## 6 Host-Induced Gene Silencing (HIGS)
Candidate parasitism genes identified in the study included 12 orthologues from other nematode species and 41 genes encoding ROS-associated genes, and five types of cell wall-modifying enzymes, thought to protect nematode from host defenses. The transcriptome of \(M\). _graminicola_ was obtained from J2 stage nematodes collected from rice roots [97]. Of 1328 candidate secreted protein genes, the authors focused on four that were expressed in the esophageal gland cells or olfactosensory organs, and were common to _Meloidogyne_ and cyst nematodes, but without sequence orthologues in humans, plants, and insects. Two genes lacked functional annotation (hypothetical protein), the third encoded a prion-like (Q/N-rich) domain-bearing protein [98] associated with conversion of soluble protein to protein aggregates in other organisms, and the fourth encoded a trehalose-6-phosphate phosphatase, thought to reduce accumulation of toxic trehalose-6-phosphate in the nematode gut [99]. After HIGS, nematode viability was 20%-56%, compared to 100% for the water control. Furthermore, the \(M\). _graminicola_ transcriptome [97] was used to obtain a full-length copy of a novel parasitism gene called \(MgGPP\)[100]. This gene encoded a protein that had limited sequence identity (37%-41%) to a family of _Meloidogyne_ virulence proteins of unknown function. The MgGPP protein was expressed in the esophageal gland cells of the nematode and accumulated in early parasitism. Overexpression of the gene resulted in enhanced susceptibility of transgenic rice lines to \(M\). _graminicola_; female nematode numbers increased 23%-67%, depending on the line. Conversely, rice plants transformed with RNAi species showed reduction in \(MgGPP\) gene expression and 50%-72% reduction in female nematode numbers. Clues to possible mechanism(s) of MgGPP action were revealed using molecular and histochemical approaches. The protein underwent host-mediated post-translational modifications that resulted in suppression of the normal host cell death resistance response and localization of the modified protein to the nucleus. Fungal pathogenicity factors, including secreted cell-wall degrading enzymes, phytotoxins, and cell death-inducing proteins, have been described [89; 101]. Certain isolates of _F. culmorum_ produce the toxins nivalenol and deoxynivalenol, which contribute to yield losses caused by _F. graminearum_ in Fusarium head blight of cereals [8; 35; 102; 103]. A possible candidate for HIGS in _F. culmorum_ arose from observations of developmental and metabolic defects associated with mutations in the \(StuA\) transcription factor gene [30]. The \(stuA\) mutants of _F. culmorum_ displayed reduced conidial, delayed spore germination, decreased mycelial diameter, length and density, decreased catalase and polygalacturonase activities, and loss of pathogenicity to the stem and root [30; 104]. These phenotypeswere independent of toxin production, rendering \(StuA\) a promising target for HIGS of stem and root rot of wheat and barley. Another promising HIGS target for _F. culmorum_ is the _CYP51B_ gene, which encodes a lanosterol C14-\(\alpha\)-demethylase essential for plasma membrane permeability and ascospore germination. Simultaneous silencing of the _CYP51A_, _CYP51A_, and _CYP51C_ genes in _F. grainnearum_ resulted in abnormal morphology and growth inhibition of the mycelium, and the resistance response in detached leaves of the model plant Arabidopsis and transgenic barley expressing the RNAi molecules [105].