Pinewood nematode (PWN), Bursaphelenchus xylophilus, the causal agent of pine wilt disease, is an inhabitant of native pine species of North America, where its presence has minor impact. In contrast, the introduction of this nematode to forests in Asia and Europe has devastated some pine stands and is recognized as a pest of significant phytosanitary concern by the National Plant Protection Organizations of several countries. The ability to detect PWN in internationally traded wood products is crucial to reduce the spread of this organism. Currently, the majority of molecular techniques for the detection of PWN rely on the presence of genomic DNA and thus fail to differentiate between living and dead PWN. The detection of dead nematodes could lead to unnecessary trade disruption. Therefore, accurate techniques for the detection of and differentiation between living and dead PWN are critical. We have developed a reverse transcription loop-mediated isothermal amplification (RT-LAMP) assay, which specifically identifies living PWN in wood by detecting the presence of mRNA encoding an expansin gene as a viability marker. This diagnostic method was found to be more sensitive, faster and less dependent on expensive laboratory equipment than PCR. In addition, unlike PCR, it allows for simple colour detection of amplification products. This method will help resolve disputes over the detection of PWN by clarifying whether it originates from live or dead organisms. Where approved treatments are implemented, unnecessary trade disruption will be avoided, thus protecting market access of wood products from PWN-infested areas.
Background Pulmonary function (PF) progressively declines with aging. Forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC) are predictors of morbidity of pulmonary and cardiovascular diseases and all-cause mortality. In addition, reduced PF is associated with elevated chronic low-grade systemic inflammation, glucose metabolism, body fatness, and low muscle strength. It may suggest pleiotropic genetic effects between PF with these age-related factors. Methods We evaluated whether FEV1 and FVC share common pleiotropic genetic effects factors with interleukin-6, high-sensitivity C-reactive protein, body mass index, muscle (grip) strength, plasma glucose, and glycosylated hemoglobin in 3,888 individuals (age range: 26-106). We employed sex-combined and sex-specific correlated meta-analyses to test whether combining genome-wide association p-values from two or more traits enhances the ability to detect variants sharing effects on these correlated traits. Results We identified 32 loci for PF, including 29 novel pleiotropic loci associated with pulmonary function and (i) body fatness (CYP2U1/SGMS2), (ii) glucose metabolism (CBWD1/DOCK8 and MMUT/CENPQ), (iii) inflammatory markers (GLRA3/HPGD, TRIM9, CALN1, CTNNB1/ZNF621, GATA5/SLCO4A1/NTSR1, and NPVF/C7orf31/CYCS), and (iv) muscle strength (MAL2, AC008825.1/LINC02103, AL136418.1). Conclusions The identified genes/loci for PF and age-related traits suggest their underlying shared genetic effects, which can explain part of their phenotypic correlations. Integration of gene expression and genomic annotation data shows enrichment of our genetic variants in lung, blood, adipose, pancreas, and muscles, among others. Our findings highlight the critical roles of identified gene/locus in systemic inflammation, glucose metabolism, strength performance, PF, and pulmonary disease, which are involved in accelerated biological aging.
Pulmonary function progressively declines with aging. Forced expiratory volume 1-second (FEV1) and forced vital capacity (FVC) are predictors of morbidity of cardiovascular diseases and all-cause mortality. Reduced pulmonary function has shown association with elevated chronic low-grade systemic inflammation and low muscle strength, and glycosylated hemoglobin (HbA1c). We evaluated whether FEV1 and FVC share common genetic factors with interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsCRP), body mass index (BMI), handgrip strength, plasma glucose, and HbA1c employing correlated meta-analysis (CMA) in up to 3888 individuals (age range: 26-106). CMA tests whether combining genome-wide association (GWA) P-values from two or more traits enhances the ability to detect variants concomitantly influencing such traits. We considered a variant pleiotropic if the univariate GWA P≤1.0x10-02 and CMA P≤5.0x10-08. We identified pleiotropic loci for FEV1 (or FVC), IL-6 and hsCRP within CYCS, CALN1, TRIM9, AXIN2, MICAL3, and CMIP; FEV1 (or FVC) and BMI within CYP2U1, LINC00871-RPL10L-MDGA2, and LOC105372472; FEV1 (or FVC) and grip strength within XXYLT1 and MAL2; FEV1 and FPG within MAF; and FVC and HbA1c within HDHD3. Some loci were reported as GWAS suggestive (P<10-6) for pulmonary function. Additionally, the identified loci harbor genes with roles in pro-inflammatory cytokine production, immune and inflammatory pathway, T-helper signaling pathway, transforming growth factor-beta, and T-cell receptor-alpha enhancer. Our findings suggest that inflammation is a feature of reduced pulmonary function with IL-6, hsCRP, BMI, low muscle strength, glucose, and HbA1c. Pleiotropic genetic associations across these traits may explain part of the correlated genetic architecture between pulmonary function and aging-related traits.
Adiponectin is involved in regulating insulin resistance (IR) and is a potential regulator of healthy aging and lifespan. To identify novel variants associated with adiponectin, we further assessed our previously identified linkage peak on 16q23.2 (LODs=3.8). We used sequence data of 632 participants (age, 24-110 years) from 47 families of European ancestry in the Long Life Family Study, a study with familial clustering of exceptional longevity in the US and Denmark. Adiponectin levels were log-transformed, and adjusted for age, sex, sites, and PCs for ancestry. We found a variant in the PKD1L2 (rs527459046, p=2e-8, MAF=3%, r2=1.5%, accounting for linkage=28%). The PKD1L2, 1.4 Mb upstream of the CDH13 (adiponectin receptor gene) is expressed in heart, liver, and adipocytes, known to function as an ion-channel regulator or a GPCR regulator for aging-related lipolysis, IR, and adiponectin/leptin secretion. Haplotyping, epistatic and bioinformatic analyses will be engaged to capture additional/functional variants and regulatory networks.
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