INTRODUCTORY PLANT PATHOLOGY
INTRODUCTORY PLANT PATHOLOGY BOT 350
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Date Created: 10/19/15
Introduction to plant Viruses Valerian Dolja Cordley Hall 4067 Tel 73 75 4 72 1898 Dmitry Ivanovsky Russia and Martinus Beij erink The Netherlands described the rst virus Tobacco mosaic virus Viruses are the major players in the genetic universe 1 cm3 of seawater contains 106109 virus particles Suttle CA 2005 Nature 437 356 g There are millions of diverse bacteriophage species in the water soil and gut x 3 Edwards and Rohwer 2005Nat Rev Microbiol 3 504 44 Viruses dominate biosphere there are 10100 viruses per each living cell The metagenomes of viruses and cellular organisms have comparable complexities VIRUSES Noncellular form of life I Obligate intracellular parasites I Exist as inert particles Virions outside the cell I Virions harbor viral genome protected by protein shell Viral form of life Genetic Diversity m Pg amp x and EFL l w b lt E m u lt M 4 CELLS VIRUSES Host Ranges of g a I Reprndllctinn Binary ssinn Assemblyfrnmthe Vlmses pnnls nfcnmpnnents Membrane All phases nfthe Only Envelnped viruses life cycle when nutside the l Translatinnal All types nfcells Nnne nfthe viruses machinery Gennme dsDNA dsnr xx DNA nr RNA 5 quotI 3 I R M amp J H mm w E55 Cnmmnn High 7 Vlrus ongms from quotquotuquot 3 at am 4 2 eukaryntic picnrnzvinlses Precellular 7m quotm 3 mmgmmgm Wigwam Gene Pool Virus particles Virions are built of a nucleic acid and a protein shell PENTAMER Icosahedral spherical Virions Elongated helical Virions Virions under EM Geminivirus ssDNA Within a double sphere Tobacco mosaic virus ssRNA Within a helical rod DNA 39 Families and Genera of Viruses infecting Plants I RNA dsDNA RT I SSDNA Caulrmovmdae Caulimo virus Gemini Vi f i dae gngVIIlke Vf Re SbCMV like Mastreyirus Nanowrus Curtovirus Begamo virus Badnavirus RTBV er j dsRNA SSRNA H SSRNA 4 Emma viridae Sequiviridae Tombusviridae gcu vgs BgnyaVI39ndae buts viridae Brama virus OSPO VIN5 ara ivirus Heo viridae M Oben39ovims 0 o 39 ymovmls Ilarvirus Phyloreovirus 6523 Umb aV rus Ofyzayirus Hhabdovlrdae Cytorhabdovirus ganq v fus Nucleorhabdovirus ph ov ms 0 Alfamovirus Comovmdae E a SSRNA RT ldaeavirus Partiriviridae r Tobamovirus Alphacryplovirus PSeUdo V dae m um m Betacryptovirus Ourmiavirus 39 139 mum AIexiw39rus Carlavirus Foveavirus Potexw rus Benyw rus w V hmlwfqvw mum Varicosavims Capllowrus Trlchowrus Vmwrus v Potyviridae Closteroviridae 100 nm Virus Life Cycle 1 Invasion Cytoplasm Cell Wall Invasion through leaves vectoring insects mechanical damage Invasion through roots vectoring nematodes or fungi mechanical damage Exception seed and pollen transmission Virus Life Cycle Virus Life Cycle Particle virion assembly Genome uncoating expression and replication 1l unmatng JJ translation II I V J deUJ III J4 41 JJ J replication I Virus Life Cycle Virus Life Cycle Systemic transport through phloem Celltocell movement quotmm m awnquot m m quotINm Mm vmuIv ylmmuh Virus Life Cycle RNA genome of TMV 64OO nts three genes and three major functions Plant to plant transmission a RNA REPLICATION RNA ENCAPSIDATION tnmntn spam will tnhnccn Host Resistance Two major types I I I Concert39 of Speci c recognition39 defense responses nonrace speci c i a ive nttt Genetics of resistance continue Genetics of resistance continued Host cultivar mum mquot M each atthe cultivavs recagmzespathagen isolate tut Wu B m Hm mm WW Mime w an 1 1 W 2m M lgg tsjlstq vecagulze isolate 2 Pathogen AVR gene avirulence gene thi ll 7 HF Racespecific resistance is based on the Gen 0 Gene Hothe5is The product of a single gene in the host specifically recognizes the product of a gene in the pat 0 en During an infection event an interaction b tween these products results in incompati ility Le a hypersensitive response and programmed cell death Host is RRz or R 1 AVRvAVR OI39 AVRI 7 re a me mam Hypothesized physical model for how Rgene and Avrgene products interaction on plasma membrane ofhost cells Pathogen protein AVR interacts with host Rgene protein Cf9 which triggers the cell death response hypersensitivity Exam an n n l2 mm mdu quotmu l7 1 Three cultivars each with a different R gene yields 8 races 23 v 7 7quot 7 77 Ten cultivars each with a different R gene could discern a possible 1024 races 2 The set of cultivars used to 39 characteri races is r a v For each ofthe boxes Indicate whether or no the races of a rust pathogen quot quot 39 infecting the host cultivars R A39 active product present 7 39 active product absent Oomycetes WOTCP molds Websites to brush u on Oomvcete diseases Diploid 2N Ovewiew of Oomvcetes a isnel oraleducationLabEm 1 icetesi To lIIIIll Hyphae are coenocytic tubes 7 I 39 Ge W0 made 0f ceHUI se Blight of PotatolTomato sexual reproduction v 1 11etomeducation lamPathLateBliomdafaulthtm oospo re quot o my mildew of grape l l 39 l l 39 l h phthora root rot of so bean net 010 enlcation Asexual reproduction sporangia and zoospores Lecture 5 Disease Cycles Example 1 Late blight of potato T111110 0 look tor spunnglum Apple scab disease cycle video spursngmm WM l mm mm m 1 m l l mnem summer 0y cle of reproduction QERWINTERI mosnmas l I a charm j are spores tomied by sexual or asexual proce s 2 which spore type is most impo aiit economically l quotlento1 plant I Generlc Dlsease cycle 39 Outside Host OVE RWINTE RING Disease cycle diagrams pro de useful information BUT what information is difficult to obtain from the drawings 9 A 39eighting 0f the practical signi cance of the various steps cycles and subcycles ary cycleVS 0 A nse 0f the length of time required by various steps cycles and subcycles U o o o 039 Lecture 5 Disease Cycles Example 1 Late blight of potato quotquot 39quotquot 39 loculum infectious propagule usually wmngium g mmquot a i 7 from an ovenyintering source that initiates muf n perpetuates the prinr 39 ease ch as opposed mm LR to infectious propagules spread disease hiring the 39 Tm season 0 ERWINTE mum 39 n r spore anmenaium 39t i W 39 2 s lly39 as i disease cycle t Secondary inoculum infectious propagules that were produced by infections that took place during the same growing season this qje of ulurn is nearly ah 39ual and the infectious p agules are relatively shortlived di ease cycle tern continued Polycyclic disease a d e where one to many cycles of infection are init Ited by secondary inoculum liar diseases e0 t grzes are pol C lic lVIonocyclic disease a disease where infectl are caused by primary inoculum only S lb rne diseases are comIm The timing ofindi 1dual infections can still I ease cycle terms continued Terms that addre the TETE REQUIRED 39 ues they relate to the period after infection but be are symptom expression the time between infection ilIlL 39 Incubation perio ex on r t ally regulated by temperature mptom 39 Latent nilar to incubation period it time the time from ii on to ne pore p Mill c on r the latent overns the speed of incret e of poly c c L Quie cent infectio nptoml inac 39c infections 7 important in man nit ro ant eedborne I ea Outside Hos OVERWINTERING Deposition msseminafion Infc on Incubation urvival E Disease Developmenf 2 0 gt o gt E E o o o 0393 Inside Reproduc iion HOS Lab Tuesday Electr n Microsco and Nematode Extraction Quiz for Viruses pp 7583 and Observation ofViral Movement in Plants p 119120 and intro sections for Electron Microscopy pp21 and Nematode Extraction 39om Soils p 84 week 1 Review of RNA silencing A wayward petunia leads to the discovery of modest little Finish Kochvs postulates reexamine symptoms molecules with enormous medical and agricultural promise Demonstration ofelectron microscopy Extract nematodes lab Observe movement ofGFP expressing virus under black light Record data on from virus inoculations Principles of Plant Disease Control Principles Of Disease CO OI Review Excl 39 Fitll l 39l 39 li 39 n Disease management strategies revolve around three manageable factors We Eradication m reduce the amount or ef cacy ofinitial inoculum Therapixh XD or amount of initial disease yD Host resistance re reduce the rate of disease develo ment r change the time frame t Protection Methods certi cation quarantine Princiles Exclusion Eradication rotation pasteurization fumigation Therapy surgery drug treatment heat therapy Host resistance Rgenes polygenic pathogenderived Protection chemical paints biological agents Avoidance planting site date depth and maturity 39 e irrigation method drainag Methods to achieve pathogen exclusion legally enforced quarantines seed certification Distribution of pathogenfree propagation stock Exclusion of pathogens Purpose to prevent the introduction of a pathogens into an area where susceptible plants will be grown this area can be as small as a green house or as large as a country Goal is to produce susceptible plants in a pathogenfree environment Pathogens distributed with propagative parts are vulnerable to control by exclusionary procedures Quarantine Governmental action to prevent spread of disease Quarantine Citrus canker quarantine and eradication legislative control ofthe propagation culture or effort in southern Florida transport of plants or plant parts to prevent the spread Quarantine m wniun cnumy of pests or pathogens Citrus canker OI39I grapefruit Citrus Canker Questions about Quarantine Disease Certification Seed and D39sease cem cat39on Propagation Stocks Governmental assurance of quality smuvcemm my sympto mneesm msezses m seed nmanes Disease TulerancE Gen w musaic n1 Putatu lealrull n 15 ring ml Wu blacklEE Pathogen free or pathogentested Questions about seed and propagation materials Certi cation purpose is to ensure little to no pathogen resides in propagation s ock llDtE l typically pathogentesting39 requires lab testing by government agency or increasingly by a rivate compan Pathogenfree or pathogentested seed and propagation materials Often goes handinhand with disease certi cation but may involve testing planting stock for the presence of pathogens btaining pathogenfree seed Grow seed crop in area isolated from the pathogen or area where the climate is not suitable for the disease dry climate Obtaining pathogenfree clonal plant material Use micropropagation to cure infected plants and to at least initially mass produce pathogenfree plants EL Example of a s eed class Field year WWW 1 m mamas a o e n Dem Plan Frenuciearpanlers and Plants microrubers maintained in Pamaloqy vim in 9th mama39s warm stark quotmm mm tested potato WWW mm seed program 1 Minn Rogued irewenm EUSA resrm deem anyDarhogen Mum gleam mm 2 Rogued Visasmg news lt mum Wmmmnee m Once propagated fr risingigarageugnitgi quotquotquotquotquotquotquotquotquotquot quot a pathogemtested Ema 4 raunmmmmm tissue culture clonal yggggjnwiig fdlem x 4 Fnunmi nn eremmn exist in the program for up to 8 years Fauna nn rGenualnnz Fauna nn eremmn a N la in IA in COMMERCIAL LISE Mmmm mm m plamnv Plus vmhavemesunv xmmeme mm m plamnv 39 mamquot meansellviblehrwminuedusemseedvmduamn mammarde Mammy PmcessmV rsnugWmquotgramme Etherdassrmimeetbluear llawu mammals whenshlvvm V 7quot European Plant Protection Organization Programs in pathogen tested planting stock PM 411 Virusfree or virustested 39uit trees and rootstocks PM 421 Pathogentested material of carnation PM 432 Pathogentested material ofpelargonium PM 441 Pathogentested material oflily PM 451 Pathogentested material ofnarcissus PM 461 Pathogentested material of Chrysanthemum PM 471 Nursery requirements recommended requirements for participation in ce i Ication offruit or ornamental cro s PM 481 Pathogentested material ofgrapevine varieties and rootstocks PM 491 Pathogentested material of Ribes PM 4101 Pathogentested material of Rubus PM 4111 Pathogentested material of strawberry PM 4121 Pathogentested citrus trees and rootstocks PM 4161 Pathogentested material ofhopPM 4171 Pathogentested olive trees and rootstocks PM 4181 Pathogentested material of Vaccinium spp PM 4191 Pathogentested material of begonia PM 4201 Pathogentested material ofNew Guinea hybrids ofimpatiens PM 4211 Pathogentested material of rose PM 4261 Pathogentested material of petunia Questions about Pathogen Tested Micro re a ation Micropropagatlon p p 9 Goals curemfmted lam obtaIn pathogenfree plants Obtain clean mother39 plants IvaIntaIn pathogenfreecondmon as numberofplants Is Increased Typically systemic obligate pathogens are targeted eg viruses 2 test for pathogens to detennIne If the new plant Is Index39 pathogen free 3 Increase Indexed plants In pathogentree envIronnIent tnen retest Example of micropropagation program Microroaation Proram continued quot Ex 25quot quotquot quotEmma s 6 7 quotquotquot E 5 Rnnl Increased Hamlets Plan III 39s JIESEII39 memum nts for f d production as transplants Increased indexed plantlets in pathogenfree and insectfree greenhouse F r PotatOFS at this quot399 39 39 39 1 point the Indexed 11 A 39 generation could he 5 m quot growna s cer Ie for several seed years Principles of Disease Control Chemical Control Exclusion preven in the entrance of inoculum or establishmento apathogen within an uninvaded EffeCtiVei eXible teChHOIOQYg area Cost can be a factor 9 Eradicatl reducing eliminating or destroying inoculum quot mm39 Users require special Tquot lmgsgarstgissztamassing 395 knowledge and training empera ure rainage Repeat treatments may be necessary Pathogenresistance to fungicides P quot3333girl 39 lllirei ili 39 3332 J39iweb3aihogen Health and environment concerns a Environmen Avoidance Avoiding disease byavoiding the patho en Chemistry continues to evolve 9 of byaltering the environment outside and insi e Dan Host resistance reducing ef ciency of inoculum via host genetics FunQICIde market Dominant uses of fungimdes 9039100 million Pounds CI emical Crop Protection Market by Field crops Seeds Nursery FOIiaQe and Soil of copper and sulfur product Class 2001 foliage in some high yield pot drenches root dips applied to fruit crops environme ts seeds stored products 40 million pounds 77 Fruits and nuts Foliage Fruit ofs nthetic or anic I I39e nd posth r chezqicals applged 0 Essential tools in most crops treatment of Spawn bads apples I apples bananas grapes potato peanuts citrus Essential for some crops value playing surfaces Mushrooms Routine Turf Essential for Vegetables Seeds Foliage maintenance of very high grapes other veges fruits cereals in high yield situations ornamentals and turf eg potato Methods of Fungicide Application Methods of Fungicide Application i w m Mummammmmmi m mgim mwm5 mip Smallfarm technology 3 Aquot quot 3 Ground or beam Air blast or air assisted sprayer for eld and sprayer for orchards and vegetable crops vineyar s Seed warehouse or farm service provider Methods of Fungicide Application Classi cation of Fungicides Protectant house paint analogy a chemical barrier protects plants from infection MOST fungicides are in this category they prevent infection but do not kill spores Eradicant kill the target organism like insecticides the chemical reduces inoculum uncommon for foliar fungicides Chemotheraputant cure infections drug therapy generally restricted to indexing programs eg injections to target a pathogen inside plant Classi cation of Protectant Fungicides Contact think house aint protect for 7 to 14 days ocall sstemic move in the apoplast xylem application to one of leaf commonly protects the other side Exam Fung de treated 39 disks placed on leaf 8 1 then inoculated with k powdery mildew benomyl Locally systemic materials imamumgu Control of this stage in ki dim am Wittluu m m Up to 96h after germination requires movemento t e chemical into tissue Olmtilbn Fauntlun M B u liMi Ipprmndum umdlaluiii and quotWilma m Iiilcduili Fungicides with this property are said to 39 have kick back activity39 Once infection has progressed to this point fungicides Contact materials DO NOT t ff t inhibit advancement are 0 e 9 3 Ive beyond these stages Locally systemic materials can move through tissue at different rates L gt Azoxvsunbin Metalaxvl wmt Synmic mm 3 day aim In ation Order of 39 39 39 39 Effective discovery Fungiades Families dose coppers Bordeaux mixture 5 High organomercuries dithiocarbamates benzimidazoles gal cal pathway inhibited at single site This strobilurins site varie fungicide family ine cone funus strobilurins are the newest Strobilg tendcellus gicide family they are based on a natural antifungal chemical produced by a Basidiomycete 0 Stratiluiin A 197i i973i Fungicide resistance Fungicide resistance example lnmally pathogen lndnnduals are sensitive to low doses of the chemical Exposure to the fungicide selects for those that row at h h chemical doses 7 Ca Example l After repeated prolonged use of fungicides atho ens unaffected by their toxic effects are 1965 selected for Number offungal g nera resistant to a fung Every family offungicides discovered in the 39 7 1 L W Fz quot39 quot b 5 399h a In I I s last 35 years has developed a probe th Low Fungmde dose High pa hogequot grow by 50 pathogens becoming resistant to their effects m quotmmquot Relative gluwth 50 Sen lt gt Strategies for managing resistance Resources for knowing When in pathogens to chemicals to Spray fungicides M39Xtures 0f fung39C39des Regional splray guidtestare wblisnedforj stfaboutevery h typical prepackaged39 strategy mix locallysystemic single frfg wiahgriquotggvngp cit ve g aelf gta icav r y quot39quot 39 e39 site at risk modeof action fungicide with a contact material that has a multisite modeof actlon Phenologybased spray guide for backyard fruit production so a Rotate chemicals Disease warning models have been developed for many foliar Alternate mng39c39de fam39ly w39th each appl39camquot diseases where fungicides are required for control These models use weather data to provide information on the liklihood that lelt usage J W C WW 7 W conditions for infection have been ful lled comprehensive disease management program inclu ing d Is Example39 California PestC st Dis se Model Database use ofdlsease warning mo e l 39 39 mnur Review of Lecture 2 Disease was de ned type ofinjury continuous irritation causal agent Three ingredients are necessary for disease to occur Host Environment Pathogen The disease triangle Disease is a condition of the host Host responses to disease are termed Symptoms Causal Agents of plant diseases abiotic biotic fungi bacteria viruses nematodes Disease symptoms Symptoms are the plant s response to disease Symptoms re ect the physiological function of the plant that is disrupted or impaired Diseases have namesll Name of Disease Apple scab Causal Agent Venturia inequalis Host apple Tissues affected leaves and fruit Primary symptom scabtype lesion Secondary symptoms Defoliation fruit deformation and drop ommon Names of Plant llll url Diseases can be categorized according to their symptoms Examples root rots leaf spots abnormal growth vascular Wilts fruit rots Signs Signs are the physical evidence of a pathogen s structure Lecture 3 Disease Dianosis Readin Assinment Website APSnetorg Education Center Main Menu Introductory Plant Pathology Topics in Plant Pathology Plant Disease Diagnosis M B Riley M R Vl lliamson and D Maloy Know what is possible Seek out literature that categorizes diseases by host APS compendia on diseases of specific hosts APS Database Common Names of Plant Diseases USDA publications PNW online guide to plant disease control Disease Diagnosis Know What is Normal Know what is possible Collect Background Information Check for Symptoms and Signs Observe Patterns Ask Questions Laboratory Consultation ampTesting Final Diagnosis Important diagnostic resources are becoming available on the web Field crops 3 Tree fruits 8 nuts 3 Grasses 3 Samples by r a crop type Vegetables 5 IO Soil Small fruits 7 26 l Herbaceous omamentals 10 Woody Miscellaneous 13 ornamentals 30 Observe Patterns Biotic Abiotic Fact 13 of problem samples submitted to OSU s Plant Disease Clinic have an abiotic cause Collect Background information Information that ma be imortant a identity ofhost to culti r b planting date and emu onmental conditions at planting seed source seed treatment if applicable seed germination disease history description of rst symptoms when rst noted spread speci c factors associated with disease appearance cultural practices chemicals and dates of application eld and crop hist y weather conditions during season and period of disease development 9er Symptoms of Abiotic Injury What s the cause Symptoms of Abiotic Injury Note uniformity and sharp transition from healthy to injured 391 1 blossom end rot Once again note the sharp transitions from healthy to injured I m What s the ab tic cause Observe Patterns Abiotic causes a often no spread is observed acute episodic b regular distribution or uniform damage c clear lines demarcating healthy vs damaged d more than one plant species may be affected e linear stripes t more common near edges of host population Biotic or abotic biotic ca symptoms are ty ical arranged irregularly the transition from injured to l1ealtl more diffuse Observe Patterns Observe Patterns WIthIn a plant populationl 39el patterns observed With biotic causes random lisn ibution P ri ma ry VS seco nda ry l 39 39 edbo111ei11oc11111111 or if t s m toms i11oc11111111 OlllLB e1 11 m anary symptoms occur at slte of Infectlon y 1 a u 39 agglegat l 039 contaglous ms lbunon examples root rots leaf spots blights kers vew co111111o11p 1tte111 galls can i11 1 1 e 11 11tio11 followed 5 d t t t d t t econ ary symp oms occur a SI e Is an 1 Inn 1105 populd 1 n from the primary symptoms and usually E later in time V examples above ground symptoms of pawl ms bullon t root rot crown rot or vascularwilt characten 10 o 1 oot 111tect111g pathogens nematode damage often delimited b to ograph or soil type ary symptom lesions on roots Secondary foliar chlorosis stunting ot and top dieback ary symptom necrotic lesion Secondary chlorosis defoliation Diagnosis is a form of Primary symptom vascular discoloration Secondary unilateral wilt of leaves e olia ion roots remain heal hy Primary symptom sunken lesion Secondary istal branch diebac othesis testing Diagnosis is detective work Multiple pieces of evidence may be required Evidence must be weighed accordingly Tynes of tests Microscopic observation of signs Incubate disease tissue in moist chamber Culture diseased tissues in petri dish ochemical test 39 serology DNA hybridization Chemical tests for abiotic causes pH nutrient deficiency etc Koch s posulates if new disease Principles of Disease Control Exclusion preven ing the entrance of inoculum or establishment of a pathogen within an uninvaded area MW Eradication reducing eliminating or destroying inoculum at the source Therapy curing diseased plants by use of chemicals drugs surgery or an altered environment temperature drainage Host resistance reducing ef ciency of inoculum via host gene cs Protection reducing the ef ciency of inoculum by interposing a barrier between host and the pathogen Avoidance Avoiding disease by avoiding the pathogen or by altering the environment outside and inside plant Three examples of Eradication Fallow Thermal inactivation heat Chemical fumigation Eradication reducing eliminating or destroying inoculum at the source Usually targeted at pathogens with monocyclic disease cycles The treatments are typically harsh but commonly an additional bene t is achieved suppression of weeds conservation of moisture Fallow is the practice of allowing a field to remain uncropped and commonly weedfree Pur oses p Accumulate soil moisture and Reduce inoculum ofplant reduce pathogen populations pathogens on high value dryland wheatsummer fallow land forest tree nursery rotation in eastern Oregon Thermal inactivation with fire Open d burning crop Propane gas aming re is debris is the fuel Practiced in grass seed elds in PNW for control of ergot blindseed disease seed gall nematode Cost per 20 per acre Thermal inactivation with hot water Used to eradicate bacterial pathogens from seed or other propagation materials budwood scions etc typical protocol 5 Cfor 20 to 25 min downside plant material can emerge from the treatment less vigorous Mflt McGrarh Thermal inactivation with steam Pasteun39zation of soil Heat soil with aerated steam want to achieve a temperature of 82 C for 30 min This kills nearly all plant pathogens but does not completely sterilize the soil Steaming media for pot culture Moving bed steamer Thermal inactivation with sunlig Solarization of a field in Israel E ctive on soilborne pathogens Verticillium w It nematodes Fusarium wilt Solarlzatlon Practiced 39 Israel Cal fornia and Australia nual crops but some success erennIals such as pIstachIos olIves Temperature C am 5 49 tarp o 3 Works best Cean t n pa5tic Treatment is 95 efficacious Wet so I Intense summer sunshine Plastic on field 3 4 weeks Also controls weeds Fumlgants am sodium Vapam not a true fumigant but in moist soil releases methyl isothiocyanate which is a fumigant very effective on fungi Applied by shank 39njector in irrigation water or as granules no tarp 1 3 dichloropropene Telone excellent actlvity on nematodes no tarp chloroplcrin tear as kills nematodes and fungi usually m Xe d with methyl bromide as a warning agent requires a plastic tarp methyl bromide highly toxic gaseous biocide requires a licensed applicator and a plastic tarp quotquot Use of methyl Fum39ants work best bromide is being llght soHs sandy low organic matter moderate temperatures moist but hot wet soil will take its place Eradication with SCI fumigants Purpose eradicate a spectrun l of soil borne diseases nematodes and weed seeds Primary uses all preplant high value food crops strawberries p ppers potato nurseries sod and cut flowers and bulbs orchard and vineyard replant situations Non rum39gatec39 c in forest tree nurse Eradication with soil fumigants Injection and tarping of soil fum gated with methyl bromidechloropicrin Chemigation of metam sodium Websites to brush 9 on TIMELINE OF INFECTION Anamorhic Ascom cetes Outside of host Inside of host Fungal winger diophore f Early blight of potato and tomato con Verticillium wilt microsclerotia i Leucostoma canker of stone fruits pycnidium An hracnose of turfgrass acervulus e CONSTITUTIVE DEFENSES chemical structural Induction of s1emic Acquired Resistance Induced biochrgmical defenses 7 mmwmpw mm V wer eci f t defenses In dlstal V Thickening 01 plant cell wallquot P mnt in ii ermine m 1 cumulation 39 noninfected parts of the plant c PR A 1 After a primary inoculation here Plants can have more than one type of acquired resistance N edwardscnii manna VIM gt lung m E Pathugenesis I related rmEl 39 39 PR1 N edwgrdson wzeo In HFL Roslstnnl llmmmnh sysknverrqulnd minimum quotEmmetquot m m Inoculated with A lam dilemma Inoculatedwith p V 39 water mildewpathogen Tl quotW3quot lt i Outside of host Inside of host Fungal pathogen P M m Hun Hum tur nmth Wild type plant tur nmtiun with inducible SAR ru mmnun u y milwm tum WWW mm F plll Mutant plant with constitutive SAR 39 39 gt mmanm mun Hp structural CONSTITUTIVE DEFENSES chemical All ofthe defenses we have talked about so far are likely operative in most plants most of the time Constitutive structural cuticlethickness Constitutive biochemical waII Iigniiications Induced structural cellular papillae tyloses gums suberin and abscission layers Induced biochemical local phytoalexins systemic SAR reactive oxygen species PRproteins such as chitinases Collectively we will refer to the above as th e concert of defenses Hypersensitivity Specific Recognition Some host cultivars can 39 recognize certain s a exhibiting an HR V O 9 Combinations oftwo or more HR induc39n more on this later A nal lnduced biochemical defense The hypersensitive response HR is a localized death of host cells at the site of infection It is the result of a speci c recognition of a pathogen attack by the host The HR is considered to be a a type of programmed cell death39 It can be a very effective form of resistance against obiigate parasites lmortant o39 In addition to disease a hypersensitive response also triggers Induced local defenses in nearby cells eg phytoalexins Systemic acquired resistance eg enhanced levels of PRproteins TIMELINE OF INFECTION Outside of host Inside of host Postinfection Huustorium formation biotroph erm tube searcn oxin orniation necrotroph Appressorium formation Detoxification of phytoulexins Penet ution peg Reproduct39on Germination 6 Host General induced Pupillue defenses formation Specific recognition gt Hypersensitivity Phytoulexins structural CONSUTUUVEDEFENSES chemical Significance of Plant Disease Current S ation 10 of all food production is lost to disease 30 to all pests The introduction of exotic plant pathogens has caused great losses American elm amp chestnut Many additional exotic threats sudden oak death soybean rust Each year suppression of plant disease costs billions of dollars worldwide Plant pathogens can restrict trade Pathogens continually evolve break resistance in host crops develop insensitivity to chemicals Course Content Up To Now Theme 1 What is a disease What do the symptoms amp signs tell us about the host39s condition Theme 2 Disease cycles Oomycetes ampAscomycetes How speci cally does the pathogen turn the primary cycle Does the pathogen turn a secondary cycle Theme 3 Pathogen life strategies How does the pathogen cope in the world of the living ofthe dead Theme 4 Timeline of infection events The dynamic struggle of attack and counterattack Disease defined Disease is the in39urious alteration of one or more physiological processes in a living system in our case a plant caused by the continuous irritation of a primary causal factor or factors H ost Pathogen Environment Disease Diagnosis KnowWhat is Normal Collect Background Information Check for Symptoms and Signs Observe Patterns Ask Questions Knowwhat is possible Laboratory Tests Final Diagnosis Disease Cycle Terminololgy Disease rnnrent prinul nd ryrle diagrams inm39 ortlie diagram were deernhed 3 eielwas de ned tsexllalgasexuall irepmtingl cycle was de ned issemi Diseases can he rategnrired intn twn typ er nf cycles xmnnryrli 39 39 39ala lbyprinury innullumnnly pnly rlir e addilinml intertinn ryrleiel initiated by eernndary iuuruiiuu Ierrue tn help understand the tirue required tn turn a cycle iuruh adnnpen39nd e rnrruiurertinn In 3311111111 erpressinn h ent period leer erat39rrn tiuiel e rnrru interdnn In new interan pnrpaguie q 7 t I iueerer t irderuin pnanl zrlnnpavlmgenI lnrmanry ow how to apply these terms to the life cycle and You need to kn biological structures of Domycete and Ascomycete pathogens I Generlc Dlsease cycleI I 4 REPEATING sue AsauAL Imlmer cm I Life strategies of plant pathogens Pal39asitism Saprophytisru TE FACULTATIVE FACULTATIVE osth TE FAR l39l39E ROFHXTE FARASITE SAFROPHTE Defquot obligate adj restricted to a particular style of life facultative adj optionally but not preferred Oufside of host Inside of hos gtlt Fungal pathoge Prei 39 39 Postinfection Haustorium formation biotroph oxin formation necrotroph Detoxification of phytoalexins IReproIduction Hosf l I General induced PapiIIae defenses Cork 6 Iignin Systemic formation layer 39 r Phytoaiexins sfrucfurul CONSUTUUVEDEFENSES chemical Website to brush up on bacterial diseases of pepper and tomato i H Ha om w it Bacterial spot Pota o blackleg and soft rot minty m Tim19iiiuiixm Crown gall U ntiip 2 3292 ixfxfiiiwr s on a rig feet at oati ilvli om P i 1 mg Livinitiwj 43311 Mi m U 6 him quot m e a T39quot F V H quot572 I 1 uif lr39lij i111 mm 3 Lr LI 82 QAHLLnL uixr u13drm U M M u L U11 11m 5 Fl 1 Methods of ovenvinterinq In host or in seed or in clonal planting stock On host as epiphyte Free living in39 soil water or debris generally rare mmm a e as t I is w 1 Wk mama Mclhods of peneu adon and invasion by bacteria Through sloma Thraugh wound Eaclerlu m neclur and Thmugh hydmhode through necinrmode it is the ability of bacteria and some fungi to grow and reproduce saprophytically 39 plant surfaces jargon to V9 in the quotrhizo sph ere oh roots or ih the phylospherie on a foliar surface or Within a biofilm Typically with bacterial pathogens if an epiphytic phase occurs prior to infection 39 Epiphyticgrowth is favored by a humid environment A bacterial epiphytic phase has been shown to influence a plant host s sensitivity to frost injury ice nucleation phenomehort Epi phytic 39preinfection phases of bacterial and fungal pathogens are frequently susceptible to biological control acteria pathogens possess the ahiity to grow and reproduce on or in a plant wthout necessarily nciting disease This growth is called growth upon the plant or within the plant Nonpathogenic bacterial epiphytes Pathogenic aSSOCIate superfICIally bacterial epiphytes ass oc39ate 39nt39matel Q g g I I y Wilson Hirano amp Lindow 1999 H202 AEM6514351443 survival of epiphytic bacteria 25 20 15 from H202 o 5 o 2 cy 6 A 39 Q n 1 r33 q lt9 lt9 G7 q o 2 lt2 lt2 lt96 lt9 6 9 of cells in sites protected Pathogen strains Bottom line Pathogens are specialized to associate intimately with their host Biological control Definition reduction of the amount of inoculum or disease producing activity of a pathogen by or through one or more organisms other than man Cook amp Baker 1983 How is it accomplished Introduce saprophytic microorganism to plant environment Modify environment or cultural methods to favor specific saprophytic microorganisms that can accomplish biocontrol Examp les Awmgm mm Mmfra gmmg I W557 9mm Wf l I gwmmafm f fr l lm by A mm fum mfg xamjjglileeg mg mi agi gia tm KMD mtg diam m m m by am c mgsmu IUD mm magm mwmwy mdlmgmyg Hi g vie3W Wm b g E oil goj aqu mfg Ieamlg rm ea gwgmm m 45 Lam mgo ng mm 1123 m m m f WEwZPfM Emma Tm m g m 1 wmmwm m m M l uy i m gimmn m m ILQGQJW39U Q o a Pathogen o 3 B iggom r oj o Psmg higm Sfra in a The importance of antibiosis to the effectiveness of K84 Tomato 39 2 A A A A Antibiosis ineffective A A I IAntibiosis effective i J Antibiosis 39nE eCt le Antibiosis is ineffective A either when K84d0esn t make its antibiotic or when the pathogen has become resistant to the antibiotic 62 Q g 621 Tj 04 Q Q 1 62 if A O I EAntibiosis effective Works best when1 The site of infection on plant supports growth of saprophytes wounds seeds owers root surfaees 39 when the biocontro l agent possesses additional tools to suppress pathogen activity t a when disease is m39onocycl39ic and the pathogen is restricted to a short window of opportunity wound heating seed emergenee idioom period Websites to brush 9 on basidiomcete diseases Brown root rot heart rot mm H Common bunt of wheat I39illl 39 du 39PIaI39IlF Stem rust of wheat o i t Rhizoctonia diseases oft rf When asking questions of how fast how many and how far the distinction between monocyclic and polycyclic disease is very important Recall Polycyclic disease a disease where one to many cycles of 39n action are initiated by secondary inoculum Many foliar diseases eg powdery mildews and rusts of grasses are polycyclic Monocyclic disease a disease where infections are caused by primary inoculum only Soi borne diseases are typically monocyclic Diseases of speci c growth stages are monocyclic smuts fruit rots Disease development in populations of plants How fast speed How many ef ciency How far movement The Late Blight Epidemiology video dealt with the question of how fast for a polycyclic pathogen O asexual repeating cycle Disease pg ress curve The amount of disease plotted as a function of time requires information on disease severity over the course of the epidemic Disease severity Question Phases of a olcclic eidemic Whyisthe curve S shaped exponential phase up to 1 disease speed of Why is the generationtime latent period important increase is limited by supply of pathogen propagules disease is increasing rapidly 100fold increase is O shortlatent period 0 longlatent period common but is unobserved because the overa amount of disease is so small logistic phase speed of increase most limited by environment Durin this phase disease increases from 1 to 50 50fold increase terminal phase 50 to 100 speed of increase is most limited by the amount of host tissue t damage is done to the crop during the terminal phase but only a 2fold increase in disease Disease severity Polycyclic diseases are best managed reducmg Speed How can the environment in uence epidemic speed Questions 100 How can host cultivar increase or decrease epidemic speed Y Use the disease triangle as to guide to thinking about epidemic speed Hijat Disease severit Disease severity En liDl imE l it Question All other things being equal will reducing the amount of overwintering pathogen primary inoculum slow the epidemic Note this idea is termed Sanitation the degree to which the amount of primary inoculum can he reduced by a management action Sanitation here isease severity In polycylic diseases the infection rate r governs the value of delta t is delay in diseasesarlltatlorl epidemic as a result of sanitation At is proportional to inverse of r One divided by infection rate r39 think of r as a potential birth rate of new lesionsinfections Is also our measure of potential epidemic speed a high value of r rate results in small benefit from sanitation a small I results increases the value of sanitation For polycyclic diseases reducing primary inoculum with sanitation is not always a tremendous value 100 Second curve was generated after an 80 reduction in primary inoculum Result Epidemic was delayed by 8 days Disease severity Assumes infection rate 139 02 per day Question How do we visualize or estimate this idea of infection rate39 Disease severity I w 100 r gt 6 gt 4 a gt a u a u m a 9 D time H011 Natural IL quotnorm Getting inside the host is sritieal 39 step is development Fungal pathogens use a 1 V to guide their way to site where infection is possible Pathogens use to establish a parasitie relationship enzymes growth regulators toxins j that pathogens are highly evolved to enter and establish a parasitic relationship with their host Use the timeline is guide when relating to an39ol eownterattaek take plaee u Sdg 0 has I I Inside f has Fungal pathogen Pr mfgc m P s mfs c m W V Haus ror39ium f39or39ma rion bioTr39oph quot 39 Toxin formation necro rr oph De roxfifica rion of phy roalex ins Rep r39oduc rion Hos r H H gmm mducgd Pg CPR amp H gmm Sys igm c dgfgmsgs gt fQPmQ HQW ayeaws iQCQJLu md PQSES B QmCQ 39 PHY B QQHQXMS sWucmml CONSTITUTIVE DEFENSES chemica a 7 lt a i Barley powdery mildew 1 an obligate biotroph is inoculated onto different host quot and nonhost plants At what point on the timeline do the spores fail nidie On SUSce ptible barley C 6 5 C nt a f Structural wax cuticla thiclmaaa Shapa and cf atcma l a pubaacamca Biochemical pragfcrmacl inhibitcl sz phanclica cilial s A M Biochemical hyperaaljiai39livity Structural papmaa abcciaaicn layar phytcalaxima gums aya lamic accguiracl lasistanca c rllt laycar amtiemicrcbial amzymaa phanclica Induced Plants respond immediately to a pathogen s attempt to get inside Wound plug papillae formation asa result of needle injury gfbilgl lsio atllPlan39tPa39tltolowline alienmaulepenetration lutml Constitutive biochemical defense In contrast to red and yellow onions white onions do not contain significant quantities of certain phenolic chemicals Onion smudge one is catechol If present these phenolics confer resistance to onion smudge Produced by gohehylgorogoahoid pathway Lari Considered secohdary metabolitesquot but plants devote 1020 of fixed carbon to their synthesis Pigments antioxidants secondary structure wood and cork an timicrobialsantibiotics attractants r Compounds include flavonoids alkaloids phytoalexins tannins 39anthocyanin s lignin and suberin Ul l gm wa dgfgnsezs ma F F 0 E cgmfgv Wei byg 39 i fl Hmdwd Tymses ma WITF WFEW F v mg UD l 1 pm mw MU 333 um weem W U bummg M MUF gyg m If imeey f rrm bwmdn y and M KUV9 m gtp W2 gprr cezw f mgm w g mo mgm Thc oma m i ggC rm by gt G f Im mt stWCtu def mes meation of M95 Dewclnpmtm of Mqu m xylem 2153ch Ty lS as W M as gums and S ng mammm HUZ damaggd xyi m Induced biochemical defenses 39 L 39 antimicrobial compounds synthesized after pathogen attack Synthesized in healthy cells an infection site Synthesis occurs in all host cultivars but the rate speed otsynthesis varies among cultivars Most plants produce several phytoalexins eg over 20 have been isolated from potato Enzymes to detoxify phytoalexins have been observed in some fungal pathogens Phytoalexin molecules Plant produced antimicrobial compounds Several hundred have been isolated and characterized from at least 15 plant families 0H s In OH luteolindin FLJngaJ r r r r 39 Example of attack and couterattack Phytoalexins are synthesized in response to pathogen attack I g3 Some pathogens counterattack producing enzymes that degrade the phytoalexin Syntheuc V39 5 degradative 39 enzymes c r enzymes 39 Jr 99 Defense J JJ Counterattack Phytoalexin synthesis Phytoalexin degradation Elicitation and detoxi cation of phytoulcxins during infection Induced biochremical defenses Resistance is the activation of defenses in distal non infected parts of the plant 1 After a primary inoculation here SAR confers j 39 v to different pathogens For example primary inoculation with a fungal leaf spot pathogen reduces susceptibility of the host plant to other fungi as well as to bacterial and viral pathogens ctr to aciot cherhicat rellateot to aeprrth e rt halithg pathway thuotveot th trahemtietoh the otefehee reepohee throughout pliath prootuce Plant is f to rapidly produce reactive oxygen species eg H202 plus antioxidants Hydrogen peroxide is directly toxic to invading pathogens Thickening of plant cell walls Production of phenolics lignin tannic acid that strengthen walls and inhibit pathogen enzymes Accumulation of pathogenesis related proteins PRproteins enzymes that degrade fungal cell quot walls chitinase s2 Bl3 Glucanases Theseenzymes accumulate in vacuole of plant cell Upon attack they directly degrade fungal cell Walls Indirectly their action results in the release of fungal wall components that elicit additional defense reactions A a 4 Um gdlw h Umm g cgdwm A um m Wisif m cawpcsm HEB Pam E31325 WMch 3mm mm mcdlm bkg W Mw am p tmtw fdh tm u cm I b F m quot i Vf39 1quot Bowling et al ThePlant Cell Vol 6 18451857 December 1994 Plants can have more than one type of acquired resistance Im new we i2 2mm Inle uuvtl lit iman Jusnmnun amp 9 Ellulum 39 A i L k I T imir 1 r iUljintiw limit 39 El icimr 39 I 7 I Elicitrm lt 5 II I h I quot i39r lrriusl I 39 u u n I I I I I I n Izmmmzm 5 I baker hm 39 l llfi illi39llL39 39 I r L 9 I Eyilmnit J i liluir d lm uu d Systemic Ht39aiilnmr 5an lh si mnct IHIH u Sdg 0 has I I Inside f has Fungal pathogen Pr mfgc m P s mfs c m W V Haus ror39ium f39or39ma rion bioTr39oph quot 39 Toxin formation necro rr oph De roxfifica rion of phy roalex ins Rep r39oduc rion Hos r H H gmm mducgd Pg CPR amp H gmm Sys igm c dgfgmsgs gt fQPmQ HQW ayeaws iQCQJLu md PQSES B QmCQ 39 PHY B QQHQXMS sWucmml CONSTITUTIVE DEFENSES chemica Review of lecture 1 S39nificance of Pla Disease Leoture 239 D39sease concept 10 of all food production is lost to disease I Eilglrgggagt wg gigz ggg gndmg a GOA to 3 peSts molecular cellular tissue organismal The Introduction of exotic plant pathogens has population and community caused great losses eg American chestnut magiskgg ongtexot39c threats sudden oak death And Plant Pathology integrates many areas of stud EaCh earv suppresswn f Plant d39sease C 5t5 plant science molecular biology genetics b39 39 quot5 f d ar5 V r39dW39de biochemistry microbiology soil science Plant pathogens restrict trade meteorology statistics economics Pathogens continually evolve break resistance in host CFDPS The Disease Concept is the link that unifies develop insensitivity to chemicals the discipline Functions of a healthy plant Healthy plants carry out several physiological functions to the best of their genetic potential grow cells and develop tissues uptake water and minerals from soil translocate of water and minerals capture energy amp synthesize sugars translocate utilize and store sugars metabolize synthesized com pounds reproduce Overhead 1 ln39 m vs insect feeding frost herbicide damage lightning Disease rot gall wilt stunt Three ingredients are necessary for disease to occur a the pathogenic agents must be present b the host must be susceptible to the agents c the environment is conducive to the interaction of pathogen and host This is commonly expressed as Disease defined Disease is the in39urious alteration of one or more physiological processes in a living system in our case a plant caused by the continuous irritation of a primary causal factor or factors back to overhead 1 The Disease Triangle Host Pathogen Environment Disease fhost X pathogen X environment Disease is a condition of the host and we need vocabulary to describe it Terms that describe a diseased condition are called symptoms If a pathogen can be seen in association with a symptom the observed pathogen structure is called a sign Examples of signs Funal spore fruiting body mycelium sclerotium pustule Bacterial streaming cells Nematodes cysts juveniles Examples of symptoms Weaked or killed tissues Necrosis chlorosis rot soft dry firm Lesion canker mosaic Abnormal in cell rowth Gall tumor curl scab knot Whole lant aearance dampingoff blight stunted dwarfing rosetting yellows wilt Homework Look up hese words in the APSnet glossary write the de ni ion in your notebook Causal Agents of plant diseases Biotic 1 fungi and funguslike organisms 2 bacteria 3 viruses 4 nematodes 57 phytoplasmas viroids higher plants Abiotic 1 air pollutants eg ozone 02 2 chemical imbalances or toxins Overhead 2 Homework Read handout 2 carefully use a glossary or die ionary to look up words you don39t understand Disease symptoms Diseases can be categorized according to their symptoms Symptoms are the plant s response to disease Examples root rots leaf spots abnormal growth vascularwilts Symptoms reflect the physiological fruit rots function of the plant that is disrupted or impaired Diseases have namesll Name of Disease Apple scab Causal Agent Venturia inequalis Host apple Tissues affected leaves and fruit Primary symptom scabtype lesion Secondary symptoms Defoliation fruit deformation and drop as Common Names of Plant l 0r r in Cankers Mosaic Signs Signs are the physical evidence of a pathogen39s structure gt Sign Bacterial strands u v 1 Three cultivars each with a diff t R yields 8 39 discern a possible 1024 races 2 Where do we see Rgene resistance used Obliate biothrohs rusts cereals pine flagtlt coffee corn smuts cereals corn eastern filbert blight Oregon hazelnuts downy mildews sunflower lettuce crucifers powdery mildews cereals cucurbits viruses many cro s nematodes sedentary endoparasites tomato cereals Facultative sarohtes apple scab bacterial leaf spots legumes cotton arabidopsis ascomycete leaf spots rice tomato bean vascular wilts crucifers tomato anana oomycetes root rot soybean late blight potato Host resistance amp Disease dynamics Quantitative nonrace secific resistance 100 Reduces the infection rate Low level of quantitative resistance Slows how rapidly disease evelo ps ls effective against all isolate of the pathogen igh level of quantitative resistance U Disease severity Generally it lasts a long time Host resistance amp Disease dynamics tys Qualitative racesecific resistance Reduces initial inoculum because only a subset of pathogen genotypes in the beginning most if not all are specifically recognized Disease Isease severi curve a er red races arises D Pathogen population Disease progress curve prior to Introduction of blue After introduct of the Rgene race the Blue39 race is recognied red race is not Fre uen th race arises later via mutation Major gene R gene 39 resistance Upside simply inherited and extremely effective Downside e Watsa mmm sonny 1 it breaks down when pathogen Resistance J I I I breakdown 1 loses its elicrtor h l resistance ie stops breaks down making the AVR gene product ms 1 ms nutm um unknown Mvnrmlulo mm In Kora period of time Rgene resistance was effective Smart de lo ment of Race s ecilic resistance yramids eory If a mutation from AVR1 recognized to avr1 ie eli occurs once every 10L to 1 asexual spores then a simultaneous mutation 39om AVRiAVR AV avriav avrg will be a very very rare event RGene pyramids have been highly effective for F control of cereal rusts Smart deloment of race seci c resistance What is this man doin 33quot so H nt He works for the government The white stuffis NaCl 39 3 The bush is Berberis a vulgaris Stem rust of wheat can turn its primary 2 39 s l FZrEnn h ucci39ni a Pathw r BER Y THE SOUTH Why was s eradication of barberry so important Elimination of iiieiosis greatlyl slows genesls of new races 39itrCUItiVal39 Mixtures Lecture Considerations in breeding for and managing host resistance iir F i irit riii sirire rusi Enl emlc nn ms are dispersal barriers 53 39 quot s Ainruierit spores induce SAR I 395 S39W by l cunmr mixiuie s besrwmi polycyclic roiiar diseases of skiririy39 piams irusts or powdery mildew of cereaisi Breeding for Minor gene polygenic resistanCi i i itii i i Pol enic minor ene resistance Wanna is needed Theme It is hard to hang on to effective minor gene resistance to maini in minor gene First generation Effective Proud parent day reSIStance at effeCtlve levels R ene resistance AND Released disease effective poiygenic resistance resistant 39 9 First generation Effective Rgene resistance AND poiygenic resistance r e e v i c nt o inue Resistance Screening And Crossin And Selection But poiygenic resistance has eroded with each crossing eneration because its effects were masked by the Rgene Principles of Di ease Control annulablpi algae Dlsease avmdance est e t t i nnentofnpnthogenw liin an uninvnded atea hng tlle pathogen or by alterlng Etatlieatioi reducing eliminating 0r destroying inoculum at de mdin 13 ppm the t 39 nn39ng t39 eased plant ofchemiczil at an altered emitpinnent ttenipeiatine drilling ei ldnlgs i Hosttesi ee educmg etieieiie wtinoculumvin host geneti targeted at one t nlore component of the tliangle Protecrio reducing the ef ciency ntiiineiiliiiii by inteipnsing a lianiei between host and the pathogen Environment Pathogen Environment Avoitlnn nitlii Ii eli wldmg hepnthogenorb39 altenng the enm onmemio e antli ldeplnntl AVOldance measures targeted at D d b df 1 lsease av01 ance mo 1 1n0 tie the pathogen 5 environment Pi iciple of control ta geted at the pathogen 39lon Eradication A ance ithere o erlap among tll ater 7 Soil 39ater tent Avoidance of the pathoge le 1 r f Y t 39 In39 lyinigrationte 1icmiuttualtingbatleyi 7 k 1 a we n Temperature greenh be storage I OIIIIIIOII bCSl nlanagemen y constrained Atmo phere istorages es oietopping ste quot III ltost range or sum capabilities orpatltogen ptopagnles 39 Planting date or hal I e ate winter wlteat 7 late planting the eases disease i Irrigation management and Verticillium Wilt soil borne disease 3 59 I quot Example Verticillium wilt of potato Suppress disease development by deficit irrigation early in the season De cit iirigation Normal iirigation Planting Tuber mmamm Disease response V M Wet soils favor infection by fungal propagules Management of Foliar Leaf Wetness Duration of wetness required by foliar pathogens to achieve successful infection 8 to 32 hour temperature dependent 0 Bo lyris Strawberry 0 Puccinia Wheat 9 to 15 hour 10 to 22 hour 0 Sclerolinia Bean Irrigation and Verticillium wilt Yield kg per plot 13925 Optimal elicit Excessive a o a a o I a a a V O O tuber harvest initiation Days after Plantmg Irrigation treatment General rule Excessive water early in season promotes fungal root rot and vascular wilt pathogens Irrigation timing and leaf wetness duration Irrigation sets started in in morning Set 1 or in afternoon Set 2 N etness periods followed by sunny day Time of start of Leaf Wetness period set 2 to Midnight 17 4 hour irrigatio period Leaf wetness intensity Duratiuon of wetness 1400 1600 1800 2000 2200 2400 Time ofday 6 am 12 pm 6 pin 12 am 6am Time of day FoliarCanop management 1 Question Examp 1th respect to 3 01dng conditions Leafremoval 0 bunch n in grapes or infection by a foliar pathogen it better to water at night during the day Leaf Removal in Grape Effect of leaf removal on bunch rot suppression gm V 7 am 39 v7 m Before m if I W93 FoliarCanop management Disease av idance by managing t susceptibility hat can we control Nature and frequency of wounds inwAumrmh wmm mn mmquot w m Nun innal of M oderate gor 39i u fmit at ha Scenai i quotHighquot C cium Fru L c Mg Direct Inhibition S enariil L L 1 Low Fruit Calcium Promotes R 9 For mom a the infections are nnated in ii39ozmds Eu d Skin Wounds vs Fruit Firmness 7 Skin Wounds vs Fruit Firmness Pa by the bin 139
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