The release of mitochondrial genome sequences provides the basis for characterizing interspecific and intraspecific variation in Brassica mitochondrial genomes.However,few B.juncea(mustard)mitochondrial genomes have b...The release of mitochondrial genome sequences provides the basis for characterizing interspecific and intraspecific variation in Brassica mitochondrial genomes.However,few B.juncea(mustard)mitochondrial genomes have been published.We assembled the mitochondrial genomes of three B.juncea subspecies and compared them with previously published genomes.The genomes were phylogenetically classified into A,B,C,and Bna clades.Two variant sites,a transversion(C→A)at nt 79,573 and a 31-bp copy-number variation between nts 65,564 and 65,596,were identified.Based on these variant sites,mitotype-specific sequence markers were developed to characterize the variation among worldwide 558 B.juncea accessions.Three mitochondrial genome types(mitotypes MT1–MT3)were identified.In terms of geographical distribution,MT1 and MT2 accessions were distributed mainly to the north and MT3 to the south of 34°N.Root mustards carried only MT1,leaf and stem mustards carried mainly MT3,and seed mustards carried all three mitotypes,implying that the mitotypes underwent selection during B.juncea domestication.A new form of oil mustard evolved by hybridization between two gene pools in southwest China.展开更多
Neurodegenerative disorders are typically“split”based on their hallmark clinical,anatomical,and pathological features,but they can also be“lumped”by a shared feature of impaired mitochondrial biology.This leads us...Neurodegenerative disorders are typically“split”based on their hallmark clinical,anatomical,and pathological features,but they can also be“lumped”by a shared feature of impaired mitochondrial biology.This leads us to present a scientific framework that conceptualizes Alzheimer’s disease(AD),Parkinson’s disease(PD),amyotrophic lateral sclerosis(ALS),and Huntington’s disease(HD)as“metabolic icebergs”comprised of a tip,a bulk,and a base.The visible tip conveys the hallmark neurological symptoms,neurodegenerative regions,and neuronal protein aggregates for each disorder.The hidden bulk depicts impaired mitochondrial biology throughout the body,which is multifaceted and may be subdivided into impaired cellular metabolism,cell-specific mitotypes,and mitochondrial behaviours,functions,activities,and features.The underlying base encompasses environmental factors,especially modern industrial toxins,dietary lifestyles,and cognitive,physical,and psychosocial behaviours,but also accommodates genetic factors specific to familial forms of AD,PD,and ALS,as well as HD.Over years or decades,chronic exposure to a particular suite of environmental and genetic factors at the base elicits a trajectory of impaired mitochondrial biology that maximally impacts particular subsets of mitotypes in the bulk,which eventually surfaces as the hallmark features of a particular neurodegenerative disorder at the tip.We propose that impaired mitochondrial biology can be repaired and recalibrated by activating“mitohormesis”,which is optimally achieved using strategies that facilitate a balanced oscillation between mitochondrial stressor and recovery phases.Sustainably harnessing mitohormesis may constitute a potent preventative and therapeutic measure for people at risk of,or suffering with,neurodegenerative disorders.展开更多
基金China Agriculture Research System(CARS-12)National Natural Science Foundation of China(U20A2029)。
文摘The release of mitochondrial genome sequences provides the basis for characterizing interspecific and intraspecific variation in Brassica mitochondrial genomes.However,few B.juncea(mustard)mitochondrial genomes have been published.We assembled the mitochondrial genomes of three B.juncea subspecies and compared them with previously published genomes.The genomes were phylogenetically classified into A,B,C,and Bna clades.Two variant sites,a transversion(C→A)at nt 79,573 and a 31-bp copy-number variation between nts 65,564 and 65,596,were identified.Based on these variant sites,mitotype-specific sequence markers were developed to characterize the variation among worldwide 558 B.juncea accessions.Three mitochondrial genome types(mitotypes MT1–MT3)were identified.In terms of geographical distribution,MT1 and MT2 accessions were distributed mainly to the north and MT3 to the south of 34°N.Root mustards carried only MT1,leaf and stem mustards carried mainly MT3,and seed mustards carried all three mitotypes,implying that the mitotypes underwent selection during B.juncea domestication.A new form of oil mustard evolved by hybridization between two gene pools in southwest China.
文摘Neurodegenerative disorders are typically“split”based on their hallmark clinical,anatomical,and pathological features,but they can also be“lumped”by a shared feature of impaired mitochondrial biology.This leads us to present a scientific framework that conceptualizes Alzheimer’s disease(AD),Parkinson’s disease(PD),amyotrophic lateral sclerosis(ALS),and Huntington’s disease(HD)as“metabolic icebergs”comprised of a tip,a bulk,and a base.The visible tip conveys the hallmark neurological symptoms,neurodegenerative regions,and neuronal protein aggregates for each disorder.The hidden bulk depicts impaired mitochondrial biology throughout the body,which is multifaceted and may be subdivided into impaired cellular metabolism,cell-specific mitotypes,and mitochondrial behaviours,functions,activities,and features.The underlying base encompasses environmental factors,especially modern industrial toxins,dietary lifestyles,and cognitive,physical,and psychosocial behaviours,but also accommodates genetic factors specific to familial forms of AD,PD,and ALS,as well as HD.Over years or decades,chronic exposure to a particular suite of environmental and genetic factors at the base elicits a trajectory of impaired mitochondrial biology that maximally impacts particular subsets of mitotypes in the bulk,which eventually surfaces as the hallmark features of a particular neurodegenerative disorder at the tip.We propose that impaired mitochondrial biology can be repaired and recalibrated by activating“mitohormesis”,which is optimally achieved using strategies that facilitate a balanced oscillation between mitochondrial stressor and recovery phases.Sustainably harnessing mitohormesis may constitute a potent preventative and therapeutic measure for people at risk of,or suffering with,neurodegenerative disorders.
