Pseudomonas syringae pv. actinidiae (Psa) biovar 3, a virulent, canker-inducing pathogen is an economic threat to the kiwifruit (Actinidia spp.) industry worldwide. The commercially grown diploid (2×) A. chinensis var. chinensis is more susceptible to Psa than tetraploid and hexaploid kiwifruit. However information on the genetic loci modulating Psa resistance in kiwifruit is not available. Here we report mapping of quantitative trait loci (QTLs) regulating resistance to Psa in a diploid kiwifruit population, derived from a cross between an elite Psa-susceptible ‘Hort16A’ and a resistant male breeding parent P1. Using high-density genetic maps and intensive phenotyping, we identified a single QTL for Psa resistance on Linkage Group (LG) 27 of ‘Hort16A’ revealing 16–19% phenotypic variance and candidate alleles for susceptibility and resistance at this loci. In addition, six minor QTLs were identified in P1 on distinct LGs, exerting 4–9% variance. Resistance in the F1 population is improved by additive effects from ‘Hort16A’ and P1 QTLs providing evidence that divergent genetic pathways interact to combat the virulent Psa strain. Two different bioassays further identified new QTLs for tissue-specific responses to Psa. The genetic marker at LG27 QTL was further verified for association with Psa resistance in diploid Actinidia chinensis populations. Transcriptome analysis of Psa-resistant and susceptible genotypes in field revealed hallmarks of basal defense and provided candidate RNA-biomarkers for screening for Psa resistance in greenhouse conditions.
Polyploidy is a key driver of significant evolutionary changes in plant species. The genus Actinidia (kiwifruit) exhibits multiple ploidy levels, which contribute to novel fruit traits, high yields and resistance to the canker-causing dieback disease incited by Pseudomonas syringae pv. actinidiae (Psa) biovar 3. However, the genetic mechanism for resistance to Psa observed in polyploid kiwifruit is not yet known. In this study we performed detailed genetic analysis of a tetraploid Actinidia chinensis var. chinensis population derived from a cross between a female parent that exhibits weak tolerance to Psa and a highly Psa-resistant male parent. We used the capture-sequencing approach across the whole kiwifruit genome and generated the first ultra-dense maps in a tetraploid kiwifruit population. We located quantitative trait loci (QTLs) for Psa resistance on these maps. Our approach to QTL mapping is based on the use of identity-by-descent trait mapping, which allowed us to relate the contribution of specific alleles from their respective homologues in the male and female parent, to the control of Psa resistance in the progeny. We identified genes in the diploid reference genome whose function is suggested to be involved in plant defense, which underly the QTLs, including receptor-like kinases. Our study is the first to cast light on the genetics of a polyploid kiwifruit and suggest a plausible mechanism for Psa resistance in this species.
Clonal trials of Pinus radiata D. Don (radiata pine), representing two populations (or breeds), one selected for growth and form (GF) and the other selected for high wood density as well as growth and form (HD), were replicated on two low-altitude New Zealand sites: Tarawera (pumice soil, 38°08′S) and Woodhill (coastal dune, 36°42′S). The GF material comprised 33 pair-crosses (19 parents) × 10 clones, and the HD material comprised 19 single-pair crosses (35 parents) × 10 clones, with six ramets per clone per site. Diameter (DBH), two tree-form variables, and needle retention (NRA) were assessed 8 years after planting, and wood density (DEN), acoustic velocity, and collapse were assessed 9 years after planting. The site differences were generally expressed more strongly in the GF population. Estimated genetic parameters were mostly similar for the two breeds, except that genotypic correlation between DBH and DEN was apparently zero in the HD population. Estimated broad-sense heritabilities (H2) were generally markedly higher than narrow-sense heritability estimates (h2), except with DEN. Estimated between-site type-B clonal genotypic correlations were generally high (>0.8) for wood properties. Overall, DBH showed adverse genetic correlations with wood properties. The Elite/Breed strategy appeared to be helpful in combating adverse genetic correlations.
Douglas-fir is New Zealand's second most important plantation species and has been grown there since the late 1800s. Recently there has been increased commercial interest in the species, especially for higher-altitude, snow-prone sites in the southern South Island. Tree improvement began in 1957 with the establishment of extensive large-plot provenance trials. These have shown that coastal fogbelt provenances from California and southern Oregon are superior in growth to those of Washington coastal origin. The Washington provenances had been used for much of the afforestation up to 1980. A first breeding program, started in 1969 from stands of Washington origin, became redundant following the provenance trial findings and, in 1988, selection of 186 plus trees in provenance trial plots of coastal Californian and Oregon provenances restarted the breeding program. In addition, open pollinated seed from 240 parents in 21 coastal Californian and Oregon populations was planted as a breeding population in 1994. An ambitious program of polycrossing and paircrossing of NZ selections failed to deliver sufficient crosses and seed, and recently a new breeding strategy based on open pollination in a clonal archive of the 1988 selections has been instituted. The breeding objectives have also been recently revised to include volume yield, log quality and timber stiffness, selection criteria being diameter, bole straightness, light well-distributed branching and outerwood density and/or sound velocity.
Linear Mixed models (LMMs) that incorporate genetic and spatial covariance structures have been used for many years to estimate genetic parameters and to predict breeding values in animal and plant breeding. Although the theoretical aspects for extending LMM to generalised linear mixed models (GLMMs) have been around for some time, suitable software has been developed only within the last decade or so. The GLIMMIX procedure in SAS® is becoming popular for fitting GLMMs in various disciplines. Applications of GLMMs to genetic analysis have been limited, probably because of the complexity of the models used. This is particularly so for Proc GLIMMIX because, unlike ASReml software, it is not specifically tailored for analysis of breeding data and some pre-procedure coding is necessary. Binary data that fits the GLMM framework is commonly encountered in breeding experiments, such as when evaluating individuals for resistance by observing the presence or absence of disease. Bacterial canker (Psa) caused by Pseudomonas syringae pv. actinidiae is a serious disease of kiwifruit in New Zealand and other kiwifruit-producing countries. Data from a progeny test trial was available to identify parents with high breeding values for resistance. We successfully applied the GLIMMIX procedure for this purpose. Heritability for resistance was moderate, and we identified two parents and their family as having high potential for Psa resistance breeding. There are several potential pitfalls when using GLMMs with binary data and these are briefly discussed.