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Iron is critical for host-pathogen interactions. While pathogens seek to scavenge iron to spread, the host aims at decreasing iron availability to reduce pathogen virulence. Thus, iron sensing and homeostasis are of particular importance to prevent host infection and part of nutritional immunity. While the link between iron homeostasis and immunity pathways is well established in plants, how iron levels are sensed and integrated with immune response pathways remain unknown. We identified a receptor kinase, SRF3 coordinating root growth, iron homeostasis and immunity pathways via regulation of callose synthase activity. These processes are modulated by iron levels and rely on SRF3 extracellular and kinase domain which tune its accumulation and partitioning at the cell surface. Mimicking bacterial elicitation with the flagellin peptide flg22 phenocopies SRF3 regulation upon low iron levels and subsequent SRF3-dependent responses. We propose that SRF3 is part of nutritional immunity responses involved in sensing external iron levels.

Iron is critical for host–pathogen interactions. While pathogens seek to scavenge iron to spread, the host aims at decreasing iron availability to reduce pathogen virulence. Thus, iron sensing and homeostasis are of particular importance to prevent host infection and part of nutritional immunity. While the link between iron homeostasis and immunity pathways is well established in plants, how iron levels are sensed and integrated with immune response pathways remains unknown. Here we report a receptor kinase SRF3, with a role in coordinating root growth, iron homeostasis and immunity pathways via regulation of callose synthases. These processes are modulated by iron levels and rely on SRF3 extracellular and kinase domains which tune its accumulation and partitioning at the cell surface. Mimicking bacterial elicitation with the flagellin peptide flg22 phenocopies SRF3 regulation upon low iron levels and subsequent SRF3-dependent responses. We propose that SRF3 is part of nutritional immunity responses involved in sensing external iron levels.

SummaryIron is critical for host-pathogen interactions. While pathogens seek to scavenge iron to spread, the host aims at decreasing iron availability to reduce pathogen virulence. Thus, iron sensing and homeostasis are of particular importance to prevent host infection and part of nutritional immunity. While the link between iron homeostasis and immunity pathways is well established in plants, how iron levels are sensed and integrated with immune response pathways remain unknown. We identified a receptor kinase, SRF3 coordinating root growth, iron homeostasis and immunity pathways via regulation of callose synthase activity. These processes are modulated by iron levels and rely on SRF3 extracellular and kinase domain which tune its accumulation and partitioning at the cell surface. Mimicking bacterial elicitation with the flagellin peptide flg22 phenocopies SRF3 regulation upon low iron levels and subsequent SRF3-dependent responses. We propose that SRF3 is part of nutritional immunity responses involved in sensing external iron levels.

Black and red raspberries (Rubus occidentalis L. and Rubus idaeus L.) are the prominent members of the genus Rubus (Rosaceae family). Breeding programs coupled with the low costs of high-throughput sequencing have led to a reservoir of data that have improved our understanding of various characteristics of Rubus and facilitated the mapping of different traits. Gene B controls the waxy bloom, a clearly visible epicuticular wax on canes. The potential effects of this trait on resistance/susceptibility to cane diseases in conjunction with other morphological factors are not fully studied. Previous studies suggested that gene H, which controls cane pubescence, is closely associated with gene B. Here, we used tunable genotyping-by-sequencing technology to identify the de novo SNPs of R. occidentalis and R. idaeus using an interspecific population that segregates for the waxy bloom phenotype. We created linkage maps of both species and mapped the identified SNPs to the seven chromosomes (Ro01&ndash, Ro07) of Rubus. Importantly, we report, for the first time, the mapping of gene B to chromosome 2 of R. occidentalis using a genetic map consisting of 443 markers spanning 479.76 cM. We observed the poor transferability of R. idaeus SSRs to R. occidentalis and discrepancies in their previously reported chromosome locations.

Raspberry cane disease, caused by a complex of fungi, is amongst the most devastating problems for raspberry production. Using resistant or highly tolerant genotypes is a promising strategy. However, until now, cultivars with good field resistance for German fruit growers as well as the primary causal pathogens of cane disease present in the eastern part of Germany, Saxony state are still unknown. The primary objective of this study was to identify the primary disease causing organisms and resistant Rubus germplasm for future breeding efforts. From 2012 to 2014, we evaluated the degree of susceptibility to cane diseases on 213 raspberry cultivars at two different locations using a rating scale. We also identified the main fungi growing on infected canes. Our results suggest that Fusarium avenaceum is the main fungus causing cane disease in Saxony. The Rubus hybrid cultivars ‘Tayberry’ (2n = 6x = 42), ‘Buckingham Tayberry’ (2n = 6x = 42) and ‘Dorman Red’ (2n = 2x = 14) displayed the highest levels of field resistance at both locations. Moreover, we established an in vitro assay for resistance evaluation which correlates significantly with field data and is particularly suitable for quick assessment of resistance against F. avenaceum in breeding material. Future breeding programs, aiming at cultivars with enhanced resistance towards cane diseases can use the presented data for parental selection and may employ our in vitro F. avenaceum inoculation method for parental testing and progeny selection.

Mechanisms underlying speciation in plants include detrimental (incompatible) genetic interactions between parental alleles that incur a fitness cost in hybrids. We reported on recessive hybrid incompatibility between an Arabidopsis thaliana strain from Poland, Landsberg erecta (Ler), and many Central Asian A. thaliana strains. The incompatible interaction is determined by a polymorphic cluster of Toll/interleukin-1 receptor-nucleotide binding-leucine rich repeat (TNL) RPP1 (Recognition of Peronospora parasitica1)-like genes in Ler and alleles of the receptor-like kinase Strubbelig Receptor Family 3 (SRF3) in Central Asian strains Kas-2 or Kond, causing temperature-dependent autoimmunity and loss of growth and reproductive fitness. Here, we genetically dissected the RPP1-like Ler locus to determine contributions of individual RPP1-like Ler (R1–R8) genes to the incompatibility. In a neutral background, expression of most RPP1-like Ler genes, except R3, has no effect on growth or pathogen resistance. Incompatibility involves increased R3 expression and engineered R3 overexpression in a neutral background induces dwarfism and sterility. However, no individual RPP1-like Ler gene is sufficient for incompatibility between Ler and Kas-2 or Kond, suggesting that co-action of at least two RPP1-like members underlies this epistatic interaction. We find that the RPP1-like Ler haplotype is frequent and occurs with other Ler RPP1-like alleles in a local population in Gorzów Wielkopolski (Poland). Only Gorzów individuals carrying the RPP1-like Ler haplotype are incompatible with Kas-2 and Kond, whereas other RPP1-like alleles in the population are compatible. Therefore, the RPP1-like Ler haplotype has been maintained in genetically different individuals at a single site, allowing exploration of forces shaping the evolution of RPP1-like genes at local and regional population scales., Author Summary In plants, naturally evolving disease resistance (R) genes can cause autoimmunity when combined with different genetic backgrounds. This phenomenon, called immune-related hybrid incompatibility (HI), leads to growth inhibition and fitness loss due to inappropriate activation of defense. HI likely reflects different evolutionary paths of immune-related genes in nature. We have examined the genetic architecture of a complex R locus present in a Central European accession (Ler) which underlies HI with Central Asian accessions of Arabidopsis. We show that expression of one gene (R3) within the Ler cluster of eight tandem R genes (R1–R8) controls the balance between growth and defense but that R3 needs at least one other co-acting member within the R locus to condition HI. We traced the R1–R8 haplotype to a local population of Ler relatives in Poland where it also underlies HI with Central Asian accessions. Occurrence of the incompatible haplotype in ∼30% of genetically diverse local individuals, suggests that it has not arisen recently and has been maintained through selection or drift. Co-occurrence in the same population of individuals containing different R genes that do not cause HI provides a basis for determining genetic and environmental forces influencing how plant immunity genes evolve and diversify.