植物生理学：植物衰老与器官脱落

PlantSenescenceandOrganAbscission

Section1PlantSenescenceanditsprogram1.1Conceptandtypesofplantsenescence1.1.1Senescence:Aprograminwhichthefunctionoforganorwholeplantnaturallydeclinestodeath.Thisisanessentialphaseofthegrowthanddevelopmentinplant。Fornutritiontransfer,suchasseed，tuberandbulb。Leafabscissioninfall——sprout，leafandflowergrowinnextspring。Fruitsmatureandfall——seedsspread。

1.1.2typesofplantsenescence

(1)OverallSenescenceSenescenceoccursinwholeplantbody,suchasannualswhichsenescestodeathafterflowerandsetting.(2)TopSenescenceThepartabovegrounddieswiththeendofgrowthseason,butthepartundergroundisaliveforseveralyears.Perennialweeds,corm(球茎)andbulb（鳞茎）——lily。InsummerInwinter(3)DeciduoussenescenceTheleaffallsinspeciousseason,insummerorwinter.Deciduoustrees(4)ProgressivesenescenceSenescenceonlyoccursinolderorganortissue.Neworganortissuedevelopswhileoldonesaresenescing.Greentrees。衰老有其积极的生物学意义，不仅能使植物适应不良环境条件，而且对物种进化起重要作用。温带落叶树的叶片，在冬前全树叶片脱落，从而降低蒸腾作用，有利于安全越冬。通常植物在衰老时，其营养器官中的物质降解、撤退并再分配到种子、块茎和球茎等新生器官中去。如花的衰老及其衰老部分的养分撤离，能使受精胚珠正常发育；果实成熟衰老使得种子充实，有利于繁衍后代。1.2ProgramforplantsenescenceSenescencecanoccuratdifferentlevels:cell,tissue,organsandwholeplant.1.2.1Cellsenescence

Membraneandorganellesenescence。1.2.1.1、Senescenceincellmembrane。(1)Lipidphasechange。Biomembranechangesitsphasefromliquid-crystallinestatetosolid-gelstate.

Hardandinextensive，fluiditydecreasesandcohesionincreases。液晶相凝固相衰老、低温六方晶相I六方晶相II混合相衰老生物膜几种相变示图liquid-crystallinestatesolid-gelstate（2）DegradationandperoxidationoflipidleadtodecreaseinlipidcontentSynthesis↓,lipase↑,

phospholipase、lipoxygenaseandactiveO2↑MDA(malonyldialdehyde）↑。

（3）Phospholipase

。磷脂酶A1、磷脂酶A2、磷脂酶B、磷脂酶C、磷脂酶D等。其中，磷脂酶D主要存在于高等植物组织中。CH2—O—C—R1CHCH2—O—P—O-XR2—C—OOOOOHA1A2BCDThedehydrationboundfordifferentphospholipases磷脂的降解磷脂游离多元不饱和脂肪酸磷脂酶脂氧合酶不饱和脂肪酸的氢过氧化物脂氧合酶自由基分解醛类（如丙二醛）和易挥发的烃类（乙烯，乙烷，戊烷）等脂氧合酶亚麻酸茉莉酸（JA）JA是一种促进植物衰老的内源物质，有人称为死亡激素。Phospholipid

↓phospholipaseAorBPolydouble-boundfatacid

↓Lox(lipoxygenase)OrganicfreeradicalsR’HC=CCH2C=CR’’-COOHHHH顺，顺—甲叉间二烯R’HC=CCHC=CR’’-COOHHHH•O2OOH•夺取氢，形成过氧自由基R’HC=CCHC=CR’’-COOHHHH•自由基：反，顺—共轭二烯重排OOH•R’HC=CCHC=CR’’-COOHHHHOOH过氧化作用反，顺—共轭二烯过氧化物（4）Biomembranedegradationandleakage.Lossequilibriumofionsanddisorderofmetabolism。1.2.1.2、Organellesenescence。

RibosomeandroughER↓→chloroplastsbreakdown→mitochondriacristaeswollen↑→vacuolebroken.Autophagyoccursandcellsenescesanddegrades.1.2.2Programmedcelldeath(PCD，程序性细胞死亡)Theorganismcontrolstheinitiationandexecutionofthecelldeathprocess,thesetypesofcelldeatharereferredtoasprogrammedcelldeath(PCD)PCD可发生在植物的各种细胞。过程：DNA断裂、染色质固缩、胞泡形成、凋亡小体形成。动物细胞PCD后产物被其他细胞吞噬利用，植物细胞PCD后产物用于本身细胞次生壁的构成。OneoftheimportantfunctionsofPCDinplantsisprotectionagainstpathogens.Whenapathogeninfectsaplant,cellsatthesiteoftheinfectionquicklyaccumulatehighconcentrationsoftoxicphenoliccompoundsanddie.Thedeadcellsformasmallcircularislandcalledanecroticlesion,whichisolatesandpreventstheinfectionfromspreadingtosurroundinghealthytissues.Thisrapidandlocaizeddeathduetopathogenattackiscalledthehypersensitiveresponse,whichisageneticallyprogrammedprocess.PCD发生过程启动阶段（initiationstage)启动细胞死亡信号的产生和传递效应阶段(effectorstage)caspase的活化和线粒体通透性的改变。Caspase属于半胱氨酸蛋白酶家族，直接导致PCD细胞原生质解体.Caspase全称为含半胱氨酸的天冬氨酸蛋白水解酶(cysteinylaspartatespecificproteinase)。caspase是一组存在于细胞质中具有类似结构的蛋白酶。Caspase与真核细胞凋亡密切相关，并参与细胞的生长、分化与凋亡调节。它们的活性位点均包含半胱氨酸残基,能特异性的切割靶蛋白的天冬氨酸残基上的肽键.酶解清除阶段(degradationstage)Fig20.4Celldeathoccursinalmostallplantcellsandtissues.PCDisinvolvedinnumerousprocesses,inclu-dingthefollowingillustrat-edinthisfiguregameteformation,includingmegasporeformation(1);embryodevelopment(2);degenerationoftissuesintheseedandfruit(3);tissueandorgandevelopment(4)through(6);senescence(7);andresponsestoenviron-mentalsignalsandpath-ogens(8and9).Fig20.9SenescenceinArabidopsisthaliana.(A)DevelopmentofArabidopsisthalianaplantsisshownatvarioustimesaftergermination.Photographsshowplantsat14,21,37,and53daysaftergermination(lefttoright).Notetheyellowingofshootsofthe53-day-oldplant.(B)Age-relatedchangesinrosetteleavesofArabidopsis7,9,and11daysafterleafexpansionhadceased.Notetheprogressiveyellowingofleaves,beginningfarthestfromthemainveinsFig20.2(A)Saccharromycescereoisiaeundergoesautophagy(自体吞噬)whenstarvedofnutrients.Theyeastshowninthisfigurewasnitrogen-starved,bringingaboutautophagy,inwhichautophagicbodies(AB)engulfthecytoplasmandtransportittothevacuole(V),whereproteasesandotherlyticenzymesreleasenitrogentocompensateforthelackofnitrogeninthemedium.(B)AutophagyoccursindyingplantcellsasinthesenescingImpomeatricolorcorollacelldiagrammedhere.Autophagicbodiesengulfaportionofcytoplasm,includingthenucleus(N),tothevacuole(s),wherebreakdownofthecell’scontentsoccurs.ThethreecellsshownrepresentdifferentstagesofPCD,Abeingtheearliest,andBandClaterstagesofautophagy.ABFig20.5Theinflorescencesofmaizecontainflowersthatareinitiallybisexual,butPCDresultsinthedeathofmaleorfemaletissuestogiverisetofemaleinflore-scence(ear)ormaleinflorescence(tassel),respectively.Inthetasselseed2mutant(A),femaletissuesinthetasseldonotundergoPCD,andtheresultingtasselflowersaremostlypistilate.Awild-typetasselinincludedforcomparison(B).Fig20.6OnevisibleexampleofPCDinplantsisseenintheornamentalplantMon-steradeliciosa.

Theleavesofthisplantexhibitdeepindentationsandholeinthelamina,whichresultfromthepro-grammeddeathofspecificregionsoftissueinthedevelopingpromor-dia.Astheleafexpands,theseareasarenotreplaced,andtheresultingleaflaminahasthecharacteristicpatternthatinspiresthecommonname,‘‘Swisscheeseplant’’Fig20.8Aerechymaformationinmaizerootsinresponsetohypoxia.Rootsweregrownunderareobic(A)andhypoxic(B)conditions.Underlow-oxygenconditions,corticalcellsbetweentheendodermisandhypodermisundergolysogenictoformairspacesthatarecontinuousthroughouttheroot,therebyallowingsubmergedrootsaccesstoatmosphericgasesobtainedbyabove-groundtissues.

1.2.3OrganSenescence

1.2.3.1Leafsenescence。（1）Photosynthesisdeclines-----slowerphaseandfasterphase。Decreaseinactivityandcontentofphotosynthetickeyenzyme(Rubisco)Decreaseinactivityofphotoelectrontransportandphotophosphorylation.Decreaseinstomatalconductance.Decreaseinchlorophyll.Leafyellow.Organelledegradation:叶绿体内基粒→（脂类小体）→内质网→核糖体→线粒体→液泡膜。（二）器官衰老1.叶片衰老2.花器官的衰老叶色-----由绿变黄根据叶色将叶片衰老分为五级花冠---雄蕊---雌蕊

花器官3.根系的衰老果实成熟意味衰老开始根系是边生长边衰老，根毛寿命很短相对值大小呼吸速率可溶性氮化物蛋白质叶绿素含量光化学活性光合速率Rubisco活力天叶片衰老期间的生理变化示意图脂质小体Fig20.13Impactofsenescenceonplastidultrastructureinleavesofwild-typeandastay-greenmutantoftheC3grassX.Festulolium.(A)Priortosenescence,thechloroplastsofawild-typeandmutantplantscontainnumerousgrana,stacksofappressedthylakoidmembranes.(B)Theseinternalmembranestructuresarelostduringsenescenceofawild-typemesophyllcell,andelectron-denselipiddropletsknownasplastoglobuliaccumulate.(C)Retentionofintrinsicthylakoidmembraneproteins,pigments,andotherhydrophobiccomponentsgivesthegerontoplasts(老年质体)ofmutanttissuesadistinctiveappearance,withpersistentgranastacksandfewplastoglobuli.Fig20.15Chlorophyllaanditsbreakdownproducts.Subcellularcompart-mentationofthepheo-phorbideapathwayofchlorophyllcatabolisminleafmesophyllcells.Fig20.19(A)Activityofkeychlorophyll-catabolizingenzymePaOisstronglyinducedinsenescingtissuesofwild-typeX.Festuloliumbutundetectableinpresenescentleavesandinastay-greenmutant.(B)Inductionofchlorophylldegradationinwild-typetissueisaccompaniedbylossofthepigment-bindingmembraneproteinLHCP,asshownbyWesternblottinganalysis.InthemutantasecondformofLHCPIIprogressivelyaccumulatesassenescenceproceeds.Asillustratedinthecartoon,degradationofLHCPIIwhichprotrudesfromthethylakoidmembraneintothestroma.(C)StabilityofRubisco,themajorstromalprotein,isenhancedveryslightlyinthemutantcomparedtowildtype.Xieyou9308Shanyou63Peiai64s/9311Xieyou9308Shanyou63Peiai64s/9311ABChangesinmRNAsofrbcS(A)andrca(B)inflagleafafterheading

1.2.3.2Seedaging。Theviabilityofseedlossinverselyfrommaturetodeath。Degradationandleakageofbiomembrane:MitochondriaandERbecomeswollen,plasmicmembranecontactsanddepartfromcellwall.DNAinjury，broken。Enzymeactivitydecreases:dehydrase。Storagematterexhausting,freefatacidrising.

1.2.4Senescenceinwholeplant：Onesettingplants:一生中只开一次花的植物-全部一年生\二年生和某些多年生的植物.Polysettingplants------graduallysenescing一生中多次开花结实的植物-木本植物\多年生宿根性草本植物.Section2SenescenceMechanismandregulation2.1

Senescencecausedbynutritionexhaustion

Nutritionexhaustion

theory：Senescencecausedbyreproductiveorgan.Suchastomato,ifsetting,survivesforoneseason,ifflowerremovedoff,survivesforseveralyear.Roottissueculture,morethan30years.龙舌兰doesnotflower,liveforseveraldecades,andfloweringalive—8-10years。Oppositeviews:Sunflowersenescespriortoflowerinitiation.Removingfloweracceleratessenescenceinmaizeandpopper自由基损伤学说：自由基有细胞杀手之称。1955年哈曼（Harman）就提出，衰老过程是细胞和组织中不断进行着的自由基损伤反应的总和。

三、植物衰老的机理与调节（一）植物衰老的机理1.营养亏缺学说

许多一年生植物在开花结实后，营养体衰老、凋萎、枯死。原因主要是营养物质的征调和同化物的再分配与再利用。即将营养体内的物质大量运输到生殖器官，促进营养体衰老。摘除果实可以延缓衰老。存在问题：

1）供给已开花结实植株充分养料，无法免除其衰老

2）雌雄异株开花后并未结实，雄株仍然死亡。如菠菜和大麻

2.DNA损伤学说差误理论要点：植物衰老是由于分子基因器在蛋白质合成过程中引起差误积累所造成的。当错误的产生超过某一阈值时，机能失常，出现衰老、死亡。这种差误由于DNA的裂痕或缺损导致错误转录、翻译，错误可能在蛋白质合成轨道一处或几处出现。这种错误可能是氨基酸排列错误，或者是多肽链折叠错误。错误的发生导致无功能的蛋白质（酶）的积累。3.遗传程序学植物衰老、死亡是由其自身基因程序所决定的。一切衰老过程都是基因控制。牵牛花的衰老很快，在开花当天即衰老，第二天脱落细胞程序性死亡（programedcelldeath）：植物体内存在特定基因控制细胞衰老事件。---DNA降解为特征外源乙烯--诱导WT拟南芥衰老对乙烯不敏感型突变体无影响生命衰老受遗传控制4.生物自由基损伤学说

衰老常伴有超氧化物歧化酶（superoxidedismutase，SOD）活性降低和脂氧合酶活性升高（lipoxygenase，LOX，催化膜脂中不饱和脂肪酸的加氧，产生自由基），导致生物体内自由基产生与消除的平衡被破坏，以致积累过量的自由基，对细胞膜及生物大分子产生破坏作用。如加强酶蛋白的降解、促进脂质过氧化反应、加速乙烯的产生、引起DNA的损伤、改变酶的性质等，进而引起衰老（1）生物自由基（FreeRadical）的概念

生物自由基（FreeRadical）是指生物体代谢产生的自由基。又称游离基，是带有未配对电子的原子、原子团、分子或离子等。（2）生物自由基种类生物自由基

氧自由基（oxygenfreeradical）（主要的生物自由基）非含氧自由基，如CH3.、（C6H5）3C无机氧自由基，如超氧自由基（O2.-）、羟基自由基（.OH）；有机氧自由基，如过氧化物自由基（ROO.）、烷氧自由基（RO.）和多元不饱和脂肪酸自由基（PUFA.）。含氧非自由基(1O2,H2O2)活性氧自由基的特点：不稳定，寿命短；化学性质活泼，氧化能力强；能持续进行链式反应。

活性氧（activeoxygen）化学性质活泼，氧化能力很强的含氧物质的总称。生物体内活性氧

--氧自由基、单线态氧和H2O2、NO、NO2等。它们能氧化生物大分子，破坏细胞膜的结构与功能，其中O2.-的氧化能力特强，能迅速攻击所有生物大分子，包括DNA，引起细胞死亡。（3）自由基的产生产生部位：细胞壁、细胞核、叶绿体、线粒体及微体等。产生途径：单电子的氧化还原；共价键的断裂；高能辐射；光分解；逆境条件A.单线态氧（1O2）的产生B.超氧自由基的产生C.羟基自由基的产生2.2Physiologyandbiochemistryduringsenescence

2.2.1Senescence-associatedgenes（SAGs）expression。

Senescenceiscontrolledbyspecialgenes.Twokindsofgenescanbefoundduringsenescence.(1)Senescence-downwardgenes，mostofgenescodeenzymesrelevanttophotosynthesis,energymetabolismandothersynthesis。(2)Senescence-upwardgenes，mostofgenescodeenzymesforhydrolase,suchasDNase,RNase,Protease,phospholipase。Senescence-associatedgenes（SAGs）referstotheirmRNAlevelsincreasewithsenescenceproceeding.Theyfunctioninmetabolismofbiomacromoleculedegradationandmobilization.Morethan40geneshavebeencloned:ProteasesinMaize,A.thaliana,rape.SAG2,See1,LSC7，SAG12，LSC790，LSC760；RNS1，RNS2，RNS3in

A.thaliana

；PEPC，MDH，MS，ICL，GAPDH,F-1,6-P,aldolaseandβ—galactosidaseinrape,cornandcucumber.StagesinBrassicanapusleafsenescence.SAGsaredividedinto10classesaccordingtotheirtemporalpatternofexpression.2.2.2Degradationofbiomacromolecules。(1).DNAdegrades，RNAchangesinqualityandquantity.RNAbreakdownfasterthanDNAdoesduringsenescence,especiallyrRNA,whichismoresensitivetosenescence.RNaseactivityrisesandDNA—RNApolymeraseactivitydeclines。(2).Proteinsynthesisdecreasesanditsdegradationincreases。Solubleprotein-----Rubiscodecreasesin85%,thylakoidmembraneproteindecrease50%,andcytochromef,bdecreasesfast。对蛋白质的伤害:由脂质过氧化过程所产生的脂性自由基（如RO.、ROO.）能引发膜蛋白（包括膜酶）发生聚合和交联,是自由基对蛋白质损伤的主要形式。丙二醛对蛋白质的交联作用。

脂质过氧化的最终产物丙二醛（MAD）能与蛋白质等生物大分子产生交联反应。

由丙二醛引发的这种交联反应既可在蛋白质分子内进行，也可在蛋白质分子间进行。

丙二醛与两个蛋白质分子交联形成的物质叫脂褐素（LPF）。5.激素平衡学说

植物体内各种植物激素相对水平的不平衡是引起衰老的原因。抑制衰老的激素（如CTK、IAA、GA）与促进衰老的激素（ETH、ABA）之间可相互作用、协同调控衰老过程。

茉莉酸（jasmonicacid,JA）茉莉酸甲脂（methyljasmonate,MJ）死亡激素

不仅抑制植物生长,且能促进植物衰老。加快叶片中叶绿素降解,提高蛋白酶和核糖核酸酶类活性,加速生物大分子的降解。它促进植物衰老的作用比ABA还强ABA和ETH----植物衰老激素Twopossiblemechanismsareillustrated.Inonecase(leftsideoffig.),occupationofbindingsitesbycofactors(e.g.,enzymesubstrates)orallostericeffectorslockstheproteinintoaconformationresistanttoproteolysis,andtheequilibriumbetweenthisstructureandthesusceptibleconformationisthusdeterminedbytheabundanceoftheseligands.Intheothercase(rightside),theproteinismarkedfordegradationbytheadditionofatagsuchasubiquitinandistherebymadeavailableforproteolysis.Fig20.20Comparisonofthe

foliarsenescence-as-sociatedproteaseSEE1frommaizewithothercysteineendopeptidases.

(A)TheaminoacidsequenceinferredfromSee1cDNAalignedwiththesequencesofotherproteasesfromthesamefamily.Conservedstructurefea-turesincludingaputativevacuolesortingmotif(residues29through34;redline),potentialglyco-sylationsites(125throu-gh127,256through258;bluelines),andthelikelycleavagepointthatremovestheprodomain(between142and143;arrowhead).Opencirclesindicatethecysteine-histidine-asparaginetriadoftheactivesite,andthegreenlinesidentitifythesurroundingconservedregions.(B)DendrogramlocatingSEE1inthesamesubfamilyasthecerealgerminationproteasesaleurainandoryzain.NotethatSAG12ofgreeofconservationofcysteineproteasestructuralmotifsinSEE1allowsathree-dimensionalmodeltobedevised.

GluconeogenesisinsenescingleleafcellsTheglyoxylatebypassisactivated(3).biomembranebreakdownsandlossesitsfunction.2.2.3Disorderofplantgrowthsubstance（1）、CTKcontentdecreases。Detached(invitro)leaf----aggravatingsenescence;Rooting----RegreeningHigherCTKcontentsofthebleedingsapintheresist-senescingcultivarsinsunflowerandrice

CTKfunctions:Blockingsomesenescence-associatedgenes(SAGs)expression;Preventinghighbiomoleculesfromdegradation;Delayingdeclinationofphotosynthesisandmaintainingregularrespiration;Makingthestomataopen;Cleaningfreeradicalsandchangingassimilatedistribution.（2）Eth.Itinduces“Cyanide-resistantpathway”，andstimulateactiveO2formationaswellashydrolasesynthesisandactivation。Fig20.26Ethylenepromotesleafsenescenceinwild-type(WT)Arabidopsis,butnotintheethylene-insensitiveetr1mutant.Fig20.28Ethyleneproduction(A)andtheexpressionofethylene-inducedgenes(B)inripeningtomatofruit.MG1throughMG4refertosequentialstagesintomatofruitdevelopment.MG,maturegreen;Imm,immature.Theinflorescencein(B)isfromaplantcarryingtheneverripemutation,whichisinsensitivetoethylenebecauseofamutationinanethylenereceptor.Asaresult,ethylenedoesnottriggersenescenceandabscissionintheseflowers.Inuntreatedwild-typeflowers,floralsenescencefollowspollination(C),whereasintheethylene-insensitivemutants,theflowersdonotsenesceafterpollinationbutinsteadremainintact,evenasthefruitbegintodevelop(D).Thus,ethyleneisakeysignalininducingfloralsenescenceafterpollinationintomato.Asthenameimplies,intheneverripemutant,thefruitdonotripen.Thetwotomatofruitsin(E)areofapproximatelythesameageandweregrownunderthesameconditions.However,thefruitontheleftisfromaneverripemutant,whereasthefruitontherightisfromthewild-typeplant,thusemphasizingtheimportaceofethylenesignalingintheinductionofrepeningFig20.29Exogenoustreatmentwithethyle-neinducessenescenceinmanyplants.Thetomatoinflorescenceontheleftin(A)wastreatedwithethylene,causingtheflowerstosenesceandabscise.wwwnrnrnrEthylenesynthesisbyleavesofcontrol(Blue)orantisenesce(red)tomatoplantsexpressingACCsynthase.MethionineSAM(S-Adenosylmethionine)SAMdecarboxylaseACCsynthaseSpd(spermidine)ACCSpm(spermine)EthFigSyntheticcompetitionofployaminetoEth

(3)ABA.

Stomatalclosureandhydrolasesynthesis

(4)JAJA(Me-JA):chlorophylldegradationandEthpromotion.2.2.4EquilibriumlossofCa2+betweenintro-andextra-cell

。UsuallyCa2+8-15mmol/Linapoplastand0.1-1μmol/Lincytoplasm.Ca2+entersthecytoplasmandcausessenescenceActivatingCaM,phospholipaseDActivatingphospholipaseAPhospholipiddegradationUnsaturatedfatacidBD,CaenterscellHydroylsuperoxidefatacid(Cachannel)LoxPhospholipidCachannel

Primaryreaction（

）andsecondaryreaction（）ofbiomembranedegradation(BD)inducedbyCaandCaM2.2.5、Freeradicalsburstandthecapacitiesofscavengersystemsdecline.

2.2.5.1feedradical

Freeradicals:ion,atomandmoleculewithfreeelectron.

Characters：instable,active,stronglyoxidativecapacityandchain-reactionsInorganicfreeredicals:、1O2andOH

；Organicfreeredicals:ROO

、RO

。O2Mostofinorganicfreeradicalsfromtheilluminatedchroloplast(1)Photochemicalfreeredicals---hvPSIIPSIO2MehlerreactionO2O2e-e-XanthineoxidaseO2OHO2(2)Xanthine+uricacid++H2O+O2+(3)Fentonreaction：OHH2O2+Fe2++OH-+Fe3+(4)Haber-WeissreactionO2OHH2O2++OH-+O2OHisthemostpoisonfreeradicalinthelivingthings2.2.5.2Freeradicalscavengingsystemsinplant(1)Non-protectiveenzymesystem—antioxidant:Cytf、glutathione、ascorbicacid、ubiquinone,vitaminEandcarotenoids。(2)ProtectiveenzymesystemsSOD、AAO、glutathionereductase、catalaseandglutathioneperoxidase.SODismostimportant.SODtypes:(1)CuandZn—SOD，dimmerwithsubunit32kD，andeachwithoneCu2+andZn+，mainlydistributesinhigherplantchloroplast(2)Mn—SODmainlydistributesinprokaryoticbacteriaaswellineucaryoticmitochondria(3)Fe—SODisabasictype，mainlylocatesingreenalga.SODcatalyticreaction：O22+2H2OH2O2+O2SODFig20.24Theassociate-glutathioneredoxcycleinsenescence.Ascorbateisregeneratedfromoxidizedformsbyacyclecatalyzedbyascorbateperoxidase(APX),monodehydroascor-batereductase(MDHAR),dehydroascorbatereductase(DHAR),andglutathionereductase(GR).Superoxidedimutase(SOD)isoneoftheenzymaticdefensesagainstthebuildupofreac-tiveoxygenspecies.Inma-tureleaves,photosyntheticelectrontransfergeneratesNADPH,whichdonateselectronstoascorbatebywayofreducedglutathione(GSH).Insenescingleaves,NADPHproductiondecreases,resultinginincreasedratiosofoxidizedglutathione(GSSG)toGSHandofdehydroascorbatetoascorbate.Theserelativelysubtlechangescanresultinsubstantialchangesincellularredoxconditionsandsignalnewpatternsofgeneexpression.PSI,PhotosystemI;*,nonenzymaticreaction.Section3MechanismforAbscissionAbscission:

aprocessduringwhichthecells,tissuesororgans,suchasflowers,fruitsandsmallbraches,aredetachedfromtheplantbody.Normalabscissioncausedbysenescenceorripening.Abnormalabscissioncausedbystresses:higherorlowertemperature,droughtorflood,insectsordiseases.Physiologicalabscission

causedbydisordersinphysiologyitself:suchasnutritionalcompetitionbetweenvegetationandregeneration,sinkandsource.第五节器官脱落的生理一、器官脱落的概念植物器官自然离开母体的现象称为脱落（abscission）。三种类型正常脱落：衰老或成熟引起的脱落---种子和果实。胁迫脱落：因环境条件胁迫和生物因素引起的脱落。生理脱落：因植物本身生理活动而引起的脱落。二、器官脱落的机理（一）离层与脱落

叶片脱落之前，离层细胞衰退，果胶酶与纤维素酶活性增强，中层分解，叶片脱落。（二）激素与脱落1.IAA脱落的生长素梯度学说(Addiccott,1955)：器官的脱落与离层两端IAA的浓度梯度有关。当远轴端/近轴端IAA比值低时，加速离层的形成，促进脱落。当远轴端/近轴端IAA比值高时，抑制或延缓离层形成，抑制脱落；2.ETH

诱导果胶酶和纤维素酶合成，提高酶活性，促进离层分解，加速脱落。3.ABA

促进脱落机理---可能与其抑制叶柄内IAA的传导和促进分解细胞壁酶类的分泌有关。（三）营养与脱落

碳水化合物和蛋白质等有机营养不足是花果脱落的主要原因之一。三、影响器官脱落的环境因素1.光照强光抑制脱落弱光促进脱落

长日照抑制脱落短日照促进脱落光强光质2.水分

干旱提高IAA氧化酶的活性，降低CTK含量，提高ETH和ABA含量，促进脱落。水淹时，也会出现落花，落果，落叶3.温度高温、低温均促进脱落。4.O2高O2、低O2都促进ETH的合成。高O2还导致呼吸的加强，光合产物消耗加大，导致脱落。5.矿质营养缺乏N、Zn、Ca能导致脱落。6.其他因素大气污染，病虫害，盐害等Budincottonis70％abscission，flowersorfruitsinsoybeanis60-70%abscission。3.1Abscissioninanatomyandphysiology3.1.1Abscissioninanatomy

AspecificPartforabscission——abscissionzone。Oneorseverallayersofcelllocateinthepetioleinwhichcellshaveasmallinsize,acloseconnectionwitheachother,adensecytoplasmandstarchgrains.DivisioncellChangeincellwallduringabscission中胶层3.1.2Enzymesrelativetoabscission(1)、Cellulase。

Cellulaseactivityincreasesinbean,cottonandcitrusduringleafabscission。

(2)、Pectinase.Inbeanpectinase↑,abscission↑.Pectincompound↓Pectinase(PEM,果胶甲酯酶)Pectin↓Pectinase(PG,多聚半乳糖醛酸酶)Smallsubunit(sugar,C5)(3)、Catalase↑,abscission↑。3.1.3Abscissionandplanthormones(1)、IAAs。

WhenIAAisappliedinthepartoutsideofabscission(远基（轴）端),abscissionpromotes,inotherway,WhenIAAisappliedinthepartinsideofabscission(近基（轴）端),abscissioninhibites.IAApromotionofabscissionIAAprotectionfromabscissionAbscissionzoneCTKandGA?

(2)、Ethylene。

InduceandsecretePG,degradecellwall.(3).ABA。Justbeforethefallingintheautumn，ABA↑.ABAinhibitsIAAtransferandpromotesdehydrolaseactivity。Section4、Environmentalfactorsinfluencingsenescenceandabscission

4.1Temperature

SenescenceandabscissionriseatTtoohighandlow.4.2Water

Senescenceandabscissionriseatdroughtbecauseof1AAoxidation，andCTKdeficiency；EthandABAincrease.Inthefloodingcondition,senescenceandabscissionrise.4.3light

Lightintensity↓,abscission↑.Notenoughphotoassimilate.ShortdayinduceABA,resultinginsenescenceandabscission.

Toohighlightintensity,abscission↑.4.4O2

10203040506070809050100O2concentration%Abscision%4.5Mineralnutrition

Anyoneofmineralnutritiondeficiencycausesincreaseinsenescenceandabscission.N、Zn——1AA，Ca——cellwall.

B——pollendevelopmentandpollentuberelongation.4.6Diseases，pests,radiationandotherstressescausesenescenceandabscission.三、脱落的调控1．防止脱落----

园艺作物（蔬菜）

2,4-D---防止茄果类植物落花，如茄子、番茄等

NAA---防止落果（缺点--提前呼吸跃变，不耐贮藏）低浓度2,4-D,NAA-----减少棉花早期幼铃脱落

GA-----能增加棉花座铃。

CCC、B9、PP333等，对防止落铃也有明显效果。