Stripe rust caused by Puccinia striiformis f. sp. tritici (Pst), is one of the most important fungal diseases on wheat worldwide and a serious threat to wheat production. Understanding the plant-microbe interaction mechanism is the basic step to assist future plant breeding aiming at increasing disease resistance. Based on the sequenced stripe rust fungus genome, several hundreds of small, secreted candidates for effector proteins are predicted. Effectors are believed to be pivotal for fungal pathogenicity with key roles in suppressing host defense. Thus, identifying key effectors and understanding their mechanisms of action is fundamentally important to guide future fights against the stripe rust disease.
In this PhD project, I studied the potential function of six stripe rust fungal effector candidates which are highly expressed in haustoria, by employing the Pseudomonas fluorescens EtHAn strain containing an engineered type-three secretion system. Results show that one of the effector candidates, PEC6, functions as a pattern-triggered immunity (PTI) suppressor in a host species-independent manner.
A host-induced gene silencing (HIGS) study revealed PEC6 as an important pathogenicity factor. By using the yeast two-hybrid system, the adenosine kinase (ADK) was identified as a host target of PEC6. Virus-induced gene silencing (VIGS) of ADK enhanced wheat susceptibility to stripe rust indicates that ADK is a positive regulator in plant defense.
Based on EtHAn-mediated effector delivery, seventy-two wheat landraces were screened to search for the presence of potential resistance (R) genes. Three landraces showed strong hypersensitive response (HR) when PEC6 was expressed in the cells, suggesting the presence of certain R gene(s) recognizing PEC6. However, these landraces did not show resistance upon Pst-inoculation.
In conclusion, the stripe rust fungal effector candidate PEC6 works as a PTI suppressor probably by targeting host ADK protein and interfering with its activity. A few wheat lines apparently carry R-genes able to recognize PEC6 but still are susceptible to Pst, so some other expressed effectors must suppress the unknown R gene-mediated HR induced by PEC6 during rust fungi infection and enable successful colonization.