection.