PLPA 301 Lecture Notes Pathology – anything that is out of the ordinary (abnormal health) What is normality? Normal is a fluid term In plant pathology, it’s fairly self-evident. A plant only has a problem when it underperforms. Plants can tolerate a certain disease or pathogen for a certain amount of time. In most cases, it’s better to encourage non-resistant, tolerant plants, because if we keep creating non-resistant plants, the bacteria or pathogens evolves and changes to become a new strain. 5 groups of pathogens - Bacteria - Fungi - Virus - Nematodes - Parasitic plants There is a constant chemical communication between a plant and a pathogen. The talk to each other; cross signal communication. Virulent means it can infect. *extension specialist Resistant vs. virulent Plant pathology – medical science for health The basic biology will be the same behind different diseases. The more we understand the cause of diseases in humans, the more we understand diseases from plants. It’s amazing how much we don’t understand in plants, about the same pathogen in humans. Think of pathogens as living organisms. They cause environmental distress. How do you know if a plant is sick? If you can visually observe the plant. What you SEE is a symptom or a sign. How to tell the difference? For example, wilting
Transcript
PLPA 301 Lecture Notes
Pathology – anything that is out of the ordinary (abnormal health)
What is normality? Normal is a fluid term
In plant pathology, it’s fairly self-evident. A plant only has a problem when it underperforms. Plants can tolerate a certain disease or pathogen for a certain amount of time. In most cases, it’s better to encourage non-resistant, tolerant plants, because if we keep creating non-resistant plants, the bacteria or pathogens evolves and changes to become a new strain.
There is a constant chemical communication between a plant and a pathogen. The talk to each other; cross signal communication.
Virulent means it can infect.
*extension specialist
Resistant vs. virulent
Plant pathology – medical science for health
The basic biology will be the same behind different diseases. The more we understand the cause of diseases in humans, the more we understand diseases from plants.
It’s amazing how much we don’t understand in plants, about the same pathogen in humans.
Think of pathogens as living organisms. They cause environmental distress.
How do you know if a plant is sick? If you can visually observe the plant. What you SEE is a symptom or a sign. How to tell the difference?
For example, wilting
What is the difference between wilting as a sign and wilting as a symptom?
Wilting is a sign, because it’s dehydrated. That’s normal, we get dehydrated, we drink water, we’re fine.
Symptom – a lesion
When you talk about disease, or the definition of the disease
- We do not mention a cause (we don’t know)- We don’t say anything about specific symptoms- We don’t say anything about the amount of money lost
We just know that the plant is diseased.
Yield losses are left out of the definition of a pathogen, or pathology
***biotic means its living organism
***abiotic means its nonliving
Abiotic pathogens cause non-infectious (non transmissible) diseases
- Abnormal temperature, too high, too low (some plants have different tolerances)- Moisture -> drought stress, or flood- Mineral nutrients -> HUGE***HUGE***HUGE -> sometimes it looks exactly like the plant has
been affected by a pathogen- Air pollutants
Biotic pathogens are infectious (transmissible)
May also be called “causal agent”
What is a disease? What is a pathogen? They are different.
WE humans create these problems, because we don’t know what we’re doing. Because we want cheap, abundant, high quality food.
Beautiful, full, uniform fields of corn -> lack of genetic diversity, they are genetically uniform
***monoculture – the same corn variety on many, many, many acres <- the most yielding
Modern Agriculture Practices
- Dense cropping systems --- plants are too close to one anothero Why does this matter? If a plant is infected by a fungal pathogen, if a bunch of plants are
too close they will become infected as well. Too close, means disease spreads. o Why do we do it? High yield per acre
- Over large areas; “economy of sale”o Huge historical problem: planted coffee over an entire island of Sri Lanka – beat out by
coffee rusto We grow coffee in brazil, Guatemala, central America nowo Coffee rust research in Guatemala
- Monocultureo Genetically uniform organismso Corn – germ last? Extremely susceptible to a particular disease
2 types of plant pathology
- Basic - Applied
Basic : study of diseased and resistant plants to determine
- The effects of the disease
- The nature of the disease
Applied : identify the most effective control techniques such as developments of new pesticides or more resistant germplasm
- Diagnosis, treatment, cure- Prevention of plant disease
Categories of diseases based on:
- Types of organs they affect and symptomso CANKER – stem, a sunken or rotted part of the stem o Plight – leaf
- Types of crops they affecto Some only affect corn, some only affect cotton
- Types of pathogens
Root Diseases:
- Rots = discoloration and decay due to disintegration and decomposition of tissues- Damping-off = seedling death just prior to (pre-emergence, type 1) or just following (post-
emergence, type 2) emergence from the soil
*** Defense is costly
Pouring water into a seed that doesn’t have a root yet is a problem.
One type of fungus can wipe the plants out, when it’s just tons of water + seeds.
Over-watering is a big problem, as big as drought.
- Cankers = localized necrotic (dead, usually dark brown to black) areas associated with death of the phloem
- Galls = hyperplasia (increase in number of cells) -> BASICALLY a TUMOR- Witch’s brooms (parasitic plants) *** spread by birds
Sterilization is important! If you cut off a diseased part of a plants, you must clean the utensils or else you spread the disease by going from plant to plant pruning.
Vascular Diseases:
a) Wilt – when transpiration exceeds absorption of water and turgor cells is lost
*** The most beautiful tulips in Holland (boom and bust) are beautiful because they’re diseased, not healthy
Different Extension Specialist
- Field crop diseases- Vegetable diseases- Fruit tree diseases- Forest diseases- Turf diseases- Diseases of ornamentals
Categories of diseases based on TYPES of PATHOGENS:
A) Fungal diseases (eukaryotes that have membrane bound nucleus and mitochondria)B) Prokaryotes (bacteria and mycoplasmas) lack nucleus and some organellesC) Parasitic higher plants (ex: dodder, mistletoe)D) Viruses and viroidsE) Nematodes
The significance of Historical Development sin plant pathology
- Man is completely dependent on plants- Every plant species is potentially subject to its particular diseases- Causes of plant diseases and methods to manage them has been recognized just recently- (most significantly since 1860, since Pasteur and others discovered that pathogens are causes of
diseases and not its consequence)
Two competing theories of causes of disease:
- Spontaneous generation- Germ theory
Diseases have had an impact since the beginning of agriculture
- Greek philosopher Theophrastus (300 BC) wrote a book about the diseases of trees, cereals, and legumes
- The early romans and Robigalia – romans made sacrifice (red dogs and sheep) to special rust god, Robigus, to prevent rust diseases of grain crops such as wheat
- People were fatalistic about the occurrence of diseases for almost 2,000 years. Real causes of diseases were not known.
- Believed that plant, human, and animal, diseases just happened spontaneously and were merely punishment from God for human sins
In 1755 Tillet in France showed that he could increase smut on wheat plants if he added smut dust to speed and reduce it if he pretreated seed with copper sulfate. He believed incorrectly that the smut dust was poisonous.
- The germ theory was first proposed by a French scientist named prevost in 1807. He repeated Tillet’s experiments and proposed.
o Causes for diseases are microscopic fungal spores that infect the plants. o Reduction of smut after seed treatment with copper sulfate results from inhibition of
spore germination- But the idea was rejected by French academy of sciences and scientists throughout Europe- People continued to believe that mildews, rots, and microorganisms found on diseased plants
were products of disease rather than the cause.
You can not propose a major hypothesis, you have to propose an alternate hypothesis.*** Must give a completely different explanation at an equal rate.
Virtually all major epidemics of pant disease have been caused by the practices of man.
Human influence often involves moving plants and/or pathogens from their point of origin.
- “New Encounter” diseases (introduced new hosts to native pathogens or native host to a new pathogen) have caused many of the most destructive epidemics
o The most infamous example of “New Encounter disease” are human diseases: measles and chickenpox devastated the American Indians when introduced from Europe.
Comply with airport security --- answering a questionnaire --- did you have any contact with agricultural products? --- Things like that.
Example: Hawaii and Bamboo- 2 Cases: both bacteria and fungal
Plant Diseases and human history *** NEED TO KNOW
- The Irish potato famine- Ergot of wheat and wye - Coffee rust in Sri Lanka (Ceylon)- Southern Corn Leaf Blight- Chestnut Blight
The Irish Potato Famine: Late Blight of Potato (& tomato)
Host: potato = solanum tuberosum
Oomycete = phytopthora infestans
***similar to fungus, genomically is related to fungi
Phyto – “plant”
Pthora – means, literally, “kill”
***need to know: none of the chemical treatments we use are working any longer, the strain we had prevented developed a resistance
The Irish Potato Famine
- Social and economic impacto 1 million people deado 1.5 million immigrated to USo Deepened the rift between the Irish and the British: British landlords refused to believe
that the famine was serious. They still demanded the drop as payment of rento Protectionist trade laws against imports of US corn repealed: import of American corn
was allowed to feed the starving Irish with boiled corn mush- All due to plant disease!
o Late blight is still one of the major diseases of potato today (20% global potato losses). Potatoes are one of the major sources of nutrition in developing countries
- Wheat and rye went to rich British people, landlord
***corn originated from Native Americans that cultivated it
SETTING THE SCENE:
- Why was it so severe?o Host: Potatoo Native to Andean highlands (Peru and Bolivia)
Staple food for Indians since 400 BC Native Indians cultivated it, and the Incan city of Matsupitsu was a potato
breeding stationo Imported to Europe by Spanish conquistadors (approximately 1570)o Widely accepted in Europe by 1800’s
Highly nutritious Easy to grow Higher yield compared to cereal
o Dependent population in Ireland!!!o Peasants consumed 8-14 lbs a day.
Potatoes grew well in cool, moist climate F F F
o Fo Fo Fo Fo F
- The pathogen: Phytopthora infestanso Imported from south America
o Hosts: potatoes and close relatives, but in South America, the broad genetic base of the host provides natural resistance
o ***weather conditions are important for diseaseo Is late blight of potato a case of “New Encounter” disease?
- Environmental conditionso Cool, moist climate conditions accelerate the rate of disease developmento Summer of 1845 started out hot and dryo Weather changed: 1.5 to 7 degrees C below normalo Continuous overcast and rain for 6 weekso Accelerates pathogen life cycle by nearly 10X!o Within a few weeks the potato crops of Ireland were destroyed.
- How do you propagate a potato?o The potato is exactly identical to other potatoes. There is no sexual reproduction. It is a
monoculture. o Very limited genetic diversity.o One problem with the host.
Impact on the Science of Plant Pathology:
Proving that the oomycete caused the disease
1. The P. Infestans pathogen: visible as white mildew on the leaves and stems of infected plantsa. Common perception: excess water caused the disease
2. Anton de Bary experiments (german botanists)a. Describe the experiments
This was a MAJOR BREAKTHROUGH for our understanding of how all diseases are initiated (both of plants and animals). It set the stage for Pasteur’s Germ Theory in 1863.
All of it combined with disease conducive environment
Last recorded epidemic of late blight:
- Germany, 1816 (700,000 dead)
- Copper fungicides had been discovered and were used to control the disease, but the German army used the copper for bullets
Ergot Wheat and Rye
Cankers are usually plant diseases
Chestnut blight – cankers
2 years, the tree is dead
This is what happened to most American chestnut
EX: NEW ENCOUNTER DISEASE
The pathogen was in Asia and was feeding on the Asian chestnut
They developed no immunity whatsoever
Asian chestnut was valued for good quality
- Microscopes allowed them to see anthrax
Every time you must identify a causal agent of disease, you use Koch’s postulates
***Obligate parasites require living organism to multiply
Koch’s Postulates (there are 4):
1. Describe the symptoms in detail. EX: wilting or necrosis2. Isolate and purify the suspected pathogen. Describe it (EX: colony color, speed of growth, spore
shape and size)3. Inoculate healthy plants with the purified pathogen. This must reproduce the disease symptoms
as described in #1.4. Re-isolate the pathogen. It must be the same as that in #2.
Saprophytes eat dead organic manner
***koch’s postulates, use full sentences
Viruses can not be confirmed by Koch’s postulates; because #2 does not work
How do we identify viruses? Later
The majority of human-microbe interactions are positive (10 times more bacterial than our own cells in our body)
Plants secrete 30% of the sugars they produce from photosynthesis into the soil
This is how they co-exist
Pathogen – attack this plant? Yes or np
Virulence is completely different from pathogens because it’s a degree of pathogenicity
More virulent strain or less virulent strain
Need to know:
***host range!!!
Whether or not this pathogen is (neco troph? Bio troph?)
Viruses are usually cause-specific
Many different mechanisms for resistance
9/22/15
Definitions:
VI. Pathogen species, pathovars, races, and special forms:
A. A species is a population of organisms with common morphological and physiological characteristics that allow for consistent reproductive success
B. Within a species of pathogen, variability may exist in what hosts may be susceptiblei. E.g. Puccinia graminis is a stem of rust cereals
C. Some individuals of this pathogen only attack wheat, others only barley, or oats – these groups are called pathovars (pv.) or special forms
i. E.g. Puccinia graminis pv. Tritici infects wheatD. Even within each special form, some races attack some varieties of the host plant but not others,
depending on the specific genetic makeup of the potential host
Species is primarily identified by consistent reproductive success.
Homosapiens -> H. sapiens
P. Puccini. pv. tritici M01234
What does the number mean? It’s a specific strain of the pathogen
The Nature of Plant Disease
A. Disease Trianglea. Virulent ****Pathogen (must be virulent = able to cause disease, the strength of
infection is important)i. Total of virulence, abundance, etc.
b. Conducive****Environmenti. Total of conditions favoring disease
c. Susceptible****Hosti. Total of conditions favoring susceptibility
Very important, *** situation and explain it
- In order to infect, you must have all these things happen- Roses/tomatoes are difficult to grow -> buy a new variety -> great to use for a few years, then
devastated by something- Today’s new variety, is tomorrow’s devastated crop
Life cycle of Phytopthora infestans:
***very cold
Infestans spores are not very hardy, they will die very quickly
The spores are produced from underneath, sticking on the stomata
Tubers, very important source of infected plant
Polycyclic – undergoes the life cycle several times a year
Can take many extreme environmental situations
- It can reproduce asexually very fast -> reproduce sexually once- Sporangia, sporangium -> asexual -> very cold conditions- Indirect germination (between sporangium and zoospores (see diagram picture))- Zoospores can move -> they can swim, flagellum- Zoospores -> sexual
Does oospore infect plant directly? Never
What they do:
- They germinate- To produce sporangia- ***sporangia is asexual- Oospores are sexual
Cold and wet -> they produce zoospores
Hot and dry -> germ tube
How the environments affects diseases progress?
- What is the right environment to infect?- 6-8-12 hours to germinate/infect tissue
The only time when spraying fungicide works -> is if you spray it when spores germinate
Only works before the pathogen is inside of the tissue/leaf
^^^ Marshall Ward
A seed once planted, doesn’t need to be watered everyday Really wet, allows swimming zoospores to colonize the root
10/1/15
No more GMS germ plasm
Southern corn leaf blight?
Supposed to be dead, in 1970’s
Why is this happening?
- Commercial hybrid- Commercial fields- Corn is dead by now, it’s harvested- Close to Houston, it rained much more in Houston than it did here- Wo different strains, race O and race T- Race O was primary cause of southern corn leaf blight- Is it another race that showed up that we haven’t seen before?- This disease has never been since 1970 in this area
o A new race of southern corn blight, much more virulent and aggressiveo Job securityo Disaster situationo Only have two more lectures before the examo The first exam will only cover material in lectureo 2nd exam is the most difficult
Pathogen:
3 different lifestyles
- Necrotroph- Biotroph- Hemibiotroph
Biotrophs pretend to live in harmony with the plant
- Fewer cell degrading (or cell wall degrading) enzymes than non-biotrophs- Intercellular, apoplast- Live between the cells, they feed on abundant sugars - Evade detection and avoid elicitation of defense responses- Very specialized feeding structures to insert into plant without detection
Necrotophs
- Smash and grab- Produces toxins and cell degradation enzymes
Toxins:
- Phyto-toxins : only effective against a plant cells- Myco-toxins: fungi that infects seeds highly carcinogenic to us
Fungal and oomycete biotrophs:
- Live right between the cell wall and plant plasma membrane- Surround themselves with something the plant will not think is foreign- They will never break through the plasma membrane- 10 days after infection, the leaves infected are dying
Haustoria/Haustorium
- Secrete special proteins to …- Prevent PCD (programmed cell death)- Completely different set of genes, expressed at any point in time- To be able to multiply without being detected- When they have built the “army” they invade the rest of the plant- Produce toxins, etc.- Targets plant machinery
1st question on exam:
- What are the pathogenistic or virulence factors produced by the pathogen that induce certain changes in the host:
o Enzymeso Toxinso Growth regulatorso Plugging substances
- Plants produce very little seedo Instead of being filled with photosynthate
It’s eaten by fungus
Very heavy cuticle layer in the tropical plants
Naming the major cell wall degraders (enzymes):
- Lipin lipase
Lignin makes plants stand tall, keeping cells turgid; skeleton of the plant cell, like bones
Cutinase important
- If you mutate genes for cutinase, they are not capable of causing disease at all
Fungi:
- Highly effective enzyme that degrades the component of tree trunks- Ligninases capable of degrading lignin- White rot fungus- To produce biofuels
Altered host metabolism:
- Toxin is entirely responsible for symptoms you would see only in an a plant attacked by a microorganism
- Only on potato (specific cultivar) and not on corn- Host specific toxin***- Doesn’t affect anything but one variety- Victoria and Victorian
Victoria Blight of Oats
- Necrotrophic- Resistance to crown rust- Gene for resistance to crown rust is required to make the oats resistant to this pathogen
T-toxin:
- Another example of a host specific toxin
AAL Toxin:
- Huge losses to tomato production
Non-host specific:
3 examples
- Tabtoxino Tobaccoo Misleading because it’s not cause specific toxino It affects other plants
- They use a molecule that mimics a hormone in the palnt- Binds to the plant 10 times more effectively than the actual hormone in the plant- Jasmonic acid (JA)
Hormone (ABA) produced in the roots but takes effect in the leaves (closes and opens stomata)
Jasmine smells because of a production of a molecule called cis-jasmine, by-product of jasmonic acid
Salicylic acid *** another human hormone – ancient Greece aspirin is salicylic acid (kills diseases)
- Aspirin is converted in the human body into salicylic acid - Aspirin binds to an enzyme to inactivate jasmonic acid
Southern Bacterial Wilt
- Plan will never recover- Bacteria reside inside vascular tissues and blocks the flow of water- Cannot grow commercially (tomato/potato) in Texas
o b/c the environment conducive to disease (more than 30 degrees Celsius) no disease below 18 degrees C
o #1 potato grown area (Idaho)o WHY GROW WHERE THERE IS NOT MUCH RAIN? PATHOGENS
Dry area, if there is a supply of water = good- Symptoms: wilting, stunting, discolored (brownish) vascular tissue, bacterial ooze in cut stems- Difference between fungal wilt and bacterial wilt!!!!
o Mechanisms of virulence:o EPSo Plant hormones
Auxin required for cell enlargement Cytokinin required for cell division
o Enzymes- Control
o Avoidance: cool climateso Eradication: crop rotation (5 yrs)o Exclusion: disease free seedo Resistant varieties: did not help (too much pathogen strains or variation)o Biological control: avirulent strain Ralstonia solanacearum cannot reproduce
virulence factors (they take up the same space of pathogenic factors though) Fills exactly the same ecological niche
Xanthonomonas: #1
- All YELLOW- Citrus canker
Rice bacterial blight #2
o Still a problem in Texaso New encounter diseaseo Known to be an epidemic to Japan and Asia, Africa, and South Americao First introduced into US In Texas in 1910 during 1912-1913, the disease was found in
Floridao Must destroy/burn infected plants
- Leaves loose ability to photosynthesize (due to leaf lesions)- Emerging panicle infected- Infects at nodes- ***alternative host (new emerging disease) *** worry
o 3 steps:o 1 – identify whether the pathogen in any part of the life cycle – does it require a
different plant species to produce a different type of spore can they find refuge in a different plant species
Bacterial spot in tomato and pepper:
- Copper sprays used- Still used
Black rot of Crucifers:
- Typical lesion on cabbage- Reminds you of….
o Bacteria penetrates through hydathodes
o Where excessive water is released from plants in early morning hours
Diseases caused by Erwinia and Pectobacterium:
- Fire blight of pear- Soft rot of vegetables/potato black leg- ***necrotrophs- Most bacteria is biotroph, and hemibiotroph
***live between cells, or haustorium the two ways bacteria live in plants without detection
Fire blight of pear:
- Best understood bacteria for ages- Erwinia amylovora
o New encounter diseaseo Pear and apple*** (hosts)
- Chestnut blight – chestnut is American plant and blight came over from Asia- This is exact opposite- No apples or pears in north America- Pathogen was in America “resident pathogen”- Then pears and apples were brought over
*** never seen this disease in Europe
- Need only one bacterial cell to create one mutated geneo Pruning is wonderful way to get rid of ito No highly resistant varieties o Some resistant varieties but not good qualityo Japan was successful with quarantine (it’s an island!)
10/20/15
- Fire blight of pear
Biological control:
- Characteristics of a desirable biocontrol agent:o Occupies the same ecological nicheo Can outcompete or antagonize Erwinia amylovorao Can be applied prior to arrival of E. amylovora inoculum (therefore a protectant)o Has resistance to antibiotics used to control E. amylovora, so that it can be used in
conjunction with present methods of control- Apples and pears brought from Europe- Pathogen was in America
o Currently, apples and pears grow in the very dry areas (like desert) because this particular pathogen needs tons of water
o Must be able to apply biological control a long time before the pathogen arrives- Next spike in yield – beneficial microorgnaisms- Why is it a bad idea to apply antibiotics
o Remember why: two types of bacteria, human bacteria (natural pathogens) or what happens when we use too much antibiotics
o Pressure on bacteria to evolve and develop a resistance against antibioticso Can be transferred from one bacteria, and even to a human bacteria
- Must use fungi that will not die of fungicide application
Nematodes
- Fumigate soil- Highly toxic- Never proven to work well
The pathogen:
- Fire blight- Recall the ecological niche of fire blight pathogen- Lives on epiphyte on pear blossoms and in cankers awaiting conditions conducive to disease
Biological Agent (competitive exclusion):
- Pseudomonas fluorescens: competes for resources on the leaf sourceso Lives epiphytically on pear blossomso Resistant to antibiotics
Bacterial soft rots of vegetables:
- Pectobacterium carotovorumo Soft rot disease of tubers and plantso Storageo Fieldo Pectinases
Pectobacterium and subspecies:
- Huge problem commercially- 3 subspecies
o Carotovorumo Atrosepticum (black leg of potatoo Dickey chrysanthemi (other plant hosts)
- Everyone of the subspecies have evolved to be at different temperature rangeso 70 – 90, 50-70, ect.o It thrives everywhereo Subspecies are localized to different locations
- Control:o Storage facilities cleano Chlorinate water
***citrus greening – huanglongbing
- How to prevent infestation- Get rid of insect factor
*** only way to control it quarantine it
- Must be destroyed- Must check with neighbors- The fruit is small and unripe
Bacterial gall disease
- BT protein toxic proteino Eat BT corn you will not die, not toxic to us or cowso Its toxic to insects
- Chemical insecticides less $$$- How were BTs introduced bacterium for gall disease (it has every gene required to insert its
own genome into the plant)- Galls: overgrowth and proliferation of tissue due to:
o Hyperplasiao Hypertrophyo Induced by two different genera:
Pseudomonas Agrobacterium
- Separately controlled by different plant hormones- Plants don’t fight tumer fasciens the tumor is where they eat; the kitchen; the tumor
Pseudomonas syringae pv. savastanoi
- Olive knot diseases- Galls - Epiculture problem
***exam question: how different pseudomonas savastonia and agrobacterium
- Compare the two- Pseudomonas only creates galls by producing one hormone (auxin)- Agrobacterium uses auxin and cytokinin - Two hormones vs. two genes- Pseudomonas produces one hormones but TWO GENES
o iaaMo iaaH
Crown gall
- specific to dicot- cant grow corn in labs- why does this bacterium not like to infect monocot?
o Tiny moleculeo Cannot penetrate directlyo Will not infect until damage/wound is createdo Wound site has molecule that helps plant healo Serves as signal to initiate infection
Insert genomeo One compound (monocot plants don’t produce this compound)
***autonomous autonomously
In order for tumors to forms it must have a 200 kb megaplasmid
What is ti-plasmid? Tumor inducing
This plasmid contains T-DNA; 10%
***memorize ti-plasmid cycle (circle)
- TI PLASMID structure- Reproduce the cycle- Listen carefully!!!!
10/22/15
Crown Gall: Scientific History continued
2 key discoveries
1. Mega plasmid is required for virulence2. Crown gall tumor cells, contain part of the Agrobacterium mega plasmid.
a. 10% of mega plasmid called Transfer DNAb. Transfer DNA contains genes to produce two hormones:
i. Auxin (IAA)ii. Cytokinin (zeatin)
***only the cells in the tumor, not anywhere else
They don’t transform (infect) the entire plant
Explain everything on the single slide of the CYCLE
***absolute detail
2 major portions of mega plasmid:
- From left T DNA border and Right T DNA border (are cut out ion out (from the inside) of the bacterial cell and is inserted into the host)
- The rest stays in the cell (conjugative transfer to Virulence region)
What are the different groups of genes?
- Need to know the names/labels- Virulence region- Origin of replication- Opine catabolism
Virulence region:
- To protect from degradation- To cut this DNA out (Right and Left)
o How do they know where to cut? Restriction enzymes?o They have enzymes to cut it out, they have enzymes to wrap it up (like a hotdog),
invade, cut chromosome and insert he whole piece
If you get rid of …
- Oncogenic genes auxin and cytokinin production and opine synthesis- There is no way for crown gall to form- All that’s left is left and right TDNA border
They can put any genes they want in there
Want only cells that contain TDNA portion to survive
- They don’t insert auxin- They just make the plant make it for them- Opine is not part of the protein - Opine amino acids great resource for energy production
o Opine can be sued only by bacterium because of opine catabolism that stays behind in the Agrobacterium
o They need the plant to synthesize Opine, then they eat it themselves
Plasmid how they exchange genetic material
Origin of replication:
- Why is it important?
Opine octopine not just a single amino acid a bunch of different species
- Why have different opine?- They don’t want to compete with brothers and sisters- They have genes that are producing a specific type of opine so they aren’t competing for food
2 categories of vir genes:
- Sensory- Transfer mechanism
One more gene: turns on transcribe all the rest of the genes
Sensory (does not infect monocots wound site signal) have to have these genes that initiate the whole PROCESS
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