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, its 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, its 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.
Its amazing how much we dont 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 its dehydrated. Thats normal, we get dehydrated, we
drink water, were fine.
Symptom a lesion
When you talk about disease, or the definition of the disease
-

We do not mention a cause (we dont know)

We dont say anything about specific symptoms

We dont 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 dont know what were 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 another
o 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 rust
o We grow coffee in brazil, Guatemala, central America now
o Coffee rust research in Guatemala
Monoculture
o Genetically uniform organisms
o 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
o
o
Types
o
Types

of organs they affect and symptoms

CANKER stem, a sunken or rotted part of the stem
Plight leaf
of crops they affect
Some only affect corn, some only affect cotton
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 doesnt have a root yet is a problem.
One type of fungus can wipe the plants out, when its 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
Witchs 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
Foliage diseases:
A) chlorosis vein clearing, mottling
B) Leaf blights, leaf blasts, leaf spots
Fruit Diseases:
a) Rots

b) Spots, scurf, sunscald, etc.

*** The most beautiful tulips in Holland (boom and bust) are beautiful because
theyre 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 organelles
C) Parasitic higher plants (ex: dodder, mistletoe)
D) Viruses and viroids
E) 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 Tillets 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
o
o
o

and economic impact

1 million people dead
1.5 million immigrated to US
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 rent
o 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: Potato
o 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 station
o Imported to Europe by Spanish conquistadors (approximately 1570)
o Widely accepted in Europe by 1800s
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 F
o F
o F
o F
o F

The pathogen: Phytopthora infestans

o 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 disease
o Is late blight of potato a case of New Encounter disease?
Environmental conditions
o Cool, moist climate conditions accelerate the rate of disease
development
o Summer of 1845 started out hot and dry
o Weather changed: 1.5 to 7 degrees C below normal
o Continuous overcast and rain for 6 weeks
o 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 plants
a. 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 Pasteurs Germ Theory in
1863.
****understand how the experiment was DONE
(Irish Potato Famine, Lessons Learned)
Caused by man:
-

Imported crop
Imported pathogen
Limited genetic base, therefore, uniform susceptibility
Vegetative propagation
Dependent population

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 Kochs postulates
***Obligate parasites require living organism to multiply
Kochs Postulates (there are 4):
1. Describe the symptoms in detail. EX: wilting or necrosis
2. 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

***kochs postulates, use full sentences

Viruses can not be confirmed by Kochs 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 its 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
susceptible
i. 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 wheat
D. 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? Its a specific strain of the pathogen
The Nature of Plant Disease
A. Disease Triangle
a. Virulent ****Pathogen (must be virulent = able to cause disease, the
strength of infection is important)
i. Total of virulence, abundance, etc.
b. Conducive****Environment
i. Total of conditions favoring disease
c. Susceptible****Host
i. 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
Todays new variety, is tomorrows 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, doesnt 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 1970s
Why is this happening?
-

Commercial hybrid
Commercial fields
Corn is dead by now, its 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 havent seen before?
This disease has never been since 1970 in this area
o A new race of southern corn blight, much more virulent and aggressive
o Job security
o Disaster situation
o Only have two more lectures before the exam
o The first exam will only cover material in lecture
o 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 Enzymes
o Toxins
o Growth regulators
o Plugging substances
Plants produce very little seed

Instead of being filled with photosynthate

Its 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***
Doesnt 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
-

Tabtoxin
o Tobacco
o Misleading because its not cause specific toxin

o It affects other plants

Phaseolotoxin
o Halo blight of bean

Viruses hardest to kill, hardest to control

Must know 7 different groups of bacteria
2 examples of bacterial immunity
All bacterial cells have circular chromosomes
Biology dogma nucleic acid (DNA) RNA transcription RNA translation
protein (amino acids)
Protein is composed of amino acids how many? 20 (normal prokaryotic cell)
In order for a gene to have function, it has to be translated into a protein
ribosomes is a must!
Bacteria do not have ribosomes how do they replicate?
They hijack ribosomes from other cells!
Texas A&M phage center
Bacterial cell contains amino acids in the cell wall
Need to remember organelles:
-

Mitochondria
Ribosomes
Endoplasmic reticulum (require to modify proteins after synthesis takes place)
Vacuoles

General bacteria must have***

Physiological attributes species specific media
Structural elements***
Fatty acid lipid by-layer
***black rot of cabbage
***fire blight of pear erwinia necotroph
***Pierces disease of grapes
***citurds greening (texas)

10/15/15
Focus on Pseudomonas Syringae!
***practice exam
Ice-Nucleation Active Bacteria
-

Gene responsible for it produces a protein

Raises freezing point so cells will rupture

3 types with INA:

-

Pseudomonas syringae
Pseudomonas fluorescens
Pantoea herbicola

Bacterial speck
-

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 EPS
o Plant hormones
Auxin required for cell enlargement
Cytokinin required for cell division

o Enzymes
Control
o Avoidance: cool climates
o Eradication: crop rotation (5 yrs)
o Exclusion: disease free seed
o 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

Still a problem in Texas
New encounter disease
Known to be an epidemic to Japan and Asia, Africa, and South America
First introduced into US In Texas in 1910 during 1912-1913, the disease
was found in Florida
o 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
o
o
o
o

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 disease
o 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
o
o
o
o

only one bacterial cell to create one mutated gene

Pruning is wonderful way to get rid of it
No highly resistant varieties
Some resistant varieties but not good quality
Japan was successful with quarantine (its an island!)

10/20/15
-

Fire blight of pear

Biological control:
-

Characteristics of a desirable biocontrol agent:

o Occupies the same ecological niche
o Can outcompete or antagonize Erwinia amylovora
o 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
antibiotics

o 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 sources

o Lives epiphytically on pear blossoms
o Resistant to antibiotics

Bacterial soft rots of vegetables:

-

Pectobacterium carotovorum
o Soft rot disease of tubers and plants
o Storage
o Field
o Pectinases

Pectobacterium and subspecies:

-

Huge problem commercially

3 subspecies
o Carotovorum
o Atrosepticum (black leg of potato
o Dickey chrysanthemi (other plant hosts)
Everyone of the subspecies have evolved to be at different temperature
ranges
o 70 90, 50-70, ect.
o It thrives everywhere
o Subspecies are localized to different locations
Control:
o Storage facilities clean
o 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 protein

o Eat BT corn you will not die, not toxic to us or cows
o 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 Hyperplasia
o Hypertrophy
o Induced by two different genera:
Pseudomonas
Agrobacterium
Separately controlled by different plant hormones
Plants dont 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 iaaM
o iaaH

Crown gall
-

specific to dicot
cant grow corn in labs
why does this bacterium not like to infect monocot?
o Tiny molecule
o Cannot penetrate directly
o Will not infect until damage/wound is created
o Wound site has molecule that helps plant heal
o Serves as signal to initiate infection
Insert genome
o One compound (monocot plants dont 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 virulence
2. Crown gall tumor cells, contain part of the Agrobacterium mega plasmid.
a. 10% of mega plasmid called Transfer DNA
b. Transfer DNA contains genes to produce two hormones:
i. Auxin (IAA)
ii. Cytokinin (zeatin)
***only the cells in the tumor, not anywhere else
They dont 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?

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 thats 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 dont 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 dont want to compete with brothers and sisters
They have genes that are producing a specific type of opine so they arent
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

FUNGI SECTION

How do fungi find each other (to reproduce?)

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Positive and negative autotropism