Bio 345 Midterm

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Define PHYTOPATHOLOGY.: Phyto=plant
Pathos=suffering
Logos=meaning
What is PP concerned with?: -what causes a plant disease
-how a pathogen attacks the plant
-how the host responds to the attack
-how pathogens are dissiminated
-how the environment influences the disease process
-how to manage plant pathogens and therbe reduce the effects of the disease on the plant
Define PLANT DISEASE: -whenever the ability of cells of plant/part to carry out 1 or more normal physiological functions is interferred by either a pathogeic microorganism or an adverse enviromental factor
-the activities of the cell are disrupted, altered, or inhibited, the cells malfunction or die, and the plant becomes diseased
-caused by biotic agents and abiotic agents
Define PATHOGEN: -an entity, usually a microorganism, that causes disease
What are the 5 kinds of pathogens?: -fungi
-prokaryotes
-viruses and viroids
-nematodes
-parasitic higher plants
Define SYMPTOM: -the external and internal reactions or alternations of a plant as a result of a disease
-the visible reaction of a plant to disease
How do you categorize disease?: -according to the types of symptoms
-according to the types of plants or there organs
-according to types of pathogens
What are the 4 significances of plant disease?: Annihilating Diseases:
-completely wipes shit out
-eg:chestnut blight, dutch elm disease, coffee rust

Devastating Diseases:
-highly dependant on host factors, happens suddenly - causes epidemcs and then dissapears
-eg: potato late blight, southern corn leaf, blight

Limiting Diseases:
-doesn't allow growth
-eg: root diseases

Debilitating Diseases:
-these diseases exist constantly but don't cause serious damage
-therefor we really don't care about these and wouldn't spray them
Who/What is Robigo?: -the Roman Rust God
-celebrated the Robiglia in spring
-diseases were from the wrath of a god
What signficant events happened between 1600-1800: **Anton von Leeuwenhoek invents the microscope
**2 French scientists (Mathieu Fillet and Isaac Benedict Prevost) shows that wheat smut is caused by a fungus, copper sulfate could reduce smut after seed treatment

-first legislation for plant disease control
What significant events happened between 1840-1900 (The Golden Age): **1860-1863, Louis Pasteur provides the basis for the germ theory of dieases
**1840's Potatoe late blight
Who developed the Germ Theory of Disease? What is it?: -Louis Pasteur developed the theory

-says that microorganisms arise only from preexisting microorganisms and that fermentation is a biologicaal phenomenon
Who is Anton deBary?: -1831-1888, considered by some to be the father of plant pathology
-confirmed that Phytophthora infestons was the cause of potato late blight
-also proved that smut and fungi are the causes, not the result of plant diseases
Who wrote 'Diseases of Cultivated Crops, Their Causes and Control'?: -German scientist, Julius Kuhn during the golden age
Who invented the pour plate method? When did he invent the Postulates?: -Robert Koch
-did the majority of his work during the Golden Age
What did Millardet discover and when did he do it?: -discovered the Bordeaux misture for the control of downy mildew of grapes
-was the first person to use chemicals for pathogen control
-did this in the golden age
What is the Golden Age?: 1840-1900
-time pd where leaps and bounds were made in PP
When did we discover that viruses were a disease causing agent?: -20th Century
When were Fungicides developed.: -first one was in 1933, an organic mercury compound
-still inventing them today
Who is Guthrie B Sanford?: -first scientist to suggest that the plant disease might be inhibited by the activity of saprophytic bacteria developing in decomposing green manure
What was the first plant used for studying resistance and signal transuction?`: -Arabidopsis was used as the model plant
What served as a good vector for bio technology in the early stages of PP?: -Agrobacterium tumefaciens
What can cause plant diseases?: -biotic agents
-abiotic agents
-infectious plant diseases
-non infectious plant diseases
What are BIOTIC AGENTS?: -living organisms which can cause disease

Includes:
-fungi
-prokaryotes
-viruses and viroids
-nematodes
-higher parasitic plants
What are Koch's Postulates?: 1)Organism must be consistently associated with the symptoms of the disease

2)Organism must be isolated and grown in pure culture

3)Organism must be inoculated onto healthy host of the same species of the original host and must reproduce the same symptoms as originally observed

4)The organism must be re-isolated and have the same characteristics as the original isolate

**there will be problems in doing this with virus and obligate bacteria since they require a living host**
What is the general suffix attached to: -Phylum -Class -Order -Family: Phylum => '-mycota'

Class => '-mycetes'

Order => '-ales'

Family => '-aceae'
What is FUNGI?: -the most important plant pathogen
-PP fungi are microscopic organisms which lack chlorophyll and developed conductive tissue
-approx 100,000 fungi spp, 50 cause disease in man, <8000 cause disease in plants
-consists of a vegetative body (mycelia[pl], mycellium[s]) made up of individual branches (hyphae) which may or many not have cross walls (septate or aseptate respectively)
What is the structure of FUNGI?: -consists of a vegetative body (mycelia[pl], mycellium[s]) made up of individual branches (hyphae) which may or many not have cross walls (septate or aseptate respectively)
-some lower fungi lack a true mycellium and consists of a naked ameboid multinucleate plasmodium (eg:myxomycetes or slime moulds)
-in the primitive or lower fungi, mycelium consists of a continous mass of cytoplasm and nuclei unbroken by septa
-in higher fungi, the mycellium is divided by septa into units shich contains one or a few nuclei
What is plasmodium?: -like a mass of cytoplasm
-looks amoeboid
With regards to PP, what are defining characteristics to the Kingdom Protista?: -has fungal like characteristics
-unicellular
-plasmodial
-colonial
-very simple multicells
-phagotrophic

-Division Myxomycota
-Division Plasmodiophoromycota
With regards to PP, what are defining characteristics to the Kingdom Chromista?: -likely to have been derived from alge, whose members have cellulosic walls among other features

-Division Oomycota
With regards to PP, what are defining characteristics to the Kingdom Fungi?: -true fungi
-have eukaryotic cells
-form mycellium with chitonous walls
-have osmotrophic nutrition
-lack an embryo
-develop from spores and produce multicellular sporocarps

-Division Chytridiomycota
-Division Zygomycota
-Division Ascomycota (most important pathogen, approx 50% of disease)
-Division Basidiomycota
With regards to PP, what are defining characteristics to the Kingdom Bacteria?: -primitive organisms classified as prokaryotes(no membrane bound organelles) therefore no mitotic apparatus
-most of the genetic info in a bac cell is carried on a single shromosome with double stranded DNA in a closed circular form
-some bac cells contain extrachromosal DNA as plasmids. These are circles of DNA which replicate independantly of the chromosomes and are important for several reasons (eg: genteic material relating to pathnogecity, fumour formation and resistance to chemical treatment)
-about 200/1600 bac spp are recognized as PP's
What does agrobacterium cause?: -tumours
-hairy root
What does clavibacter cause?: -potatoe ring rot
-fruit spot
What does pseudomonas cause?: -leaf spots
-galls
What does erwinia cause?: -blight
-wilt
-soft rot
-stinks
-fermentation therefor can be anaerobic
What does xanthomonas cause?: -leaf spots
-black venation
What does streptomyces cause?: -potatoe scab
What are Mollicutes?: -mycoplasma like organisms (MLO's)
-prokaryotic cells without cell walls
-MLO's are similar to bacteria in that they are prokaryotes and lack an organised bounded nucleus
-MLO's difer from bac in that they lack rigd cell walls, being surounded only by unit membranes. This allows them to be highly pleomorphic nd they assum a vast array of shapes and sizes
-diameter of MLO's vary from 300um to 1um
-MLO's include the smalles known cells able to multiply independantly of other living cells
-70 diseases affecting over 300 genera of plants have been attributed to MLO's
-spread via vector, usually an insect
-can't grow MLO's on artificial growth media
-tetracyclines are antibiotic substances that have been used to kill some MLO's in plants
What is SPIROPLASMA?: -mollicutes with helical structures
What is PHYTOPLASMA?: -mollicutes with ound and elongate structure
With regards to PP, what are defining characteristics to viruses and viroids?: -are parasites therefore needs a living host in order to live and reproduce
-can cause disease in man, animal, plants, fungi, bacteria and MLO's
-500/1000 well characterised and classified viruses cause diseases in plants
-plants may be simultaneously affected by more than 1 virus
-one of the smallest PP's
-not made up of cells but a protein coat
-nucleic acid core is either single stranded or double stranded RNA or DNA
-difficult to come up with a cure against viruses b/c you'll usually end up killing the host aswell
What's the diff between a virus and a viroid?: -viroids are smaller than viruses
-they act like viruses but the infectious particle is simply a strand of RNA/DNA
-has no proteins
With regards to PP, what are defining characteristics of Nematodes?: -belongs to the Kingdom Animalia, Phylum Nematoda
-small eel like worms which are usually too small to see with the naked eye
-parasitic nematodes feed on plants my means of a miniature hypodermic-like structure called a STYLET, which is used to suck liquid nutrients out of plant cells
-reproduce by laying eggs, larvae develope through a series of 4 molts until they become adults
-life cycle can be as short as 30 days
-pathogenic nematodes can be parasitic on the surface plant tirrues (ECTOPARASITES) or wriggle inside the tissue and feed from within (ENDOPARASITES)
-cause damage by injuring cells, removing cell contents, or changing normal plant growth process
-facilitates other pathogen penetration and transmission
With regards to PP, what are defining characteristics of Higher Parasitic Plants?: -they produce seeds that are parasitic on other plants, therefor considered pathogens
-most have modified root-like structures that attach to plant tissues to obtain nutrients and water, but do not have a root system that can absorb nutrients from the soil
eg: mistletoe
-usually lacks chlorophyll
-common vector are birds
**roots grow into the plant, NOT the soil**
With regards to PP, what are defining characteristics of Abiotic Agents?: -cause Abiotic Disease (AKA Phyiological Disorder)
-like non-infectious disease in humans
Causes are extreme environmental factors:
-temp
-soil moister and air humidity
-soil nutrients-too much/little
-air and soil pollutants
-light
acid rain and soil pH
-herbicides
-occurs in the absence of pathogens
-often occurs within a larger area
-associated with historical events (ie:hot yesterday, diseased today)
***if you inoculate an abiotic infected plant, you usually get nothing***
Define PARASITISM: -a pathogenic relationship in which the parasite lives in or on the host, from which it derives its food
Define SYMBIOSIS: -a mutually benificial association of 2 or more different kinds of organisms
Define PARASITE: -an organism or virus that lives on or in another living thing and gets food from that organism
Define HOST: -living organism from which parasites/symbionts obtain nutrients
Define HOST RANGE: -the variety of plant genera and species that may be attacked by a pathogen
Define PATHOGENESIS: -strategies for making disease
Define RESISTANCE: -AKA Susceptibility
-ability of host to reduce the growth, reproduction, or disease-producing activity of the pathogen
Define PATHOGENICITY: -the capability of a pathogen to cause disease
-a 'yes/no' type of question
Define VIRULENCE: -the degree of pathnogenicity of a given pathogen
-how effective the pathogen is at causing disease
Define AVIRULENCE.: -inability of a pathogen to cause a compatible (susceptible)reaction on a host cultivar with gentic resistance. If the pathogen gains this gene, it loses ability to do shit...
-pretty much the opposite of pathogenicity
Define AGGRESSIVENESS: -races of pathogens that differ in the severity of their pathological effects but do not interact differentially with host varieties or cultivars are said to differ in aggressiveness
-the more they don't give a shit, the more aggressive they are
What are the 4 types of parasitism?: 1)Symbiont
2)Biotrophic
3)Hemibiotrophic
4)Necrotrophic
Define and give an example of SYMBIONT: -the small participant in the symbiotic relationship, living in or on the host

eg:
-ectomycorrhizea: a coat of myccorhizae covering root
-VA mycorrhizea: mycorrhizae root system in most and has external hyphae
Define and give an example of BIOTROPH: -AKA an OBLIGATE PARASITE
-an organism that can live and multiply ONLY on or in another living organism

eg:
-rust, powdery mildew, downy mildew
Define and give an example of HEMIBIOTROPH: -a microorganism that parasites in living tissue for a period and continues its life cycle on dead tissue
-so has biotrophic and necrotrophic life stages

eg:
-Magnoportha
-Colletotrichum
Define and give an example of NECROTROPH: -a microorganism that kills and then feeds on the dead tissue

eg:
-Sclerotinia
-Botrytis
-Pythium
Define CONIDIA: -an asexual spore
Define APPRESSORIUM: -the swollen tip of a hyphae or a germ tube that facilitates attachment and penetration of the host by the fungus
-a penetrative structure found on fungal pathogens
-has a penetrative pore that punctures via turgor pressure
Define HAUSTORIUM: -the root like structure that takes nutrients from the host cell
Define HYPHAE: -grows on surface, continues to produce hyphae
-produces CONIDIAPHORE which produce CONIDIA
What is a RUST PATHOGEN?: -similar to Downey Mildews
-penetrates the plant through the stoma
-can infect leaves and stem too
-hyphae growth in extracellular space (around the cell)
-produces haustoria and inserts into the cell
-nutrients can also be taken up in extracellular space
Define FACULTATIVE PARASITE: -usually saprophytic but may become parasitic
Define FACULTATIVE SAPROPHYTE: -usually parasitic but may live as a saprophyte
Define SAPROPHYTE: -obtains nutrients from dead organic material
**DOESN'T KILL THE ORGANISM, ORGANISM IS ALREADY DEAD!**
Define DISEASE TRIANGLE: -a concept describing the simulaneous occurrence of:
1)virulent pathogen
2)susceptible host
3)favorable environment
-needs all of the 3 factors to be able to cause a disease
Define DISEASE CYCLE: -AKA infection cycle
-the chain of events involved in disease developement
-includes the stages of developement of the pathogen and the effect of the disease on the host
Define LIFE CYCLE: -the stage or successive stages in the growth and development of an organism that occur between the appearance and reappearance of the same stage of organism
What are the primary events in a disease cycle?: Inoculation
-arrival or transfer of pathogen onto host

Infection
-establishment of parasite within a host plant

Dissimination of the pathogen
-the transfer of inoculum to healthy plant tissue

Survival of pathogen
-overwintering or oversummering
Define INOCULUM: -parts or forms of a pathogen that come in contact with the host and can cause disease
Define PRIMARY INOCULUM: -the overwintering/oversummering pathogen propagules that cause primary infection
Define SECONDARY INOCULUM: -inoculum produced by infections that took place during the same growing season
What are the stages involved in the INFECTION CYCLE?: Penetration
-the initial invasion of a host by a pathogen

Host Recognition
-recognition determines the specificity of host-parasite interaction, following by a compatible or incompatible relationship
-if recognized, pathogen is rejected; if unrecognized, pathogen infects

Invasion/Colonization
-the spread of a pathogen into the host (local & systemic)

Reproduction
Define PRIMARY INFECTION: -infection caused by the primary inoculant
Define SECONDARY INFECTION: -infection caused by the secondary inoculant
Define LATENT INFECTION: -the state in which a host is infected with a pathogen but does not show any symptoms for a period
Define PREPENETRATION PHENOMENA: -the attachment, germination and differention of a pathogen on a host
What are the 3 methods of penetration?: 1)Direct penetration through the intact plant surface

2)Penetration through wounds

3)Penetration through natural openings
Define LOCAL INFECTION: -the infection involves a single cell, a few cells or a small area of the plant

eg:colletotrichum
Define SYSTEMIC INFECTION: -the plant pathogen occurs throughout the plant

eg: fusarium
What are the methods of Dissimination?: -air
-rain (splash, runoff and wind transport)
-gremplasm (infected seeds, seed bound pathogens)
-human activity
-vectors (insects, mice, etc.)
What is the difference between and ALTERNATE HOST and an ALTERNATIVE HOST?: ALTERNATE HOST
-a host needed in order to complete the pathogens life cycle

ALTERNATIVE HOST
-just another host
What are some basic overwintering/oversummering strategies of pathogens?: -stay in soil
-stay in infected plants
-stay in plant debris
-survive via contaminated/infected germplasms
-survive via alternate and/or alternative hosts
-can stay in vectors, especially viruses
What are the overwintering strategies of fungi?: -overwinter as spores
-mycelium and sclerotia in infected tissues of the plant
-plant debris
-in the soil
What are the over wintering/summering strategies of bacteria?: -spores
-in infected tissues of plants
-plant debris
-in the soil
What are the over wintering strategies of viruses/viroids?: -don't really have one, need a host to survive, so if the host survives, the virus should as well
What are the overwintering/summerring strategies of nematodes?: -overwinter/summer as eggs in the soil
-as eggs or nematodes in plant roots
-as eggs or nematodes in debris
Define PATHOGENICITY FACTOR: -a factor essential for the pathogen to cause disease
Define VIRULENCE FACTOR: -a factor that causes a sever disease and produces the symptoms typical of the disease in a susceptible host
Define AVIRULENCE FACTOR: -a factor that imposes the pathogen unable to cause disease
What are the 2 types of APPRESORIA?: 1)Melanized Appressoria
-able to produce more pressure since the cell wall is re-enforced with melanin
-eg: Colletotrichum, Magnaporth

2)Non-Melanized Appressoria
-not able to produce as much pressure, therefor penetration method is kind of unknown (enzymes???)
-eg: Erysiphe

**Melanization = browning**
**stopping melanization = no melanin = lack of pressure = no penetration**
Aside from the obvious, what are other roles of APPRESSORIA?: -a protective structure from UV radiation (like an umbrella/sunscreen against UV) and draught stress (the melanized one)
-an infection apparatus generating turgor pressure for penetration
How much pressure can appressorium generate? How is this pressure measured?: -8.0Mpa OR 8N/mm^2

Determined by:
a) direct penetration of non-biodegradeable membrane, exhibiing a range of surface hardness
b) cytorrysis, a technique related to plasmolysis
c)measurement of glycerol concentration (>3M) within the appressorium
d)a microscopic method using elastic optical wave guides
What are the chemical weapons of pathogens?: ***Enzymes***
1)Cutinases
2)Pectinases
3)Cellulases and B-glucosidases
4)Secrete Lipase
What are Cutinases: -wall degrading enzyme
-cutin is the main component of the cuticle
-cutinases can break cutin molecules and release monomers as well as oligomers of the component fatty acid derivatives
What are the roles of Cutinases?: -penetration of the host cuticle
-cutinases are produced by pathogenic fungi
-reach their highest expression level at the penetration point
-correlation of cutinase level's and fungal
-cutinase inhibitors or antibodies protect the infection
-cutinase deficient mutants show reduced virulence
-cutinase gene changes the pathogen type from wounding infection to direct penetration
-cutin monomers also elicit plant defense responses
What are Pectinases?: -AKA Pectolytic enzymes
-pectic substances constitue the min components of the middle lamellae and also make up a large portion of the primary cell wall in which they form an amorphous gel filling the spaces between the cellulose microfibrils
-pectic substances are polysaccharides consisting mostly of chains of galacturonan molecules (B-1,4 linked) interspread with a much smaller number of rhamnose molecules and small side chains of galacturonan and some other 5-C sugars
-pectin degradation results in liquifaction of the pectic substances that hlod plant cells together and in weakening of cell walls, leading to tissue maceration
What are some types of Pectinases?: -pectin methyl transferase
-pectate lyase
-pectin lyase
-polygalacturonase
What are the roles of pectinases.: -as a virulence/pathogenicity factor:
--the first cell wall degrading enzymes to be produced by pathogens in extracted host cell walls or in infected tissues
--corelations between the presence of pectic enzymes, disease symptoms and relativne virulence
--some pectic enzymes alone macerate host tissues

-specific antibodies raised against pectic enzymes reduce virulence
--contribute to the broad host range
--essential for pathogenicity demonstrated by:
---a single gnen desruption
---disruption of 2 inducible gnese
---breakdown of secretion pathway
--as inducers of host defense responses (endogenous elicitor):
---pectic enzymes, and their oligogalacturinate products can elicit plant defense reactions
What are Cellulases and B-Glucosidases?: -cellulose is also a polysaccharide, but consists of chains of B-1,4 linked glucose molecules
-cellulose occurs in all higher plants as the skeletal substance of cell walls in the form of microfibrils, which can be perceived as bundles of iron bars in a reinforced concrete building
-several groups of cellulases degrade cellulose to the disaccharide cellubiose
-finally, cellubiose is degraded by the enzyme B-Glucosidases into glucose
What are Secreted Lipases?: -breaks triglycerides
-can also hydrolyze ester bonds
Where do pathogens derive the majority of their nutrients?: -cytoplasmic proteins
-starch
-fats
-nucleic acids
**these can be utilized only after degredation by enzymes secreted by the pathogen**
T/F Fungi, bacteria, nematodes and higher plants produce different sets of wall degrading enzymes.: T
-they have different hosts therefore need different enzymes
T/F Cell wall degrading enzymes are redundant amont the pathogens.: T
-it is believed that cell wall degrading enzymes work in a concert.
-the individual only plays a partial role in the pathogenesis
T/F Cell wall degrading enzymes are continuously produced.: F
-the ezymes are often expressed and function when they are needed
-constitutive, substrate inducible and in planta expression
T/F a disruption of all functionally redundant genes is required to demonstrate the role of cell wall degrading enzymes in pathogens.: T
-flip the card if you wanna read it again.
In phytopathology, what is a TOXIN?: -toxic chemicals (chemopathogens) able to cause effects similar to those of disease symptoms induced by microorganisms
What are MICROBE TOXINS?: -different from PHYTOTOXINS and MYCOTOXINS
-most microbe toxins are LOW MOLECULAR WEIGHT, compounds with diverse structures
-they act as +'ve agents of virulence on pathogenecity
-pathogenic fungi and bacteria can produce toxins in infected plants as wiell as in culture medium
-they are effective in VERY LOW concentrations
What are PHYTOTOXINS?: -any product of a living organism toxic to plants
What are MYCOTOXINS?: -produced by several fungi in infected seeds, feeds, or foods and capable of causing illness of varying severity an death to animals and humans that consume such substances
List the action sites of toxins. [3]: -target the cellular membranes by affecting the permeability
-inactivate or inhibit enzymes
-inhibit or disturb the signal transduction
What 3 things have the toxin resistence of plants been associated with?: -detoxification (HC-toxin reductase, HM1 gene)
-altered affinity
-the absence and mutation of the toxin targets (T-toxin target: T-urf 13)
What are NON HOST SPECIFIC/SELECTIVE TOXINS? (non-HST's): -produce all or part of disease syndrome not onl on the host plant but also on other spp's of plants that are not normally attacked by the pathogen in nature
-increasees the extent of disease caused by a pathogen but are not esential for the pathogen to cause disease
-are not primary determinants of host range
What are some typical bacterial non-HST's?[4]: -Phaseolotoxin
-Tabtoxin
-Fusarium toxins
-Oxalate
What are PHASEOLOTOXINS?: -a bacterial non-HST
Structure
-a modified ornithine-alanine-arganine tripeptide carrying a phoshosulfinyl group

Production
-by Pseudomonas syringae pv. phaseolicola which causes the halo blight of bean and some other legumes

Plant Phenotypical reactions:
-shows the local and systemic chlorotic symptoms and reduce growth of newly expanding leaves
-disruption of apical dominance
-accumulation of ornithine

Site and Mode of Action
-plant enzymes cleave the peptide bonds of phaseolotoxin and releases alanine, arganine and phosphosulfinylornithine
-latter is a biologically functional moiety of phaseolotoxin, which affects cells by binding to the active site of and inactivating the enzme ornithine carbamoyl transferase
-this causes accumulation of ornithine and depletes levels of citruline and arginine
What are TABTOXINS?: -a bacterial non-HST

Production
-by P. syringae pv tabaci which causes the wildfire disease of tobacco, also by other strain or pathovars

-cause of the chloroic halos surrounding the necrotic white spots of tobacco leaves
-inactivating glutamine synthase therefor reduce the concentration of L-glutamate
What are FUSARIUM TOXINS? List the 3 possibilities.: -a bacterial non-HST
*different fusarium species produce a complex of several toxins

Fumonisin B:
-produced by Rusarium monliforme and by Alternaria alternata f.sp. lycopersici as AAL-toxin

Fusaric acid (5-butylpicolinic acid):
-these toxins show toxicty (1-5ppm) to a broader range of organisms and threaten animal and human health
-although these toxins are also toxic to plants, their role in Fusarium pathogenesis is unclear

Trichotherene:
-vomitoxin: Deoxynivalenol(DON), Zearaleone(ZEN), T-2 toxin etc.
-produced by F. graminearum and other Fusarium spp
What are OXALATES?: -a bacterial non-HST

Production
-by Sclerotinia, Sclerotium and other fungi
-functions as a non-HST for fungal virulence/pathnogenicity
-serves as a cofactor for host cell wall degrading enzymes
-directly inhibits the onset of plant defenses

Transgenic approaches have been applied for resistence based on oxalate catabolism by 2 major pathways:
1)Decarboxylation: occurs either by activation of oxalic acid to oxalyl-CoA by means of oxalyl-CoA decarboxylase or directly to CO2 and formic acid by oxalate decarboxylase
2)Oxalate oxidation: has been detected in plants where oxalic acid is broken down to CO2 and H2O2 by oxalate oxidase
What is the difference between hormones found in animals and hormones found in plants?: Animal: produced in one cell and targets a different cell

Plant: produced in one cell and may target the same cell
What are HOST SPECIFIC/SELECTIVE TOXINS? (HSTs): -are toxic only to the hosts of that pathogen and shows little or no toxicity against non susceptible plants
-are determinants of host range or specificity in that plant species, varieties, or genotypes
-in general, all known HST's have been produced by certain necrotrophic fungi. Most known HST's are produced by species or pathotypes in 2 genera. ***Cochliobolus*** and ***Alternaria***
What are the 2 types of Cochliobolus HST's?: 1)Victorin

2)T-toxin
What is VICTORIN?: -a Cochliobolus HST
-one of the first HST's discovered with a remarkable toxicity (effects have been recorded at 10pM)

Structure:
-a polypeptide linked to a nitrogen containing sesquiterpene

Production:
-by Cochliobolus victoriae
-causes foot and root rot and leaf blight of certain oat cultivars

Plant phenotypical reactions and disease epidemics:
-cause of some general changes in the physiology of host that are common to infectious plant diseases

Site and mode of action:
-major 100kD victorin binding protein was purified, and its gene encodes one subunit of glycine decarboxylase (GD)
-GD is located in the mitochondrion and has a central role in the photorespiration
-Victorin inhibits GD in a host selective manner in intact tissues, but exhibits no different effect on FD in isolated, intact mitochondria
-thus, selectivity might be due to uptake
What is a T-TOXIN?: -a Cochliobolus HST

Structure:
-a mixture of linear, long (35C to 45C) polyketols

Production:
-by race T isolate of C. heterostrophus, a causing agent of the Southern corn leaf blight.
-race O of C. heterostrophus, which does not produce T-toxin, is a minor pathogen of corn

Plant phenotypical reactions and disease epidemics:
-attacked corn, destroyed 15% of the crop in 1970

Site and Mode of Action:
-active at ~10nM against Tcms
-active at ~10um against maize with normal cytoplasm
-mitochondria in vitro and in situ are quickly and specifically pertrubed morphologically and biochemically by T-toxin
-T-toxin rearranges mitochondrial genome of Tcms plants that results in the production of a chimeric open reading frame, T-urf13, which encodes a 13-kD protein (URF13) localized n the inner mitochondrial membrane
-URF13 forms oligomeric pores in membranes in the presence of T-toxin
What are Alternaria HST's?: -a host specific toxin
-eg: AAL-toxin (SAM)
What is AAL-toxin(SAM)?: -an Alternaria HST

Structure:
-related to sphinganine

Production:
-by A. alternata f.sp. lycopersici as AAL-toxin
-by Fusarium moniliforme as Fumonisin B1 (Spinganine-Analog Mycotoxins, SAM)
-AAL-toxin is essential for the pathogenesis of AAl in tomato, because the toxin deficient mutants cannot infest healthy compatible tomato leaves
-SAMs producing F.moniforme are not pathogenic on the AAL compatible tomatoe isoline, indicating that the toxin produced by F. moniforme is not sufficient for virulence on tomato

Plant phenotypical reactions, toxicity and resistance:
-functions as PHYTOTOXIN against plant, and MYCOTOXIN against mammalian
-toxic to all tissues of sensitive tomato induces APOPTOSIS in some mammalian cell lines and is toxic to animals and suspected to be conditionally carcinogenic in humans
-resistance and susceptibility to both AAL and SAMs in tomato is determined by the Althernaria stem canker (Asc)locus
-it inherits in a single codominant fashion
-plants heterozygous or the Asc locus (Asc/asc) have an intermediate sensitivity to the toxin

Site and Mode of Action:
-competitively inhibit de novo sphingolipid (ceramide) biosynthesis in vitro
-besides their role as structural components of biomembranes, sphingolipids can be determinants in the proliferation or death of cells, depending on the type of cells studied
What are plant growth regulators?: -act in very low concentration
-naturally occurring compounds in plants and coordinate the activities of plant cells and tissues
eg: auxin, gibberellins, ethylene
What is AUXIN?: -a plant growth regulator
-Indole Acidic Acid (IAA) levels were changed in many diseased plant tissues
-several diseased plants show a typical gall symptom due to the incresed levels of IAA
-Ti plasmid (Tumor inducing) is introduced by the pathogen into the infected cell. T-DNA fragment is integrated into the plants nuclear DNA. T-DNA from Agrobacterium contains several genes including genes for IAA and cytokinin biosynthesis.
-infected plant cells are forced to express genes encoded in T-DNA and to produce elevated levels of IAA and cytokinin, thus transformed normal plant cells are transferred into tumor cells
What causes crown gall?: Agrobacterium tumefaciens
What are Ti-plasmids?: -Tumor Inducing
-integrated into host cells, and induces IAA production, causing swelling and galls
-the disarmed Ti-plasmid has become the most widely used plant transformation vector
-many other fungal and bacterial pathogens are also capable of producing IAA, either by themself or stimulated production
What are GIBBERELLINS?: -a plant growth regulator
-high concentrations during seed germination
-cause of foolish seedling disease (pathogen adds too much gibberellins)
-Gibberella fujikuroi fungus produced hyper elongation of rice stems by secreting the chemical gibberellin
-over 80 different gibberellins
-sometimes used as a spray to overcome stunted/diseased symptoms
What is ETHYLENE?: -a plant growth regulator
-production is dramatically induced in infected tissues
-considered as a signal in plant for wounding and senesces(maturing) responses
-may play a role in plant defense responses of several pathosystems along with another signal component, jasmonic acid.
What are the 3 structures of fungi?: 1) lower fungi
-lack a true mycellium and consists of a naked ameboid multinucleate plasmodium (eg: Myxomycetes or slime molds)

2) Primitive/lower fungi:
-mycelium consists of a continous mass of cytoplasm and nuclei unbroken by septa

3) higher fungi
-the mycellium is divided by septa into units which contains one or a few nuclei
Which nematodes can encyst?: -Heterodera spp
Define OBLIGATE PARASITE: -can grow and multiply only on or in living organisms
Give 8 different types of enzymes that plant pathogens can make: -cutinases
-pectinases
-xylanases
-cellulases
-glucanases
-proteinases
-xylosidasees
-arabinosidases
---others

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Number of cards 141