Grain protein concentration (GPC) is an important trait in durum cultivar development as a major determinant of the nutritional value of grain and end-use product quality. However, it is challenging to simultaneously select both GPC and grain yield (GY) due to the negative correlation between them. To characterize quantitative trait loci (QTL) for GPC and understand the genetic relationship between GPC and GY in Canadian durum wheat, we performed both traditional and conditional QTL mapping using a doubled haploid (DH) population of 162 lines derived from Pelissier × Strongfield. The population was grown in the field over 5 years and GPC was measured. QTL contributing to GPC were detected on chromosome 1B, 2B, 3A, 5B, 7A, and 7B using traditional mapping. One major QTL on 3A () was consistently detected over 3 years accounting for 9.4-18.1% of the phenotypic variance, with the favorable allele derived from Pelissier. Another major QTL on 7A () detected in 3 years explained 6.9-14.8% of the phenotypic variance, with the beneficial allele derived from Strongfield. Comparison of the QTL described here with the results previously reported led to the identification of one novel major QTL on 3A () and five novel minor QTL on 1B, 2B and 3A. Four QTL were common between traditional and conditional mapping, with and detected in multiple environments. The QTL identified by conditional mapping were independent or partially independent of GY, making them of great importance for development of high GPC and high yielding durum.
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http://dx.doi.org/10.3389/fpls.2021.642955 | DOI Listing |
J Neurophysiol
January 2025
Department of Anesthesiology, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
J Transl Med
December 2024
Department of Ophthalmology, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou, 510282, China.
Background: Diabetic retinopathy (DR) is the most important complication of Type 2 Diabetes (T2D) in eyes. Despite its prevalence, the early detection and management of DR continue to pose considerable challenges. Our research aims to elucidate potent drug targets that could facilitate the identification of DR and propel advancements in its therapeutic strategies.
View Article and Find Full Text PDFMetabolism
December 2024
Department of Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai National Clinical Research Center for Metabolic Diseases, Key Laboratory for Endocrine and Metabolic Diseases of the National Health Commission of the PR China, Shanghai Key Laboratory for Endocrine Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address:
Background: Delineating the shared genetic architecture of type 2 diabetes with muscle mass and function and frailty is essential for unraveling the common etiology and developing holistic therapeutic strategies for these co-existing conditions.
Methods: In this genome-wide pleiotropic association study, we performed multi-level pairwise trait pleiotropic analyses using genome-wide association study summary statistics from up to 461,026 European ancestry individuals to dissect the shared genetic factors and causal relationships of type 2 diabetes and seven glycemic traits with four muscle mass- and function-related phenotypes and the frailty index.
Results: We first identified 27 pairs with significant genetic correlations through the linkage disequilibrium score regression and high-definition likelihood analysis.
J Neuroinflammation
December 2024
Department of Neurosurgery, Stanford University School of Medicine, 1050 Arastradero Road, Building A, Palo Alto, Stanford, CA, 94304, United States of America.
Norepinephrine (NE) modulates cognitive function, arousal, attention, and responses to novelty and stress, and it also regulates neuroinflammation. We previously demonstrated behavioral and immunomodulatory effects of beta-adrenergic pharmacology in mouse models of Alzheimer's disease (AD). The current studies were designed to block noradrenergic signaling in 5XFAD mice through (1) chemogenetic inhibition of the locus coeruleus (LC), (2) pharmacologic blocking of β-adrenergic receptors, and (3) conditional deletion of β1- or β2-adrenergic receptors (adrb1 or adrb2) in microglia.
View Article and Find Full Text PDFFront Immunol
December 2024
Department of General Surgery, The First Medical Center, Chinese PLA General Hospital, Beijing, China.
Background: It has been reported that COVID-19 patients have an increased risk of developing IBS; however, the underlying genetic mechanisms of these associations remain largely unknown. The aim of this study was to investigate potential shared SNPs, genes, proteins, and biological pathways between COVID-19 and IBS by assessing pairwise genetic correlations and cross-trait genetic analysis.
Materials And Methods: We assessed the genetic correlation between three COVID-19 phenotypes and IBS using linkage disequilibrium score regression (LDSC) and high-definition likelihood (HDL) methods.
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