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Bohne, D.

Publications and source records attributed to Bohne, D..

2 recordsLinked to original sources

Identification and characterization of innate immunity in Actinidia melanandra in response to Pseudomonas syringae pv. actinidiae

Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) has decimated kiwifruit orchards growing susceptible kiwifruit Actinidia chinensis varieties. 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, and A. melanandra). Diploid male A. melanandra recognises several effectors, sharing recognition of at least one avirulence effector (HopAW1a) with previously studied tetraploid kiwiberry vines. Sequencing and assembly of the A. melanandra genome enabled the characterisation of the transcriptomic response of this non-host to wild-type and genetic mutants of Psa3. A. melanandra appears to mount a classic effector-triggered immunity (ETI) response to wildtype Psa3 V-13, as expected. Surprisingly, the type III secretion (T3S) system-lacking Psa3 V-13 {Delta}hrcC strain did not appear to trigger pattern-triggered immunity (PTI) despite lacking the ability to deliver immunity-suppressing effectors. Contrasting the A. melanandra responses to an effectorless Psa3 V-13 {Delta}33E strain and to Psa3 V-13 {Delta}hrcC suggested 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 within A. melanandra further enables breeding for durable resistance in future kiwifruit cultivars.

plant biology↗

Contrasting effector profiles between bacterial colonisers of kiwifruit reveal redundant roles and interplay converging on PTI-suppression and RIN4

O_LITesting effector-knockout strains of the Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) for reduced in planta growth in their native kiwifruit host revealed a number of non- redundant effectors that contribute to Psa3 pathogenicity. Conversely, complementation in the weak kiwifruit pathogen P. syringae pv. actinidifoliorum (Pfm) for increased growth identified redundant Psa3 effectors. C_LIO_LIPsa3 effectors hopAZ1a and HopS2b and the entire exchangeable effector locus ({Delta}EEL; 10 effectors) were significant contributors to bacterial colonisation of the host and were additive in their effects on pathogenicity. Four of the EEL effectors (HopD1a, AvrB2b, HopAW1a, and HopD2a) redundantly contribute to pathogenicity through suppression of pattern-triggered immunity (PTI). C_LIO_LIImportant Psa3 effectors include several redundantly required effectors early in the infection process (HopZ5a, HopH1a, AvrPto1b, AvrRpm1a, and HopF1e). These largely target the plant immunity hub, RIN4. C_LIO_LIThis comprehensive effector profiling revealed that Psa3 carries robust effector redundancy for a large portion of its effectors, covering a few functions critical to disease. C_LI

plant biology↗