Southern corn rust is one of destructive diseases in maize caused by Puccinia polysora Undrew. A mapping population of tropical sweet corn recombinant inbred lines (RILs) derived from a cross between hA9104 and hA9035...Southern corn rust is one of destructive diseases in maize caused by Puccinia polysora Undrew. A mapping population of tropical sweet corn recombinant inbred lines (RILs) derived from a cross between hA9104 and hA9035 inbred lines were set up to detect quantitative trait loci (QTLs) involved in partial resistance to southern corn rust. Eighty nine RILs were used to evaluate resistance levels using nine-point relative scale (1-9) at Sweet Seeds, Suwan Farm, Thailand include combined analysis. A genetic linkage map was constructed with 157 SSR markers, with a total length of 2123.1 cM, covering 10 chromosomes. Broad-sense heritability of individual location ranged from 0.76 and 0.82 and combined across locations was 0.87. Multiple QTL mapping (MQM) was applied for the identification of the QTLs. Fifteen QTLs were detected on chromosome 1, 2, 5, 6, 9 and 10 in both locations and combined across locations. QTLs on chromosome 1, 5 and 6 were contributed by alleles of resistant parent hA9104 while others were contributed by alleles from the susceptible parent, hA9035. Phenotypic variance of each QTL explained ranged from 6.1% to 41.8% with a total of 69.8% - 81.9%. QTL on chromosome 1, 6 and 10 were stable QTLs detected in both locations.展开更多
Background:Transmembrane 4 L six family member 5(TM4SF5)translocates subcellularly and functions metabolically,although it is unclear how intracellu-lar TM4SF5 translocation is linked to metabolic contexts.It is thus ...Background:Transmembrane 4 L six family member 5(TM4SF5)translocates subcellularly and functions metabolically,although it is unclear how intracellu-lar TM4SF5 translocation is linked to metabolic contexts.It is thus of interests to understand how the traffic dynamics of TM4SF5 to subcellular endosomal membranes are correlated to regulatory roles of metabolisms.Methods:Here,we explored the metabolic significance of TM4SF5 localization at mitochondria-lysosome contact sites(MLCSs),using in vitro cells and in vivo animal systems,via approaches by immunofluorescence,proximity labelling based proteomics analysis,organelle reconstitution etc.Results:Upon extracellular glucose repletion following depletion,TM4SF5 became enriched at MLCSs via an interaction between mitochondrial FK506-binding protein 8(FKBP8)and lysosomal TM4SF5.Proximity labeling showed molecular clustering of phospho-dynamic-related protein I(DRP1)and certain mitophagy receptors at TM4SF5-enriched MLCSs,leading to mitochondrial fis-sion and autophagy.TM4SF5 bound NPC intracellular cholesterol transporter 1(NPC1)and free cholesterol,and mediated export of lysosomal cholesterol to mitochondria,leading to impaired oxidative phosphorylation but intact tri-carboxylic acid(TCA)cycle andβ-oxidation.In mouse models,hepatocyte Tm4sf5 promoted mitophagy and cholesterol transport to mitochondria,both with positive relations to liver malignancy.Conclusions:Our findings suggested that TM4SF5-enriched MLCSs regu-late glucose catabolism by facilitating cholesterol export for mitochondrial reprogramming,presumably while hepatocellular carcinogenesis,recapitulating aspects for hepatocellular carcinoma metabolism with mitochondrial repro-gramming to support biomolecule synthesis in addition to glycolytic energetics.展开更多
文摘Southern corn rust is one of destructive diseases in maize caused by Puccinia polysora Undrew. A mapping population of tropical sweet corn recombinant inbred lines (RILs) derived from a cross between hA9104 and hA9035 inbred lines were set up to detect quantitative trait loci (QTLs) involved in partial resistance to southern corn rust. Eighty nine RILs were used to evaluate resistance levels using nine-point relative scale (1-9) at Sweet Seeds, Suwan Farm, Thailand include combined analysis. A genetic linkage map was constructed with 157 SSR markers, with a total length of 2123.1 cM, covering 10 chromosomes. Broad-sense heritability of individual location ranged from 0.76 and 0.82 and combined across locations was 0.87. Multiple QTL mapping (MQM) was applied for the identification of the QTLs. Fifteen QTLs were detected on chromosome 1, 2, 5, 6, 9 and 10 in both locations and combined across locations. QTLs on chromosome 1, 5 and 6 were contributed by alleles of resistant parent hA9104 while others were contributed by alleles from the susceptible parent, hA9035. Phenotypic variance of each QTL explained ranged from 6.1% to 41.8% with a total of 69.8% - 81.9%. QTL on chromosome 1, 6 and 10 were stable QTLs detected in both locations.
基金This work was supported by Basic Science Research Pro-gram through the National Research Foundation of Korea(NRF)funded by the Ministry of Science,ICT&Future Planning(NRF-2021R1A6A3A01087300 to JEK,NRF-2021M3H9A2098553 to YL,NRF-2022M3E5F3080873 to SC,NRF-2022R1A4A1018900 to LKH,NRF-2020R1A2C3008993,and NRF-2021M3A9D3024752 to JWL).
文摘Background:Transmembrane 4 L six family member 5(TM4SF5)translocates subcellularly and functions metabolically,although it is unclear how intracellu-lar TM4SF5 translocation is linked to metabolic contexts.It is thus of interests to understand how the traffic dynamics of TM4SF5 to subcellular endosomal membranes are correlated to regulatory roles of metabolisms.Methods:Here,we explored the metabolic significance of TM4SF5 localization at mitochondria-lysosome contact sites(MLCSs),using in vitro cells and in vivo animal systems,via approaches by immunofluorescence,proximity labelling based proteomics analysis,organelle reconstitution etc.Results:Upon extracellular glucose repletion following depletion,TM4SF5 became enriched at MLCSs via an interaction between mitochondrial FK506-binding protein 8(FKBP8)and lysosomal TM4SF5.Proximity labeling showed molecular clustering of phospho-dynamic-related protein I(DRP1)and certain mitophagy receptors at TM4SF5-enriched MLCSs,leading to mitochondrial fis-sion and autophagy.TM4SF5 bound NPC intracellular cholesterol transporter 1(NPC1)and free cholesterol,and mediated export of lysosomal cholesterol to mitochondria,leading to impaired oxidative phosphorylation but intact tri-carboxylic acid(TCA)cycle andβ-oxidation.In mouse models,hepatocyte Tm4sf5 promoted mitophagy and cholesterol transport to mitochondria,both with positive relations to liver malignancy.Conclusions:Our findings suggested that TM4SF5-enriched MLCSs regu-late glucose catabolism by facilitating cholesterol export for mitochondrial reprogramming,presumably while hepatocellular carcinogenesis,recapitulating aspects for hepatocellular carcinoma metabolism with mitochondrial repro-gramming to support biomolecule synthesis in addition to glycolytic energetics.
