Sclerotinia stem rot,caused by Sclerotinia sclerotiorum,is a destructive soil-borne disease leading to huge yield loss.We previously reported that Klebsiella variicola FH-1 could degrade atrazine herbicides,and the ve...Sclerotinia stem rot,caused by Sclerotinia sclerotiorum,is a destructive soil-borne disease leading to huge yield loss.We previously reported that Klebsiella variicola FH-1 could degrade atrazine herbicides,and the vegetative growth of atrazine-sensitive crops(i.e.,soybean)was significantly increased in the FH-1-treated soil.Interestingly,we found that FH-1 could promote soybean growth and induce resistance to S.sclerotiorum.In our study,strain FH-1 could grow in a nitrogen-free environment,dissolve inorganic phosphorus and potassium,and produce indoleacetic acid and a siderophore.The results of pot experiments showed that K.variicola FH-1 promoted soybean plant development,substantially improving plant height,fresh weight,and root length,and induced resistance against S.sclerotiorum infection in soybean leaves.The area under the disease progression curve(AUDPC)for treatment with strain FH-1 was significantly lower than the control and was reduced by up to 42.2%within 48 h(P<0.001).Moreover,strain FH-1 rcovered the activities of catalase,superoxide dismutase,peroxidase,phenylalanine ammonia lyase,and polyphenol oxidase,which are involved in plant protection,and reduced malondialdehyde accumulation in the leaves.The mechanism of induction of resistance appeared to be primarily resulted from the enhancement of transcript levels of PR10,PR12,AOS,CHS,and PDF1.2 genes.The colonization of FH-1 on soybean root,determined using CLSM and SEM,revealed that FH-1 colonized soybean root surfaces,root hairs,and exodermis to form biofilms.In summary,K.variicola FH-1 exhibited the biological control potential by inducing resistance in soybean against S.sclerotiorum infection,providing new suggestions for green prevention and control.展开更多
家族性高胆固醇血症(familial hypercholesterolemia,FH)的临床特征为血总胆固醇升高,尤其是低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-c)升高,沉积于组织,形成皮肤或肌腱黄色瘤,导致动脉粥样硬化甚至早发冠心病。F...家族性高胆固醇血症(familial hypercholesterolemia,FH)的临床特征为血总胆固醇升高,尤其是低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-c)升高,沉积于组织,形成皮肤或肌腱黄色瘤,导致动脉粥样硬化甚至早发冠心病。FH的发病机制为LDL受体(LDL receptor,LDLR)或apoB基因突变引起LDL受体途径功能缺陷,主要为常染色体显性遗传疾患,具有基因剂量效应;部分患者为常染色体隐性遗传,机制为LDL受体衔接蛋白1(LDL receptor adaptor protein 1,LDLRAP1)失功能型突变,导致LDL内化活性降低。罕见的人类枯草溶菌素转化酶9(proprotein convertase subtilisin/kexin type 9,PCSK9)发生功能型突变也可引起严重的FH表型。PCSK9通过降解LDLR蛋白间接下调LDL受体途径,其失功能突变可致血浆LDL水平下降。因此PCSK9是目前降脂药物的研究热点。展开更多
基金financially supported by the grants from the Inter-governmental International Cooperation Special Project of National Key R&D Program of China(2019YFE0114200)the Natural Science Foundation Project of Science and Technology Department of Jilin Province,China(20200201215JC).
文摘Sclerotinia stem rot,caused by Sclerotinia sclerotiorum,is a destructive soil-borne disease leading to huge yield loss.We previously reported that Klebsiella variicola FH-1 could degrade atrazine herbicides,and the vegetative growth of atrazine-sensitive crops(i.e.,soybean)was significantly increased in the FH-1-treated soil.Interestingly,we found that FH-1 could promote soybean growth and induce resistance to S.sclerotiorum.In our study,strain FH-1 could grow in a nitrogen-free environment,dissolve inorganic phosphorus and potassium,and produce indoleacetic acid and a siderophore.The results of pot experiments showed that K.variicola FH-1 promoted soybean plant development,substantially improving plant height,fresh weight,and root length,and induced resistance against S.sclerotiorum infection in soybean leaves.The area under the disease progression curve(AUDPC)for treatment with strain FH-1 was significantly lower than the control and was reduced by up to 42.2%within 48 h(P<0.001).Moreover,strain FH-1 rcovered the activities of catalase,superoxide dismutase,peroxidase,phenylalanine ammonia lyase,and polyphenol oxidase,which are involved in plant protection,and reduced malondialdehyde accumulation in the leaves.The mechanism of induction of resistance appeared to be primarily resulted from the enhancement of transcript levels of PR10,PR12,AOS,CHS,and PDF1.2 genes.The colonization of FH-1 on soybean root,determined using CLSM and SEM,revealed that FH-1 colonized soybean root surfaces,root hairs,and exodermis to form biofilms.In summary,K.variicola FH-1 exhibited the biological control potential by inducing resistance in soybean against S.sclerotiorum infection,providing new suggestions for green prevention and control.
文摘家族性高胆固醇血症(familial hypercholesterolemia,FH)的临床特征为血总胆固醇升高,尤其是低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-c)升高,沉积于组织,形成皮肤或肌腱黄色瘤,导致动脉粥样硬化甚至早发冠心病。FH的发病机制为LDL受体(LDL receptor,LDLR)或apoB基因突变引起LDL受体途径功能缺陷,主要为常染色体显性遗传疾患,具有基因剂量效应;部分患者为常染色体隐性遗传,机制为LDL受体衔接蛋白1(LDL receptor adaptor protein 1,LDLRAP1)失功能型突变,导致LDL内化活性降低。罕见的人类枯草溶菌素转化酶9(proprotein convertase subtilisin/kexin type 9,PCSK9)发生功能型突变也可引起严重的FH表型。PCSK9通过降解LDLR蛋白间接下调LDL受体途径,其失功能突变可致血浆LDL水平下降。因此PCSK9是目前降脂药物的研究热点。
