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Hybrid Lethality in Interspecific F1 Hybrid N. gossei ×N. tabacum Involves a MAP-Kinases Signalling

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ResearchPaper

Abstract:Aculturedcellline,GTH4(NicotianagosseiDomin×N.

tabacumL.),whichexhibitshybridlethality,diedat268C,but

notat378C.Pharmacologicalexperimentsusinginhibitorsof

proteinphosphatasesandproteinkinasesindicatedtheinvolve-

mentofaproteinkinasesignallingpathwayinthecelldeathpro-

cess.Immunoblotanalysisrevealedthatsalicylicacid-induced

proteinkinase(SIPK)wasphosphorylatedsoonaftertheshift

intemperaturefrom378Cto268C.Culturedcellsofthehybrid

ofN.gossei×transgenicN.tabacumharboringasteroid(dexa-

methasone;DEX)-inducibleNtMEK2DDorNtMEK2KR,constitu-

tivelyactiveandinactiveformsofNtMEK2,respectively,were

established.InductionofNtMEK2DDbyDEXinthehybridcellsin-

ducedtheactivationofSIPK,thegenerationofhydrogenper-

oxide(H2O2),andcelldeathat378C.TheactivationofSIPK,gen-

erationofH2O2,andcelldeathat268Cwerecompromisedby

DEXtreatmentinhybridcellsharbouringNtMEK2KR.Thisstudy

providesevidencefortheinvolvementofMAPKsignallingin

theregulationofcelldeathinhybrids.

Keywords:Hybridlethality,MAPKsignalling,Nicotiana,oxida-

tiveburst,programmedcelldeath,SIPK,WIPK.

Introduction

Lethalityinspecieshybridsisamajormechanismofisolation

andhelpstosplitonespeciesintotwoinbothanimalsand

plants(OrrandPresgraves,2000;BurkeandArnold,2001).

TheprocessinvolvesamitoticdefectinDrosophila(Orretal.,

1997),andprogrammedcelldeath(PCD)controlledbytem-

perature(Yamadaetal.,2001;Minoetal.,2002)andoxidative

burstinthegenusNicotiana(Minoetal.,2004,2005).Thus,

themechanismwhichinducescelldeathmaybeamajorcause

ofhybridlethality,andathoroughunderstandingofthecell

deathprocesswillbeimportantforanalyzingthegenesimpli-

catedinexpressionoflethality.WehavepreviouslyreportedthatcelldeathintheF1hybridof

NicotianagosseiDomin×N.tabacumL.involvedPCD,inwhich

hydrogenperoxide(H2O2)actsasamajormediator(Minoet

al.,2002,2004,2005).However,themechanismswhichcon-

trolthegenerationofreactiveoxygenintermediates(ROI)and

celldeathinaninterspecifichybridarenotclear.Ithasbeen

reportedthatH2O2isamajorsignallingmoleculeevokinghy-

persensitiveresponse(HR)celldeathinplantsinfectedwith

pathogens(GrantandLoake,2000;Pellinenetal.,2002).PCD

inanimalcellsoccurswhenincreasedlevelsofH2O2leadtoac-

tivationofeffectorcomponentsofthecell’sapoptoticmachin-

eryviaadropinthecytosolicpH(PervaizandClément,2002).

ItwasreportedthatHRcelldeathcausedbyROIoccurred

downstreamofadisruptionoftheredoxbalanceinthecell,

andtheprocesswasunderthecontrolofamitogen-activated

proteinkinase(MAPK)cascade(Renetal.,2002).Thebasic

assemblyoftheMAPKcascadeisathree-kinasemoduleinall

eukaryotes.MAPK,thelastkinaseinthethree-kinasecascade,

whoseThrandTyrresiduesinaTXYmotifarephosphorylated

byMAPKkinase(MEK).MEKis,inturn,activatedbyMAPKK

kinase(MAPKKK)inresponsetoextracellularstimuli.Intobac-

co,twoMAPKs,salicylicacid-inducedproteinkinase(SIPK)

andwounding-inducedproteinkinase(WIPK),wereactivated

inculturedcellsorplantstreatedwithanelicitororinfected

withapathogen(delPozoetal.,2004;PedleyandMartin,

2005).Studiesoftobaccoleavesinfectedbytobaccomosaic

virusindicatedthatbothSIPKandWIPKwereactivatedbyan

Nresistancegene,precedingHRcelldeath(ZhangandKlessig,

1998).However,itwasreportedthatSIPKaloneisenoughto

activatethesedefenceresponses(ZhangandLiu,2001).Direct

evidenceforaroleforMAPKinHRcelldeathwasobtainedin

tobaccousingasteroid-inducibletransientassayofNtMEK2DD

(ZhangandLiu,2001;Jinetal.,2003).TheNtMEK2DD,inwhich

theconservedThr227andSer233weresubstitutedwithAsp

(D),hasmuchhigherkinaseactivitythanwild-typeprotein,

andthismutantproteineventuallyactivatesendogenousSIPK

andWIPKwithoutanupstreamsignallingcue(Jinetal.,2003).

AstrictcorrelationbetweentheexpressionofNtMEK2DD

andtheactivationofendogenousSIPKandWIPKwasfound

intransgenicplants.ExpressionofNtMEK2DDinducedHR-

likecelldeathinthetransgenicplants.Ontheotherhand,

NtMEK2KRaninactiveformofMEKinwhichthecatalytically

essentialLys111(K),importantforthebindingofATP,wasre-

placedwithanArg(R),wasnolongerabletoactivateSIPKand

WIPK(Yangetal.,2001;Jinetal.,2003).Allthissuggeststhat

activationofbothSIPKandWIPKiscontrolledbyupstreamHybridLethalityinInterspecificF1HybridNicotianagossei×

N.tabacumInvolvesaMAP-KinasesSignallingCascade

M.Mino1,M.Kubota1,T.Nogi1,S.Zhang2,andM.Inoue1

1GraduateSchoolofAgriculture,KyotoPrefecturalUniversity,1-5Hangi-cho,Shimogamo,Sakyo-ku,Kyoto606-8255,Japan2DepartmentofBiochemistry,UniversityofMissouri-Columbia,117SchweitzerHall,Columbia,MO65221,USA

Received:June22,2006;Accepted:September29,2006

PlantBiol.9(2007):366–373©GeorgThiemeVerlagKGStuttgart·NewYorkDOI10.1055/s-2006-924725·PublishedonlineJanuary19,2007ISSN

1435-8603366

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水稻叶色突变体高光合特性研究

水稻叶色突变体高光合特性研究

作物学报 ACTA AGRONOMICA SINICA 2011, 37(10): 1860−1867 /zwxb/ ISSN 0496-3490; CODEN TSHPA9 E-mail: xbzw@

本研究由怀化学院民族药用植物资源研究与利用湖南省重点实验室项目(SYSXM200905)资助。 作者联系方式: E-mail: ou9572@ Received(收稿日期): 2011-01-31; Accepted(接受日期): 2011-05-25; Published online(网络出版日期): 2011-07-28. URL: /kcms/detail/11.1809.S.20110728.1003.015.html

DOI: 10.3724/SP.J.1006.2011.01860

水稻叶色突变体的高光合特性

欧立军

怀化学院生命科学系 / 民族药用植物资源研究与利用湖南省重点实验室 / 湘西药用植物与民族植物学湖南省高校重点实验室, 湖南怀化418008

摘 要: 标810S是温敏核不育系810S中的淡黄绿叶自然突变株, 具有较高的光合速率。本文对突变体的光合色素、

光合速率、荧光参数和光合关键酶活性等研究发现, 标810S光合色素约为810S的一半, 强光条件下标810S光合速

率(Pn)比对照高, 且没有明显的“午休”现象。标810S气孔导度(Gs)显著增加, 叶绿素荧光动力学参数显示, 标810S

光量子转化效率高; 光合酶1,5-二磷酸核酮糖羧化酶(RuBPCase)活性是对照的69.80%, 磷酸烯醇式丙酮酸羧化酶

(PEPCase)和NADP-苹果酸酶(NADH-ME)却比810S分别上升79.50%和69.06%。研究结果认为, 光合色素含量下降

Salmon et al. Molecular Ecology 2005

Salmon et al. Molecular Ecology 2005

Molecular Ecology (2005)

14

, 1163–1175doi: 10.1111/j.1365-294X.2005.02488.x

© 2005 Blackwell Publishing Ltd

Genetic and epigenetic consequences of recent

hybridization and polyploidy in

Spartina

(Poaceae)

ARMEL SALMON,

*

MALIKA L. AINOUCHE

†

and JONATHAN F. WENDEL

‡

*

UMR 118 INRA-Agrocampus Rennes, Amélioration des Plantes et Biotechnologies Végétales, Station de Génétique et Amélioration

des Plantes, F-35653 Le Rheu, France,

†

University of Rennes 1, UMR CNRS 6553 Ecobio, Equipe Evolution des Génomes et Spéciation.

Bat. 14 A Campus scientifique de Beaulieu. 35 042 Rennes cedex, France,

‡

Iowa State University, Ames IO, USA

Abstract

To study the consequences of hybridization and genome duplication on polyploid genome

evolution and adaptation, we used independently formed hybrids (

Spartina ×

townsendii

受多逆境诱导表达的GhWRKY64基因启动子克隆与功能分析

受多逆境诱导表达的GhWRKY64基因启动子克隆与功能分析

作物学报 ACTA AGRONOMICA SINICA 2015, 41(4): 593600 / ISSN 0496-3490; CODEN TSHPA9 E-mail: xbzw@

本研究由国家转基因生物新品种培育重大专项(2011ZX08005-004), 江苏省农业科技自主创新资金项目[cx(14)2065]和江苏省现代作物生产协同创新中心(JCIC-MCP)资助。 * 通讯作者(Corresponding author): 郭旺珍, E-mail: moelab@, Tel: 025-84396523 Received(收稿日期): 2014-10-17; Accepted(接受日期): 2015-02-06; Published online(网络出版日期): 2015-03-02.

URL: /kcms/detail/11.1809.S.20150302.0301.004.html DOI: 10.3724/SP.J.1006.2015.00593

受多逆境诱导表达的GhWRKY64基因启动子克隆与功能分析

杜 皓 丁林云 何曼林 蔡彩平 郭旺珍*

南京农业大学作物遗传与种质创新国家重点实验室 / 教育部杂交棉创制工程研究中心, 江苏南京210095

摘 要: WRKY蛋白属于锌指型转录调控因子, 参与植物生长发育及耐逆响应。以陆地棉遗传标准系TM-1为材料,

克隆GhWRKY64 (KF031101)基因上游1064 bp的启动子序列, 并对其调控元件及功能进行分析。生物信息学分析表明,

该区域含18个组织器官表达及诱导表达关键元件, 分别为6个ROOTMOTIFTAPOX1根特异调控元件, 4个CACTFTPPCA1叶肉特异性调控元件、4个OSE2ROOTNODULE病菌诱导元件、2个GTIGMSCAM4盐调控元件和2

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abbreviateissnimpact_facsubjectCA-CANCER J CLIN0007-9235153.459ONCOLOGYNEW ENGL J MED0028-479351.658MEDICINE, GENERAL & INTERNALREV MOD PHYS0034-686144.982PHYSICS, MULTIDISCIPLINARYCHEM REV0009-266541.298CHEMISTRY, MULTIDISCIPLINARYNAT REV GENET1471-005641.063GENETICS & HEREDITYLANCET0140-673639.060MEDICINE, GENERAL & INTERNALNATURE0028-083638.597MULTIDISCIPLINARY SCIENCESNAT REV MOL CELL BIO1471-007237.162CELL BIOLOGYANNU REV IMMUNOL0732-058236.556IMMUNOLOGYNAT MATER1476-112235.749CHEMISTRY, PHYSICALNAT MATER1476-112235.749MATERIALS SCIENCE, MULTIDISCIPNAT MATER1476-112235.749PHYSICS, APPLIEDNAT MATER1476-112235.749PHYSICS, CONDENSED MATTERNAT GENET1061-403635.209GENETICS & HEREDITYNAT REV CANCER1474-175X35.000ONCOLOGYADV PHYS0001-873234.294PHYSICS, CONDENSED MATTERNAT REV IMMUNOL1474-173333.129IMMUNOLOGYNAT REV DRUG DISCOV1474-177633.078BIOTECHNOLOGY & APPLIED MICRONAT REV DRUG DISCOV1474-177633.078PHARMACOLOGY & PHARMACYNAT BIOTECHNOL1087-015632.438BIOTECHNOLOGY & APPLIED MICROCELL0092-867431.957BIOCHEMISTRY & MOLECULAR BIOLCELL0092-867431.957CELL BIOLOGYNAT REV NEUROSCI1471-003X31.673NEUROSCIENCESNAT NANOTECHNOL1748-338731.170MATERIALS SCIENCE, MULTIDISCIPNAT NANOTECHNOL1748-338731.170NANOSCIENCE & NANOTECHNOLOGSCIENCE0036-807531.027MULTIDISCIPLINARY SCIENCESPHYSIOL REV0031-933330.174PHYSIOLOGYJAMA-J AM MED ASSOC0098-748429.978MEDICINE, GENERAL & INTERNALANNU REV BIOCHEM0066-415427.681BIOCHEMISTRY & MOLECULAR BIOLNAT PHOTONICS1749-488527.254OPTICSNAT PHOTONICS1749-488527.254PHYSICS, APPLIEDPROG POLYM SCI0079-670026.383POLYMER SCIENCEIEEE ENG MED BIOL0739-517526.303ENGINEERING, BIOMEDICALIEEE ENG MED BIOL0739-517526.303MEDICAL INFORMATICSNAT IMMUNOL1529-290826.199IMMUNOLOGYANNU REV PATHOL-MECH1553-400625.794PATHOLOGYCELL STEM CELL1934-590925.315CELL BIOLOGYCELL STEM CELL1934-590925.315CELL & TISSUE ENGINEERINGLANCET ONCOL1470-204525.117ONCOLOGYCHEM SOC REV0306-001224.892CHEMISTRY, MULTIDISCIPLINARYCANCER CELL1535-610824.755CELL BIOLOGY数据来源：/journal/hust2012.php2012年以后，不再划分A、B、C、D类，而是采用JCR的分区概念，与之前的分类对应关系如下： T类 1区和2区中影响因子大于等于20的，T类不再分T1和T2类 A类 1区和2区中均属A类，T类是A类的子集 B类 3区 C类 4区 D类 不再划分D类分区说明： 1区 该期刊的影响因子排名位于其所在学科排名的前5% 2区 该期刊的影响因子排名位于其所在学科排名的前20%但未进入5% 3区 该期刊的影响因子排名位于其所在学科排名的前50%但未进入20%的 4区 该期刊的影响因子排名位于其所在学科排名的50%CANCER CELL1535-610824.755ONCOLOGYLANCET NEUROL1474-442223.917CLINICAL NEUROLOGYANNU REV PLANT BIOL1543-500823.654PLANT SCIENCESNAT METHODS1548-709123.565BIOCHEMICAL RESEARCH METHODANNU REV ASTRON ASTR0066-414623.333ASTRONOMY & ASTROPHYSICSPROG MATER SCI0079-642523.194MATERIALS SCIENCE, MULTIDISCIPPHYS REP0370-157322.929PHYSICS, MULTIDISCIPLINARYNAT MED1078-895622.864BIOCHEMISTRY & MOLECULAR BIOLNAT MED1078-895622.864CELL BIOLOGYNAT MED1078-895622.864MEDICINE, RESEARCH & EXPERIMENAT REV MICROBIOL1740-152622.490MICROBIOLOGYPHARMACOL REV0031-699722.345PHARMACOLOGY & PHARMACYLIVING REV RELATIV1433-835122.333PHYSICS, PARTICLES & FIELDSNAT CHEM1755-433021.757CHEMISTRY, MULTIDISCIPLINARYANNU REV PHARMACOL0362-164221.543PHARMACOLOGY & PHARMACYANNU REV PHARMACOL0362-164221.543TOXICOLOGYACCOUNTS CHEM RES0001-484220.833CHEMISTRY, MULTIDISCIPLINARYNAT CELL BIOL1465-739220.761CELL BIOLOGYANNU REV NEUROSCI0147-006X20.614NEUROSCIENCESLANCET INFECT DIS1473-309919.966INFECTIOUS DISEASESIMMUNITY1074-761319.795IMMUNOLOGYANNU REV PHYSIOL0066-427819.547PHYSIOLOGYNAT PHYS1745-247319.352PHYSICS, MULTIDISCIPLINARYBEHAV BRAIN SCI0140-525X18.571BEHAVIORAL SCIENCESBEHAV BRAIN SCI0140-525X18.571NEUROSCIENCESJ CLIN ONCOL0732-183X18.038ONCOLOGYANNU REV CELL DEV BI1081-070617.983CELL BIOLOGYANNU REV CELL DEV BI1081-070617.983DEVELOPMENTAL BIOLOGYECOL LETT1461-023X17.949ECOLOGYNANO TODAY1748-013217.689CHEMISTRY, MULTIDISCIPLINARYNANO TODAY1748-013217.689MATERIALS SCIENCE, MULTIDISCIPNANO TODAY1748-013217.689NANOSCIENCE & NANOTECHNOLOGANNU REV GENET0066-419717.436GENETICS & HEREDITYCLIN MICROBIOL REV0893-851217.313MICROBIOLOGYBRIT MED J1756-183317.215MEDICINE, GENERAL & INTERNALMICROBIOL MOL BIOL R1092-217216.417MICROBIOLOGYASTROPHYS J SUPPL S0067-004916.238ASTRONOMY & ASTROPHYSICSANNU REV MATER RES1531-733116.179MATERIALS SCIENCE, MULTIDISCIPTRENDS COGN SCI1364-661316.008BEHAVIORAL SCIENCESTRENDS COGN SCI1364-661316.008NEUROSCIENCESNEURON0896-627315.766NEUROSCIENCESPSYCHOL BULL0033-290915.575PSYCHOLOGYNAT REV NEUROL1759-475815.518CLINICAL NEUROLOGYTRENDS ECOL EVOL0169-534715.389ECOLOGYTRENDS ECOL EVOL0169-534715.389EVOLUTIONARY BIOLOGYTRENDS ECOL EVOL0169-534715.389GENETICS & HEREDITYSURF SCI REP0167-572915.333CHEMISTRY, PHYSICALSURF SCI REP0167-572915.333PHYSICS, CONDENSED MATTERMOL CELL1097-276515.280BIOCHEMISTRY & MOLECULAR BIOLMOL CELL1097-276515.280CELL BIOLOGYANNU REV PSYCHOL0066-430815.265PSYCHOLOGYPLOS MED1549-167615.253MEDICINE, GENERAL & INTERNALNAT NEUROSCI1097-625615.251NEUROSCIENCESCIRCULATION0009-732215.202CARDIAC & CARDIOVASCULAR SYS