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Impactsofchillingtemperaturesonphotosynthesisinwarm-climateplants低温对热带植物光合作用的影响TrendsinPlantScience,Volume6,Issue1,1January2001,Pages36-42167940010张东芳Abstract•Photosynthesisinwarm-climateplantsissubstantiallyreducedafterchilling.Tropicalandsubtropicalspeciesoffertheopportunitytostudytheeffectsoflowtemperatureonphotosyntheticprocessesundisguisedbythemyriadofprotectiveresponsesobservedintemperatespecies.Inthisarticle,wehighlighttheprimarycomponentsofphotosynthesisthatareaffectedbyashortchill,inboththedarkandthelight,anddiscusswhatisknownofthemechanismsinvolved.Recentworkimplicatesimpairedredoxandcircadianregulationamongotherprocesses.•在低温处理的情况下，热带植物的光合作用效率大幅降低。热带和亚热带的物种为我们研究低温对各物种光合作用过程的影响提供一个机会。在这篇文章中，我们强调由一个短暂的低温处理和黑暗或光照的组合影响的光合作用，并讨论什么是已知参与的机制。最近的研究发现其中包括氧化还原受损和昼夜调控。Keywords/关键字•Lowtemperature;Photoinhibition;Oxidativestress;Carbonreductioncycle;Circadianrhythm•低温;光抑制;氧化应激;减碳循环;昼夜节律Lowtemperatureisamajorfactorlimitingtheproductivityandgeographicaldistributionofmanyspecies,includingimportantagriculturalcrops.Theformationoficeinsideplantcellsisdevastating.Freeze-tolerantplantshaveseveralstrategiestoreducetheprobabilityofthisoccurring,evenwhenairtemperaturedropsbelowzero,includingmaintaininghighintracellularsoluteconcentrationsandencouragingicenucleationoutsidethecells.Theseplantsalsocommonlyexhibitxerophyticadaptationstosurvivethereducedwateravailabilitywithintheplantandthesoil.Temperaturesof−5°Ccankillanunhardenedwinterwheatplanteventhoughithasthegeneticcapacitytoacclimatize,hardenandacquiretoleranceoffreezingdownto−20°C.Thecold-hardeningmechanismsconferringfreezetolerancehavebeendescribedelsewhere.andincludechangesinlipidcomposition,increasesinactive-oxygen-scavengingenzymes,anthocyaninaccumulationandalteredgrowthmorphology.低温是限制了许多物种的产量和地理分布的一个主要因素，其中包括重要的农业作物。在植物细胞内冰的形成是毁灭性的。植物对冷冻有多种策略，以减少这种情况发生的概率，即使在气温降到零度以下，策略包括维持细胞内高浓度的溶质。这些植物通常也表现出适应旱生。-5°C的温度可以杀死一个未硬化的冬季小麦植株即使它有适应环境，硬化，并获得冷冻低至-20°C的耐受性遗传能力。赋予冷冻硬化的机制已在别处描述。1.Thylakoidelectrontransport1.1.Photodamage(chronicphotoinhibition)andrepairItseaseofmeasurementmeansthattheratioofvariabletomaximalchlorophyllfluorescence(Fv/Fm)indark-adaptedleavesisoftenusedtoidentifyphotosystemII(PSII)photodamage,aninhibitionofPSIIphotochemistrythatisnotrapidlyreversible.Theamountofthatcanbindtotheplastoquinone-reductasesiteofPSIIinisolatedthylakoids,producesamoredirectandquantitativeassessment.1，类囊体膜上的电子传递1.1光损伤（慢性光抑制）和修复在暗适应的条件下，叶绿素荧光（FV/FM）的比值经常被用于识别光系统II（PSII）的光损伤，PSII光化学抑制是不能快速逆转的。在孤立的类囊体上，C-阿特拉津（C-atrazine）可以绑定到PSII的质体醌还原酶上，并计算其数量，产生更直接定量的对光损伤评估。Photodamageisrarelyobservedimmediatelyafterchillingofeventhemostextremethermophilicspeciesiflowtemperaturesareexperiencedinthedark.Bycontrast,thecombinationoflowtemperaturewithhighlighthasthepotentialtoinducechronicphotoinhibitionofPSII(Fig.1).Thisispartlybecauseloweringthetemperaturegenerallyreducesreactionratesandcanthereforelimitthesinksfortheabsorbedexcitationenergy(light),particularlyCO2fixationandphotorespiration.SmallersinksforabsorbedexcitationenergyincreasesthepotentialforoxidativedamagetoPSII,notablytheD1componentoftheD1–D2heterodimeratthecoreofthePSIIfunctionalcenter.Inaddition,photodamagebecomesapparentaslowtemperaturesinterferewiththenormalreplacementrateofD1intheturnover–repaircycle.在黑暗中经历低温后，即使是最喜光的物种遭遇冷害，光损伤是很少被看到。相比之下，低温与强光的组合具有诱导光系统II的光抑制（光损伤）的潜力。（图1）这部分是由于降低温度通常会降低反应速率，因此可以限制接收器吸收激发能量（光），特别是CO2固定和光呼吸。因为接收器吸收的激发能量较小，因此增加了对PSII的氧化损伤的潜力，特别是在PSII官能中心的D1-D2二聚体芯部的D1组件。此外，光损伤变得明显，因为低温会干扰D1的正常反应速率。缩写：ATPsynthase，叶绿体ATP合酶B6F，细胞色素b6f复合体RuBP，核酮糖1,5-二磷酸FBP酶，叶绿体果糖-1,6-二磷酸酶SBPase，景天庚酮糖1,7-二磷酸酶淡蓝色的剪刀代表了光照与低温组合的影响深蓝色的剪刀代表一个黑暗与低温组合的主要影响ThishasbeenattributedtochangesintheexpressionofpsbA,theplastidgenethatencodesD1,anddirecttemperatureeffectsonmembranes.LowtemperaturereducesmembranefluidityandthusisbelievedtoreducetherateofD1turnoverbyslowingthediffusionofphotodamagedD1proteinsmarkedfordegradationtonon-appressedregionsofthethylakoid.Geneticmanipulationofthylakoidlipidstodecreasethesaturationoffattyacidscanpartiallymitigatehigh-light–low-temperaturephotoinhibition,presumablybyenhancingdiffusionandtherebyfacilitatingrepair.Nevertheless,photodamageofPSIIisfrequentlynotprimarilyresponsibleforlight-chill-inducedinhibitionofphotosynthesisinthermophilicplants.这已经被归因于改变psbA基因（质体基因）的表达，其编码D1蛋白和膜上直接温度效应的表达。低温降低了膜的流动性，因此被认为光损伤是通过降低D1的扩散速率，以减少D1的周转率。通过遗传操作类囊体的膜脂，以减少脂肪酸的饱和度可以部分减轻高光低温条件下的光抑制，大概是通过增强扩散，从而促进修复。然而，PSII的光损伤往往不是抑制光合作用主要原因。1.2.Photoprotectionanddownregulation(dynamicphotoinhibition)TherapidlyreversibledownregulationofPSIIquantumefficiencyplaysanindispensablephotoprotectiveroleinleaves.Thisprocessinvolvestheinterconversionofxanthophyllpigmentsandthedevelopmentofatransthylakoidprotonelectrochemicalpotentialdifference,andisclearlyacrucialprotectivemeasureagainstthemoreperniciousimpactofphotodamage.ChangesinthequenchingofexcitationenergyintheantennaeofPSIIcaneasilybeestimatedusingmodulatedchlorophyllfluorescence.BothFv′/Fm′(theefficiencyofexcitationenergytransfertoopenPSIIreactioncenters)andnon-photochemicalquenchingareparameterswide