NbATG1 participates in the development of disease symptoms and defense related cell death in Nicotiana benthamiana

Abstract

To defend themselves against pathogens plants have evolved two interconnected immune responses. Pattern-triggered immunity (PTI) is activated by the perception of microbe-associated molecular patterns (MAMPs), while effector-triggered immunity (ETI) depends on the recognition of effectors. Usually ETI culminates in a hypersensitive response (HR) with programmed cell death (PCD). In some tomato lines, resistance to Pseudomonas syringae pv. tomato (Pst) DC3000 relies on the recognition of AvrPto and AvrPtoB effectors by Pto and Prf. We demonstrated that NbATG1-silenced N. benthamiana plants exhibit delayed AvrPto/Pto-mediated PCD and disease-associaded symptoms. To further assess NbATG1 participation in ETI, we infiltrated N. benthamiana silenced plants with Pst DC3000 to evaluate if PCD due to the recongition of another bacterial effector (HopQ1-1 through Roq1) is affected. We observed a delayed PCD response in NbATG1 silenced plants compared with Ec1 control. We also shown a PCD delay using different pairs of resistance proteins and non-bacterial elicitors. In all cases PCD was delayed in NbATG1-silenced plants. Similar experiments were performed using Bax, a murine proapoptotic protein that triggers cell death in plants, and no differences were found between NbATG1- and Ec1- silenced plants. Taken together these results indicate that NbATG1 is required for the development PCD associated to two bacterial effectors and to non-bacterial elicitors.