Biology subjects

Patterson, H. R.

Publications and source records attributed to Patterson, H. R..

4 recordsLinked to original sources

bioRxiv2025

Diverse Pseudomonas species engage in beneficial and suppressive interactions with the kiwifruit pathogen Psa across Actinidia germplasm

In 2010, a Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) incursion into New Zealand kiwifruit orchards devastated susceptible Actinidia chinensis cultivars. In contrast, many Actinidia species maintained in germplasm collections were resistant to Psa3 and showed limited symptoms. Recent genome biosurveillance revealed the emergence of widespread leaf spot symptoms in Psa3-resistant Actinidia germplasm. Surprisingly, few Psa3 isolates were recovered from symptomatic tissues, despite the frequent isolation of phenotypical Pseudomonas isolates on selective agar. Despite the poor recovery of Psa3 isolates, Psa3 was found in all symptomatic leaf tissue through qPCR and metabarcoding analysis. Metabarcoding revealed stark differences in bacterial community composition from samples taken from lesion-carrying or lesion-free material from the same leaf. Host genotype also appeared to influence community composition but to a lesser extent. Whole genome sequencing of diverse Pseudomonas spp. isolates revealed that many belonged to the P. syringae species complex. Curiously, the kiwifruit-associated P. syringae pv. actinidifoliorum (Pfm), was never recovered, nor were any other phylogroup 1 pathovars. Pathogenicity and competitive assays revealed that while individually diverse Pseudomonas isolates were not more pathogenic than Pfm or Psa3 on resistant Actinidia hosts, they could interact with Psa to sometimes improve their growth, suggesting that these isolates may form pathogenic consortia in these disease-associated phyllosphere communities on typically Psa3-resistant hosts. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=116 SRC="FIGDIR/small/635981v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@1e48d68org.highwire.dtl.DTLVardef@1ffa8d7org.highwire.dtl.DTLVardef@1a5c47corg.highwire.dtl.DTLVardef@6bd39_HPS_FORMAT_FIGEXP M_FIG C_FIG

plant biology↗

bioRxiv2024

Genomic biosurveillance of the kiwifruit pathogen Pseudomonas syringae pv. actinidiae biovar 3 reveals adaptation to selective pressures in New Zealand orchards

In the late 2000s, a pandemic of Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) devastated kiwifruit orchards growing susceptible yellow-fleshed cultivars. New Zealands kiwifruit industry has since recovered, following the deployment of the tolerant cultivar Zesy002. However, little is known about the extent to which the Psa population is evolving since its arrival. Over 500 Psa3 isolates from New Zealand kiwifruit orchards were sequenced between 2010 and 2022, from commercial monocultures and diverse germplasm collections. While effector loss was previously observed on Psa-resistant germplasm vines, effector loss appears to be rare in commercial orchards, where the dominant cultivars lack Psa resistance. However, a new Psa3 variant, which has lost the effector hopF1c, has arisen. The loss of hopF1c appears to have been mediated by the movement of integrative conjugative elements introducing copper resistance into this population. Following this variants identification, in planta pathogenicity and competitive fitness assays were performed to better understand the risk and likelihood of its spread. While hopF1c loss variants had similar in planta growth to wild-type Psa3, a lab-generated {Delta}hopF1c strain could outcompete wild-type on select hosts. Further surveillance was conducted in commercial orchards where these variants were originally isolated, with 6.6% of surveyed isolates identified as hopF1c loss variants. These findings suggest that the spread of these variants is currently limited, and they are unlikely to cause more severe symptoms than the current population. Ongoing genome biosurveillance of New Zealands Psa3 population is recommended to enable early detection and management of variants of interest.

genomics↗

bioRxiv2024

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↗

bioRxiv2021

Assessing the effectiveness of oxathiapiprolin towards Phytophthora agathidicida, the causal agent of kauri dieback disease

Phytophthora species cause disease and devastation of plants in ecological and horticultural settings worldwide. A recently identified species, P. agathidicida, infects and ultimately kills the treasured kauri trees that are endemic to New Zealand. Currently there are few options for controlling or treating P. agathidicida. In this study, we sought to assess the toxicity of the oomycide oxathiapiprolin against several lifecycle stages of two geographically distinct P. agathidicida isolates. Half maximal effective concentration (EC50) values were determined to be approximately 0.1 ng/ml for inhibiting mycelial growth, indicating that P. agathidicida mycelia are more sensitive to oxathiapiprolin than those from most other Phytophthora species that have been studied. Oxathiapiprolin was also highly effective at inhibiting the germination of zoospores (EC50 = 2-9 ng/ml for the two isolates) and oospores (complete inhibition at 100 ng/ml). In addition, oxathiapiprolin delayed the onset of detached kauri leaf infection in a dose-dependent manner. Collectively, the results presented here highlight the significant potential of oxathiapiprolin as a tool to aid in the control of kauri dieback disease.

microbiology↗