Abstract
AbstractPseudomonas syringaepv.actinidiaebiovar 3 (Psa3) has decimated kiwifruit orchards growing susceptible kiwifruitActinidia chinensisvarieties. Effector loss has occurred recently in Psa3 isolates from resistant kiwifruit germplasm, resulting in strains capable of partially overcoming resistance present in kiwiberry vines (A. arguta, A. polygama, andA. melanandra). Diploid maleA. melanandrarecognises several effectors, sharing recognition of at least one avirulence effector (HopAW1a) with previously studied tetraploid kiwiberry vines. Sequencing and assembly of theA. melanandragenome enabled the characterisation of the transcriptomic response of this non-host to wild-type and genetic mutants of Psa3.A. melanandraappears to mount a classic effector-triggered immunity (ETI) response to wildtype Psa3 V-13, as expected. Surprisingly, the type III secretion (T3S) system-lackingPsa3 V-13 ΔhrcCstrain did not appear to trigger pattern-triggered immunity (PTI) despite lacking the ability to deliver immunity-suppressing effectors. Contrasting theA. melanandraresponses to an effectorless Psa3 V-13 Δ33Estrain and to Psa3 V-13 ΔhrcCsuggested that PTI triggered by Psa3 V-13 was based on the recognition of the T3S itself. The characterisation of both ETI and PTI branches of innate immunity responses withinA. melanandrafurther enables breeding for durable resistance in future kiwifruit cultivars.
Publisher
Cold Spring Harbor Laboratory