Fig. 5

Model representing flow of events occurring during rice-gall midge compatible and incompatible interactions. Representation of flow of events related to rice-gall midge compatible and incompatible interactions (separated by dotted lines). Text within green and red boxes represents outcome of compatible and incompatible interactions, respectively. The attack by the Asian rice gall midge on a resistant host induces extensive transcriptomic and metabolomic reprogramming leading to an array of events that induce hypersensitive response (HR)-mediated host resistance against gall midge. The deregulation of carbon and nitrogen metabolism induces overexpression of genes involved in GABA shunt and accumulation of GABA that could be toxic to the feeding maggots (Ref 1) along with the concomitant release of reactive oxygen species, i.e. singlet oxygen, that trigger HR in the host. The disintegration of photosynthetic machinery leads to generation of singlet oxygen (Ref 2), which further mediates defense signaling involving phytohormones (Ref 3) and transcription factors (Ref 4). Singlet oxygen also induces lipid peroxidation (Ref 5) causing lipid mobilization that plays a role in defense signaling through release of free fatty acids (Ref 6). On the other hand, C/N shift towards nitrogen, during compatible interaction (Ref 7), favors maggot growth by promoting formation of nutritive tissue (Ref 8). Up-regulation of genes involved in cell cycle and organization during compatible interaction (Ref 9) also promotes establishment of nutritive tissue at feeding sites (Ref 10). In contrast, host cellular machinery breaks down at the site of HR during incompatible interaction. Therefore, the host cell death, during HR at feeding site, limits nutrient supply to the feeding maggots and prevents formation of nutritive tissue. The flow of events in the given model is re-constructed based on information available from the current study (text within black boxes) and earlier studies on other insect-plant interactions for which appropriate references have been cited in Additional file 11 : References S1