No abstract

Glucosinolates (GSLs) are a major class of secondary metabolites. The content of seed GSL is largely regulated by environments in rapeseed (Brassica napus). However, the genetic control of seed GSL content responsible for environment in B. napus has been poorly understood. In the current study, a doubled haploid (DH) population from a cross between winter and semi-winter lines of rapeseed was grown in two distinct eco-environments, Germany and China, to evaluate the eco-environment effect and dissect the quantitative trait loci (QTL) responsible for environment for seed GSL in rapeseed. The deviation value of GSL content between eco-environments (GSLE) was calculated for each line in the DH population and the QTLs for GSLE were detected. GSLE ranged from −46.90 to 36.13 μmol g−1 meal in the DH population, suggesting the prominent eco-environmental effects for seed GSL in rapeseed. Four QTLs for GSLE were identified on chromosomes A04, A06, and A09 explaining 4.70∼9.93% of the phenotypic variation. Comparison of QTLs of seed GSL content between different eco-environments found three QTLs for GSL on A02 from 37.6 to 45.4 cM, A04 from 0 to 17.2 cM, and A09 from 67.0 to 98.6 cM exhibited significant difference of QTL effect between the German and Chinese eco-environments (P < 0.01), indicating the environment sensibility of these loci on seed GSL content. Moreover, flowering time (FT), an important environment adaptation trait in plant, was also investigated in this study. Comparative QTL analysis among GSLE, GSL, and FT revealed that three regions on chromosomes A02, A04, and A09 not only exhibited significant differences in QTL effect between Germany and China, but also co-located with the QTL intervals of GSLE and FT. Our results revealed that most of the GSL loci can influence GSL accumulation under different eco-environments, whereas the three QTL intervals on A02, A04, and A09 might be sensitive to the eco-environments for seed GSL content.

Longevity was influenced by many complex diseases and traits. However, the relationships between human longevity and genetic risks of complex diseases were not broadly studied. Here, we constructed polygenic risk scores (PRSs) for 225 complex diseases/traits and evaluated their relationships with human longevity in a cohort with 2178 centenarians and 2299 middle‐aged individuals. Lower genetic risks of stroke and hypotension were observed in centenarians, while higher genetic risks of schizophrenia (SCZ) and type 2 diabetes (T2D) were detected in long‐lived individuals. We further stratified PRSs into cell‐type groups and significance‐level groups. The results showed that the immune component of SCZ genetic risk was positively linked to longevity, and the renal component of T2D genetic risk was the most deleterious. Additionally, SNPs with very small p‐values (p ≤ 1x10‐5) for SCZ and T2D were negatively correlated with longevity. While for the less significant SNPs (1x10‐5 < p ≤ 0.05), their effects on disease and longevity were positively correlated. Overall, we identified genetically informed positive and negative factors for human longevity, gained more insights on the accumulation of disease risk alleles during evolution, and provided evidence for the theory of genetic trade‐offs between complex diseases and longevity.

Helicobacter pylori is a causative pathogen of many gastric and extra-gastric diseases. It has infected about half of the global population. There were no genome-wide association studies (GWAS) for H. pylori infection conducted in Chinese population, who carried different and relatively homogenous strain of H. pylori. In this work, we performed SNP (single nucleotide polymorphism)-based, gene-based and pathway-based genome-wide association analyses to investigate the genetic basis of host susceptibility to H. pylori infection in 480 Chinese individuals. We also profiled the composition and function of the gut microbiota between H. pylori infection cases and controls. We found several genes and pathways associated with H. pylori infection (P < 0.05), replicated one previously reported SNP rs10004195 in TLR1 gene region (P = 0.02). We also found that glycosaminoglycan biosynthesis related pathway was associated with both onset and progression of H. pylori infection. In the gut microbiome association study, we identified 2 species, 3 genera and several pathways had differential abundance between H. pylori infected cases and controls. This paper is the first GWAS for H. pylori infection in Chinese population, and we combined the genetic and microbial data to comprehensively discuss the basis of host susceptibility to H. pylori infection.