分子生物学课件第七章part1.ppt

单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,单击此处编辑母版标题样式,单击此处编辑母版文本版式,第二层,第三层,第四层,第五层,*,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,单击此处编辑母版标题样式,*,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,被,EULEC,识别的,N-end,aa,marker of targeting protein,Met,Gly,Ala,Ser,Thr,Val,20 hrs(,稳定因子,),Ile,Glu,30 (,不稳定因子,),Gln,10,Leu,Phe,Asn,Lys,3 (,极不稳定因子,),Arg,2,Pro,7,N-end aa of targeting protein halflife,-,决定与,Ubiquitin,发生,isopeptide bond,的难易程度,-,决定被,E3,识读结合难易程度,-N,端氨基酸种类对蛋白质寿命的决定性，从原核到,真核生物高度一致,泛素,/26S,蛋白酶体通路与,植物激素应答,植物抗病反应,植物光形态建成,高等植物有性生殖,植物环境胁迫抗性,Molecular Biology,Gibberellin Signaling Pathway,a de-repressible system,moderated by DELLA-p,degradation induced by GA,Green Revolution,第一次绿色革命；,粮食作物增产,20%,Norman E.Borlaug,Director of wheat program,(CIMMYT),1970 Nobel Peace Prize,Green Revolution Gene,Semi-dwarf rice cultivars containing rice G.R gene,sd1,Green Revolution Gene,Semi-dwarf maize cultivars containing the G.R gene,d8,Highly conserved in,G.R,.gene,Arabidopsis:,(,RGA,GAI,RGL1,RGL2,RGL3),maize:,(d8),wheat(Rht),rice:,(,SLR1,),barley(SLN1),grape:,(VvGAI1),Brassica rapa,(BrRGA1),phosphotyrosine binding domain,The DELLA subfamily of GRAS proteins,Choke back growth,A conserved and unique N-terminal domain,named DELLA,after a,DELLA motif,Wild type DELLA proteins,localize in cell nuclei,and,disappear by GA treatment,phosphotyrosine binding domain,DELLA,domain-mutated are resistant,(,G.R.gene,)to GA-induced degradation,(GA-insensitive),By using immunoblot analysis and GFP fusion protein analysis,it is shown that,GA induces rapid degradation of the wild type DELLA proteins,such as,GFP,-,At-,RGA,GFP,-Os-,SLR1,From Silverstone et al.,Plant Cell,2001,13:1555-1566,The disappearance of GFP-RGA protein on GA treatment,-GA,+GA,GFP-(rga-17)proteins are,resistant,to GA-induced degradation,+H,2,O,+GA,3,(,rga-17,has the same,17AA deletion in the DELLA region,as in,gai-1,),GFP-RGA,GFP-(rga-17),GFP-(rga-17),From Dill et al.,Proc Natl Acad Sci USA,2001,98:14162-14167,Scheme of the functional domains of SLR1 for GA signaling pathway,Poly S/T/V,From Itoh et al.,Plant Cell,2002,14:57-70,A model of GA induced degradation of DELLA proteins,via,E3 ubiquitin ligase enzyme complex(EULEC),From Itoh et al.,Trends Plant Sci,2003,8:492-497,DELLA,DELLA,Involvement of the ubiquitin-proteasome pathway in degradation of DELLA proteins,In response to GA,DELLA proteins are rapidly degraded by the ubiquitin-proteasome pathway,Ubiquitylating enzyme E3 complex,Negative,G.R.,gene,？,),6.3.,真核生物基因表达与调控的特殊模式,以,positive control,为主的基因表达调控,真核生物染色质的状态对基因表达的调控,m,5,C,与基因表达的相关,转录后多种方式的加工调节,个体发育的阶段调控,真核生物基因表达调控的特异性,6.3.1.mRNA,的结构对翻译水平的调控,Leading seq.(5-Untranslation region,UTR),Cap,具有增译作用,Cap+poly(A),具有增译的协同效应,Cap,对,eIF4b,的相对浓度的选择,Shatkin(1976),-m,7,GpppN(Cap),-AUG flanked seq.effect,5 L.S,存在,AUG,对第一个,AUG,密码的起译产生负控效应,5-AUG-,AUG,-NNN-,L.S,错误起译,改变读框,降低速率,Effect of multiple replicas of the translation initiation site,immunoprecipitatd proinsulin-containing polypeptides,the farthest upstream AUG codon was used which,is again consistent with the scanning model,Kozak(1987),699,种脊椎动物，植物，酵母和原生动物,-,A,-3,NNAUG,G,+4,-,具有促译性，普遍性,A,-3,CC,AUG,G,+4,也是核糖体小亚基对翻译密码的扫描信号,-AUG flanked consensus seq(-3A,+4G),Kozak model,Kozak(1986),Rat pre,proinsulin,gene under the control of,SV40 promoter,mutagenized,Nt,at-3 and+4 position,introduction them into monkey cell,Effects of single base changes in positions,-3(A)and+4(G),Rat preproinsulin gene under the control of an an SV40 promoter,Kozak Cell 44(31)Jan 1986,mutation,mutation,Kozak model,35S-Met,-5UTR,二级结构的影响,5,端高度结构化的,mRNA,是核糖体进入的位点并通过富集核糖体和起始因子促进基因的表达,Hairpin(Stem-loop),顺式阻扼,40s subunit of ribosome,迁移,G/C,多，阻扼强,G/C,近,AUG,阻扼强,cap,C,hloramphenicol,A,cetyl,T,ransferase,氯霉素乙酰转移酶,Higher stability,62,kca/mol,lower stability,30,kca/mol,1)30-kcal stem loop only 12 nt downstream of the cap strongly inhibits translation,because it interferes with binding of the 40S ribosome and factors at the cap.,2)62-kcal stem loop placed 71 nt downstream of the cap completely blocked,appearance of the CAT protein.,Why?,6.3.2,染色质重建对基因表达的控制,表观遗传及其分子机制,Epigenetic and Molecular Mechanism,Epigenetic inheritence:,The ability of different states,which may have different phenotype consequences,to be inherited without any change in the DNA sequence.,在,DNA,序列没有发生任何改变的情况下，不同表型效应具有可以遗传的能力,（,Ww in euchromatin,）,w,Ww Red eye,（,W (near heterochromatin)be silenced,W,w,Ww white eye,Position effect of variegation in Drosophila eyes,Epigenetic phenomena,Spot eye,Cellular Memory:,Arabidopsis Vernalization,Epigenetic phenomena,One X chromosome is,inactived at random,parental imprinting,B,C,D,A,Allelic interaction(paramutation),-Position-effect variegation,-Inactivation of chromosome X,-Cell-type conversion,-Allelic interaction(paramutation),-Transgene silencing,-Parental imprinting,Cell memory:Vernalization,Heterosis,！？,Epigenetic phenomena,染色质结构的调整,核小体的松弛,组蛋白的乙酰化,组蛋白的甲基化,沉默子,.,染色质重建,Chromatin Remodeling,Epigenetic and Molecular Mechanism,Basic unit of chromatin,Nucleosome(-body,200bp,),Histone 1+linker DNA of,20-60bp,(,diff.From diff.creature,),2 H,2A,H,2B,H,3,H,4,Octamer+core DNA of,146 bp,1.75 cycle,6.3.2.1,染色质结构,6nm,11nm,30 nm,10nm fibre,Heterochromatin,Euchromatin,组蛋白中富含,Lys,+,Arg.,+,量大，进化保守，与,DNA,无专一性结合区,N,端外露,Arg,与,DNA14,个小沟结合,富含,Lys,的,N,端（特别是,H4,）能保证,Histone,间的稳定性和与,DNA,的结合,N,端磷酸化、乙酰化等能,降低组蛋白正电荷,，使组蛋白间以及与,DNA,的结合状态发生,松弛,Histone acetyltransferase(HAT),Histone deacetylase(HDAC),Histone methyltransferase(HMT),Lys,Arg,Lys,Ser,Lys,Histone Codon,Histone code,组蛋白一个位点的修饰可以激活或抑制另一个位点的修饰，这种信号的组合可以寓意染色质的类型与性质。这种组合也被称为组蛋白密码,6.3.2.2 chromatin,状况与基因表达相关,Euchromatin,gene on,Heterochromatin,gene off,Heterochromatin,；,Constitutive Heterochromatin:,组成型异染色质,除,DNA,复制以外，一直处于高度致密的固缩状态，,DNA,从不转录（高度重复序列，着丝点，端粒等）,Facultative Heterochromatin:,特异型异染色质,有时处于异染色质状态，有时为常染色质状态,转录活化区,/,非,转录活化区,chromatin,的结构差异,DNase,S,Nucleosome,incomplete,No Histone,1,in linker DNA,in transcriptional activated region,表达非常活跃的,rDNA,区,无,核小体,结构,凡被,Trans-factor,结合的区域,均能阻止,nucleosome,再形成,H,2A,、,H,2B,、,H,3,、,H,4,acetylated,降低组蛋白的正电荷,组蛋白解聚,-body,松弛,80%H,3,H,4,乙酰化,丁酸钠,（,去乙酰化酶,抑制剂,）,Hela cell,基因高效表达,Pazin,Kadonaga,1997 Cell.89:325-328,从酵母中分离出,组蛋白,去乙酰化酶,A,B,以及相应的催化组分,HDAC1,RPD3,HDAC1,RPD3,基因突变导致,H3/H4,超乙酰化,引起基因高效表达,Over acetylation,Model for,participation of histone deacetylase in transcription repression,histone deacetylase cooperator HDAC1,Nucleosome relaxed,Nucleosome reconstructed,Histone methylation causes,inactive chromatin,Heterochromatin protein 1,分离得到与甲基化,DNA,结合,抑制转录的,MeCP2,Jones P.L.1998.,Methylated DNA and MeCP2 recurit histone deacetylase to repress transcription.,Nature Genet,.19:187-191,组蛋白去乙酰化酶,A(dHAT-A),dHAT-A,的催化因子,(SIN3),MeCP2(m,5,C,结合蛋白,),complex,MeCP2,SIN3,dHAT-A,MeCP2,与,m,5,C,结合阻止,TFII,与,DNA,结合,Histone,去乙酰化作用,重建核小体,抑制基因表达,Histone methylation causes,inactive chromatin,Heterochromatin protein 1,HP1 may propagate heterochromatin,Inactive Chromatin,6.3.2.3.m,5,C,对基因表达的调控,a)m,5,C,是真核生物,DNA,中的主要修饰成分,多发生在,CpG,序列中,不同细胞间,m,5,C,相差甚大,胚胎细胞与特化体细胞相差,10,6,b)m,5,C,对基因转录抑制的表现,DNA,大沟内的,m,5,C,影响与,T.F.,间氢键的形成,DNA,大沟内的,m,5,C,导致空间拥挤,破坏构象的平衡,使,B-DNA,Z-DNA,T.F.,结合空间的改变,染色质重建,降低转录因子与,DNA,的结合,Genome and gene imprint,in Eukaryots,一定组织和细胞中，某些基因在,DNA,水平上的表达程度及表达时空受到一种“后成修饰，表观修饰”（,epigenetic modification,相同的,DNA,结构，不同的表型,）机制控制。使仅来自双亲中某一亲本的基因得以表达。这一现象也称为“基因组印记”,DNA,的甲基化、异染色质化是“,imprint”,的重要机制,染色体,区域性印记中,相邻印记基因具有“相反”的印记作用模式,父本基因印记,母本基因印记,合子及幼胚期，,DNA,去,甲基化程度高，,gene,imprint,被抑制,，表现了细胞的“全能性”,Genome/gene imprint,表现的特点,Genome imprint,具有染色体,区域性或整体性,印记现象具有组织细胞的特异性,基因印记的发生常与该基因的编码区，,启动子区及其上下游的,CpG,序列甲基化相关,Genome/gene imprint,表现的特点,印记效应会因,去甲基化而消失,(,水稻白叶枯病成株抗性？,),One X chromosome is,inactived at random,Two X chro.Euchromatin in 16 day precursor cell,One X chro.inactived at random,Variegation,Prader-willi,症,(PWS),：肌肉无力、矮小、神经疾病,Argelmen,症（,Ag,）：平衡性差、过分兴奋与发笑,共同的病因：,15q11-q13,缺失，基因型相同,子女的,父 父,染色体,母 母,病症：,Ag PWS,母本基因印记,父本基因印记,被,异染色质化,的,X,染色体,常染色质化,导致雌性哺乳动物宫颈癌，胃癌,双重遗传病因：缺失,/,印记,3 types of modification affect chromatin,甲基化的,CpG,序列可招募组蛋白去乙酰化酶，抑制基因的表达。,Vernalisation,植物低温春化现象的分子机理,After,Vernalization FLC Leafy MADS Flowering,FLC methylation,N,5,-C,的春化效应,Without,Vernalization FLC Leafy MADS Flowering,低温春化处理消除对,MADS Box,基因表达的负控制效应,Vernalization,低温春化,引起脱乙酰化、甲基化修饰,导致异染色质化,Regulation of the,floral repressor,FLC by histone deacetylation(FLD),yes,No,No,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,AC,mut.,-Chromatin structureand remodeling,-DNA methylation,-Histone modification(Ac&Me),-Relationship between DNA,Me,and Histone,Me,-Creation of repressive domain,-,ncRNA,-Heterochromatin formation,Chromatin modification&remodeling,as the epigenetic basis,No-coding RNA ncRNA,看家,RNA,rRNA,，,tRNA,，,UsnRNA,，,telomere RNA.,调节,RNA,microRNA,（,miRNA,），,siRNA,，,anti-sense RNA.,What is microRNA?,MicroRNAs are a newly identified class of small single-stranded non-coding RNAs;,MicroRNAs regulate their target genes via two main mechanisms:,target mRNA cleavage,translational repression,.,The characters of miRNA,Length:18-25 nt;,Single-strand;,Conserved among species;,Encoded by internal DNA sequences,which are located in the whole genome,mostly in the interval regions of coding genes,centromeres,or,occasionally in the introns;,Temporally and tissue-specifically expressed,The biogenesis of miRNA,Review:Geogre S Mack,Nature Biotech.,2007,dsRNA,由,Dicer,加工成,21Nt,siRNA,，在,RDRP,的作用下可以扩增，,siRNA,与靶,mRNA,来源与同一基因,60,100nt,，,3,具有,2Nt,突起茎环结构的,pre,miRNA,，由,Dicer,加工成一条双链的,21,miRNA,，与靶,mRNA,来自不同的基因,siRNA,miRNA,来源于,mRNA,，病毒,RNA,，转座子，外源,RNA,来源于基因组内的,microDNA,、剪切的,intron.,（内源性）,与靶基因可不完全配对，,因此可调控若干不同的基因,在近缘物种间具有较高的保守性,与靶基因完全配对，专一性强,不同内源,siRNA,具有较大的差异,与,mRNA,结合，,或,剪切,mRNA,，抑制翻译，沉默基因表达,(,特别是转录因子,),。进入,RISC,体系，在转录后水平上沉默基因表达,进入,RISC,体系降解靶,mRNA,，转录后水平上沉默基因表达，,RNAi works by generating siRNA,Dicer,RISC,置换,Lin14,蛋白调节秀丽新线虫的幼虫发育，但受,lin4,基因的控制,Lin4,编码,22Nt,的,microRNA,与,Lin14mRNA3,端非翻译区出现,7,次重复的,10Nt,序列互补,，抑制,Lin14,蛋白的翻译,common mechanism for microRNA,RNAi and heterochromatin formation,6.3.4.2.Programmed Cell Death(PCD),and development,2002 Nobel Prize,John Sulston,USA,Sydney Brenner,Japan,田中 耕一,H.Robert Horvitz,Switzerland,细胞的“生”,发育、分裂、繁殖、分化、成熟,细胞的“死”,.?,-,高等生物的诞生,发育,成长,死亡,即,寿命,是生物固有的特征,-,死亡是生物体不可缺少的生命内容,是生物借以存活的需要,并贯穿寿命的全部周期中,PCD gene,的发现与克隆,人类长寿,癌症发生,提高产量,-,细胞死亡的发生及过程是在长期进化中已形,成的遗传程序（,PCD,）,这一程序表达的失控,个体发育受阻、病变、畸形、蹼趾、有尾,.,癌症（白血病）,-,细胞周期变短,增殖过快,pcd,失控,细胞死亡速率变低,细胞增殖与细胞死亡平衡失调,癌症的发生,-,皮肤,指,(,趾,),甲,(,细胞从有生命经,PCD,向无生命的转化,),pcd,无皮，无鳞，无爪,失去保护与防御功能,-pcd,白细胞不分化，不死亡，不代换,41,天,51,天,在细胞自身遗传程序的控制下，有关基因的正常表达，细胞裂解成,apoptotic bodies,逐渐死亡的现象,a)PCD,的概念,细胞的死亡；,necrosis(accidental cell death),坏死,外因,细胞急速死亡，病变死亡,Programmed Cell Death(PCD),或,Apoptosis,凋亡,细胞程序性死亡,Apoptosis,细胞变园变小,与邻近细胞脱离,胞浆浓缩,染色质凝集成月牙状,内质网扩张成泡状,并与膜融合,PCD,的,细胞学特征,膜内陷，细胞呈沸腾运动，,细胞自行解体成若干有膜包围，,内容物不外溢的凋亡小体,被巨噬细胞吞噬,核内,DNA,被核酸酶,在核小体单位间降解,电泳检测呈,ladder of 180-200bp,apoptotic bodies,Apoptosis:,active cell death;,cell suicide,Necrosis:,accidental cell death;,cell murder,images of nuclei from apoptotic and necrotic cells,促进,PCD,的基因,Ces(cell death specification),细胞凋亡特异基因,p53,抑癌基因,Caspase,（半胱氨酸酶家族，蛋白降解途径）,.,抑制,PCD,的基因,LAP(inhibitor of apoptosis),凋亡抑制剂基因,Cystatin.,b),与,PCD,相关的基因,Caspase,p53 pathway,cystatin,BI-1,植物的,PCD,表现与机制,植物抗病的过敏性反应,Hypersensitive Response,PCD,枯斑的形成,花药的发育（,CMS,？）,木质部的分化,绒毡层的退化,禾本科植物胚乳的发育,缺氧条件下诱导的玉米根部通气组织的形成与根冠的形成,具有与动物细胞相似的,细胞学表型与生化特征,植物,PCD,的相关基因与机制,半胱氨酸酶家族（,Caspase,）,衰老叶片，果实，花器发育中木质部的形成,Caspase,乙烯在,PCD,中起重要作用,缺氧条件下，乙烯诱导玉米根部胞内,Ca,+,增加,气生组织的形成,小麦胚乳形成中，乙烯调节,DNA,降解,acd1,acd2,（,accelerated cell death,）,基因,Acd,负控制,Arabidopsis HR,诱导的,PCD,过程,-,植物抗病的,PCD,表现,Acd,(Accelerates Cell Death),Lsd,(Lesions Stimulating Disease Resistance),Programmed Cell Death,Neg.control,Constitutive,Pathogen,Plant,PCD,负调控关闭,PCD,系统表达,Oxidative burst,H,2,O,2,-OH,O,-2,2,升高,NADPHoxidase,Acd/Lsd repressor,失活,枯斑停止扩大,高浓度,H,2,O,2,消失,枯斑形成,限制病原物扩展,H,2,O,2,induced cytoplasm shrinkage,a typical marker of plant PCD.,在发育进程中，,PCD,何时启动？如何决定,某一细胞执行,PCD?,机体内是否存在真正杀手基因,（,killer gene,）,?,Killer,只在,PCD,细胞中表达！,其产物可使细胞走向死亡！,PCD,的信号，传递？,Prok.,与,Euk.,基因结构及表达的差异,Repetitive gene Overlapping gene,Retro-,transposon,Non-coding region(function?),Splitting gene,Eukaryote Prokaryote,DNA,，,RNA,protein,DNA+,histone,chromatin Naked DNA,and,chromatin Remodeling,Enhancer&Silencer,Attenuater,Monocistron,polycistron,(,operon,),m,5,C,gene off,acetylation,phosphorylation,mathylation,glucosylation,T.F,active form,Eukaryote Prokaryote,Post-transcription Transcription&translation,RNA processing Synchronizely,Housekeeping,gene(constitutive,),Basic promoter+T.F.,Luxury gene(inducible),多种组合的,Trans-Factor,Multiple gene family,Cluster gene,Quantitative Trait loci,Positive control,严谨性，专化性，复杂性,single gene,(cAMP+CAP)site+,UPE+pribnow box,单一类型,保险性,Negative control,Eukaryote Prokaryote,多细胞生物,单细胞生物,细胞分化,组织特化,个体发育,结构简单,遗传，代谢复杂,遗传，代谢简单,线粒体，叶绿体,质粒（,plasmid,）,Eukaryote Prokaryote,Cell,细胞膜,外界信息的感知与传递,细胞信号传递,细胞核,第,7,章,基因突变与交换,Gene Mutation,&,Crossing-Over,7.1.Point mutation,的类型,7.2.,突变发生的机理,7.3.,保证遗传稳定的机制,7.4.,基因重组交换的分子生物学,7.1.Point mutation,的类型,dNt insertion,or,deletion,Indel,=3,dNt,n,Amino acid,=3 dNt,Framshift,conversion(,取代,),transition(,转换,),Py Py,Pu Pu,transvertion(,颠换,),Py,Pu,conversion effect,-Samesense mut.,GA,A,(E)GA,G,(E),-Missense mut.,G,AA(E),A,AA(K),-Nonsense mut.,G,AA(E),T,AA(stop),南京大学,田大成等发现的遗传突变新,效应,Nature,，,doi:10.1038/nature07175,，,Dacheng Tian,，,Jian-Qun Chen,第一，基因组各区域的突变率很不相同，,Indel,的数量和密度,是度量,自发突变,发生位点的重要标准,；,第二，生物多样性的最初变异主要,源自,Indel,；,第三，自然选择在很大程度上是通过对,Indel,的选择而实现,;,突变的,表达,类型,-,获得突变型是遗传学研究的重要前提,-,非条件型突变；,allele in DNA level(,RFLP,RAPD,),allele in phenotype,(,红花,/,白花，糯,/,非糯,),条件型突变；,突变的表现,=,突变基因型,+,诱导条件,（,光，温敏感不育，,Ts,su,-,）,突变的,表达,类型,无效突变,Null mutation,：,完全消除了基因功能的突变（缺失）,功能丧失型突变（,loss-of-function mutation,）,无效突变或其他阻止基因功能的突变,功能获得型突变（,gain-of-function mutation,）,突变使蛋白质获得新的功能,沉默突变（,silent mutation,）,没有明显表型效应改变的突变,突变的,表达,类型,DNA level RAPD F1?,RFLP F1?,Protein level F1?,7.2.,突 变 发 生 的 机 理,(,自发突变，诱发突变,),7.2.1.,自发突变,7.2.1.1.,碱基异构式引起,DNA,复制过程的错误,a),碱基异构式,A(amino)A(imino),C(a)C(i),G(keto)G(enol),G(k),G(e,i),T(keto),T(enol-2)or T(enol-4),A(a),A(i),C(a),C(i),G(k),G(e),G(e,i),T(k),T(2e),T(4e),b),碱基异构式引起,DNA,复制的错配,碱基异构式引起,DNA,复制的错配,碱基异构式引起,DNA,复制的错配,A(a)T(k),G(k)C(a),正确配对,错误配对,G(k),T(e),A(a),C(i),A(i,anti)A(a,syn)A(i,anti)G(k,syn),G(e,i,anti)G(k,syn)G(e,i,anti)A(a,syn),A(i),C(a),G(e),T(k),C(i),A(a),T(k),A(a,anti),T(k,anti),C(a,anti),A(a),A(a,anti),碱基异构式引起,DNA,的错配突变,C(i),C(a),G(k,syn),G(k,syn),G(k,anti),G(k),7.1.2.3.,增变基因（,mutator gene,）,w.t.,维持遗传的稳定性,mut.,随机引起其他各类基因的突变,but be wronged,增变基因类别,DNA polymerase,相关基因,3,5 editing function mutation,错配修复系统的基因,MCE(mismatch correction enzyme),DNA,损伤修复系统基因,错配修复功能丧失 突变率升高,修复过程是基因突变的重要来源,7.1.2.4.,不对称交换,内源转座子,（,Retro-transposon,Helitron,）,Indel,7.2.2.,诱发突变,7.2.2.1.,物理诱变,a),电离辐射诱变；,Co,60,()()ray,Cs,137,()()ray,H,3,()ray,P,32,S,35,()ray,卫星搭载诱变；,高真空，强辐射，微重力,()()ray,穿透性,（外照射处理）,()()ray,非穿透性,（内标记处理）,dNt,电荷及结构改变,卫星搭载育种 太空蔬菜,微重力,高辐射,强射线,b),非电离辐射,Ultra Violet light(U.V),-pyrimidine dimer(TT dimer)is generated by,covalent links,between adjacent