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Cracking susceptibility of full-sibs of a cross of a cracking tolerant and cracking susceptible sweet cherry: Relation to cuticle characteristics, microcracking and calcium.
PLoS One
January 2025
INRAE, Biologie du Fruit et Pathologie, Université de Bordeaux, UMR 1332, Villenave d'Ornon, France.
Rain cracking compromises quality and quantity of sweet cherries worldwide. Cracking susceptibility differs among genotypes. The objective was to (1) phenotype the progeny of a cross between a tolerant and a susceptible sweet cherry cultivar for cuticle mass per unit area, strain release on cuticle isolation, cuticular microcracking and calcium/dry mass ratio and (2) relate these characteristics to cracking susceptibilities evaluated in laboratory immersion assays and published multiyear field observations.
View Article and Find Full Text PDFSmall RNA sequencing analysis provides novel insights into microRNA-mediated regulation of defense responses in chickpea against Fusarium wilt infection.
Planta
January 2025
ICAR-National Institute for Plant Biotechnology, New Delhi, 110012, Delhi, India.
Small RNA sequencing analysis in two chickpea genotypes, JG 62 (Fusarium wilt-susceptible) and WR 315 (Fusarium wilt-resistant), under Fusarium wilt stress led to identification of 544 miRNAs which included 406 known and 138 novel miRNAs. A total of 115 miRNAs showed differential expression in both the genotypes across different combinations. A miRNA, Car-miR398 targeted copper chaperone for superoxide dismutase (CCS) that, in turn, regulated superoxide dismutase (SOD) activity during chickpea-Foc interaction.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Washington University School of Medicine, Saint Louis, MO, USA.
Background: The recent European-ancestry based genome-wide association study (GWAS) of Alzheimer disease (AD) by Bellenguez2022 has identified 75 significant genetic loci, but only a few have been functionally mapped to effector gene level. Besides the large-scale RNA expression, protein and metabolite levels are key molecular traits bridging the genetic variants to AD risk, and thus we decided to integrate them into the genetic analysis to pinpoint key proteins and metabolites underlying AD etiology. Few studies have generated more than one layer of post-transcriptional phenotypes, limiting the scale of biological translation of disease modifying treatments.
View Article and Find Full Text PDFComplex genetic interactions affect susceptibility to Alzheimer's disease risk in the BIN1 and MS4A6A loci.
Geroscience
January 2025
Biodemography of Aging Research Unit, Social Science Research Institute, Duke University, Erwin Mill Building, 2024 W. Main St, Durham, NC, 27705, USA.
Genetics is the second strongest risk factor for Alzheimer's disease (AD) after age. More than 70 loci have been implicated in AD susceptibility so far, and the genetic architecture of AD entails both additive and nonadditive contributions from these loci. To better understand nonadditive impact of single-nucleotide polymorphisms (SNPs) on AD risk, we examined individual, joint, and interacting (SNPxSNP) effects of 139 and 66 SNPs mapped to the BIN1 and MS4A6A AD-associated loci, respectively.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Laboratory of Neurobiology, Department of Neurology, Poznan, Poland.
Background: Alzheimer's disease (AD) is characterized by an acquired, progressive impairment of cognitive functions. The pathogenesis of this disease remains unknown. It is explained based on the following theories: amyloid cascade, inflammation, vascular, and infection hypothesis.
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