Identification of resistance to citrus black spot using a novel in-field inoculation assay

Citrus black spot is an important fungal disease of citrus resulting in fruit drop and rind blemish in tropical and subtropical production areas. The disease is incited by the fungus Phyllosticta citricarpa (McAlpine) van der Aa (synonym: Guignardia citricarpa Kiely), with control currently relying on the application of fungicides. Because the presence and expression of resistance is poorly understood, we sought to develop a method for inoculating fruit in the field that gives reproducible symptoms of citrus black spot consistent with natural field infection. We subsequently validated this method by screening 49 citrus accessions and characterized their qualitative expression of citrus black spot symptoms. Challenge inoculations were undertaken with a known isolate of P. citricarpa, and control fruit were inoculated with water or the endophyte P. paracapitalensis Guarnaccia & Crous. Our results showed that all mandarin, sweet orange, lemon and papeda types were susceptible; pummelo, lime, and sour orange types expressed immunity; while various hybrids were susceptible, resistant and immune. Hybrid progeny from crosses using pummelo [Citrus maxima (Burm.) Merr.] as a parent showed preliminary evidence of segregation for citrus black spot immunity. The implications of these results to achieve genetic improvement for citrus black spot resistance in citrus breeding programs are discussed

Inoculum dynamics and infection of citrus fruit by Phyllosticta citricarpa

Citrus black spot, caused by , is characterized by fruit blemishes and premature fruit drop, resulting in significant economic losses in summer rainfall areas. The pathogen forms both conidia and ascospores during its life cycle. However, the occurrence of these spores and their contributions to infection of fruit in field conditions are not well understood. Our research using direct leaf litter monitoring and volumetric spore trapping in Queensland orchards revealed that pseudothecia and ascospores in leaf litter as well as trapped ascospores had low abundance, while pycnidia and conidia were highly abundant. Both and endophytic spp. were identified, with being dominant. In replicated field trials, we determined that infection of Imperial mandarin fruit by occurred from fruit set until week 20 of fruit development, with the key infection events taking place between weeks 4 and 16 in Queensland subtropical conditions. These results demonstrate that protecting fruit during weeks 4 to 16 significantly reduced infection. We found no significant correlation between the disease incidence in fruit and conidial abundance in leaf litter or ascospore abundance measured by volumetric spore trapping. Therefore, it is suggested that inoculum sources in the tree canopy other than those detected by spore trapping and direct leaf litter monitoring may play a major role in the epidemiology of citrus black spot. Improved knowledge regarding epidemiology of and an understanding of propagules causing infection may aid in development of more effective disease management strategies

Yield of Familial Hypercholesterolemia Genetic and Phenotypic Diagnoses After Electronic Health Record and Genomic Data Screening

Background Data mining of electronic health records to identify patients suspected of familial hypercholesterolemia (FH) has been limited by absence of both phenotypic and genomic data in the same cohort. Methods and Results Using the Geisinger MyCode Community Health Initiative cohort (n=130 257), we ran 2 screening algorithms (Mayo Clinic [Mayo] and flag, identify, network, deliver [FIND] FH) to determine FH genetic and phenotypic diagnostic yields. With 29 243 excluded by Mayo (for secondary causes of hypercholesterolemia, no lipid value in electronic health records), 52 034 excluded by FIND FH (insufficient data to run the model), and 187 excluded for prior FH diagnosis, a final cohort of 59 729 participants was created. Genetic diagnosis was based on presence of a pathogenic or likely pathogenic variant in FH genes. Charts from 180 variant‐negative participants (60 controls, 120 identified by FIND FH and Mayo) were reviewed to calculate Dutch Lipid Clinic Network scores; a score ≥5 defined probable phenotypic FH. Mayo flagged 10 415 subjects; 194 (1.9%) had a pathogenic or likely pathogenic FH variant. FIND FH flagged 573; 34 (5.9%) had a pathogenic or likely pathogenic variant, giving a net yield from both of 197 out of 280 (70%). Confirmation of a phenotypic diagnosis was constrained by lack of electronic health record data on physical findings or family history. Phenotypic FH by chart review was present by Mayo and/or FIND FH in 13 out of 120 versus 2 out of 60 not flagged by either (P<0.09). Conclusions Applying 2 recognized FH screening algorithms to the Geisinger MyCode Community Health Initiative identified 70% of those with a pathogenic or likely pathogenic FH variant. Phenotypic diagnosis was rarely achievable due to missing data

Lithospheric dismemberment and magmatic processes of the Great Basin-Colorado Plateau transition, Utah, implied from magnetotellurics

To illuminate rifting processes across the Transition Zone between the extensional Great Basin and stable Colorado Plateau interior, we collected an east-west profile of 117 wideband and 30 long-period magnetotelluric (MT) soundings along latitude 38.5°N from southeastern Nevada across Utah to the Colorado border. Regularized two-dimensional inversion shows a strong lower crustal conductor below the Great Basin and its Transition Zone in the 15–35 km depth range interpreted as reflecting modern basaltic underplating, hybridization, and hydrothermal fluid release. This structure explains most of the geomagnetic variation anomaly in the region first measured in the late 1960s. Hence, the Transition Zone, while historically included with the Colorado Plateau physiographically, possesses a deep thermal regime and tectonic activity like that of the Great Basin. The deep crustal conductor is consistent with a rheological profile of a brittle upper crust over a weak lower crust, in turn on a stronger upper mantle (jelly sandwich model). Under the incipiently faulted Transition Zone, the conductor implies a vertically nonuniform mode of extension resembling early stages of continental margin formation. Colorado Plateau lithosphere begins sharply below the western boundary of Capitol Reef National Park as a resistive keel in the deep crust and upper mantle, with only a thin and weak Moho-level crustal conductor near 45 km depth. Several narrow, steep conductors connect conductive lower crust with major surface faulting, some including modern geothermal systems, and in the context of other Great Basin MT surveying suggest connections between deep magma-sourced fluids and the upper crustal meteoric regime. The MT data also suggest anisotropically interconnected melt over a broad zone in the upper mantle of the eastern Great Basin which has supplied magma to the lower crust, consistent with extensional mantle melting models and local shear wave splitting observations. We support a hypothesis that the Transition Zone location and geometry ultimately reflect the middle Proterozoic suturing between the stronger Yavapai lithosphere to the east and the somewhat weaker Mojave terrane to the west. We conclude that strength heterogeneity is the primary control on locus of deformation across the Transition Zone, with modulating force components.Philip E. Wannamaker, Derrick P. Hasterok, Jeffery M. Johnston, John A. Stodt, Darrell B. Hall, Timothy L. Sodergren, Louise Pellerin, Virginie Maris, William M. Doerner, Kim A. Groenewold, and Martyn J. Unswort