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gen bio exam 1
Terms in this set (126)
Four groups of eukaryotes
excavata- all protists
SAR- all protists
Archeplastida- algae, land plants
Unikonta- fungi and animals
shared derived traits
traits that organisms have acquired from their ancestors and share with other members of the group
shared ancestral trait
a character that originated in an ancestor of the taxon
Occam's Razor (Law of Parsimony)
when two competing theories exist to explain the same phenomenon, the simpler of the two theories is generally preferred
group that consists of a single ancestral species and all its descendants and excludes any organisms that are not descended from that common ancestor
composed of some but not all members descending from a common ancestor
an unnatural group that does not include the most recent common ancestor
Problems with using derived traits to determine taxonomy and phylogenies
1. highly derived
2. derived traits can be lost
3. analogous traits can be confusing
1.highly derived, ancestor was terrestrial
2.loss of hind limbs
3. convergent evolution with sharks
uses molecular data (DNA, RNA, developmental genes, hox genes)
genes derived from the same ancestral gene that have accumulated random mutations that make their sequences slightly different (yeast and humans, 3rd nucleotide not preserved, neutral/silent variation)
vertical gene transfer
transfer of genes from an organism to its offspring
horizontal gene transfer (HGT)
(also, lateral gene transfer) transfer of genes between unrelated species
Resolving "Deep branches" using slowly evolving genes
-Highly conserved and slowly evolving genes are good for looking at
evolutionary relationships that date back billions of years (deep branches)
Example - ribosomal RNA (rRNA)
rRNA are components of the ribosome that are absolutely essential for translation (they actually catalyze the enzymatic reactions)
highly conserved due to important cellular function - if you don't have rRNA functioning properly you are super dead.
no changes in every third position since rRNA does not code for a polypeptide (slowly evolving)
High conservation and slowly evolving makes rRNA an excellent gene to examine deep branches of the tree of life (speciation events that happened a long time ago in evolutionary history).
Resolving "branch tips" of a phylogenetic tree using quickly evolving genes
To determine phylogenetic relationships between two closely related
species you need to use rapidly evolving genes.
-Rapidly evolving genes pick up changes very quickly so you can detect evolutionary relationships between species that arose from a relatively
recent speciation event.
Example - Phylogeny of the primates using mitochondrial genes
Mitochondrial genes are in the DNA in the mitochondria (nuclear genes are on chromosomes in the nucleus)
Mitochondrial genes are rapidly evolving
-The DNA polymerase that replicates them is error prone
Divide more often than the host cell
i. mitochondria divide independently of the host cell ii. remember the mitochondria is a bacterial cell living
inside our cells)
iii. more divisions = more replication of the DNA = more chances for errors
How does HGT happen?
Conjugation - mating between two cells
Transformation - picking up freely floating DNA that was released
by another cell.
c. Viruses - can inadvertently move DNA between organisms
One cell engulfs another cell, but does not digest it. the engulfed cell lives inside the host cell
This type of event gave rise to the mitochondria and eukaryotic cells
Over time, mitochondrial genes are slowly "migrating" from the mitochondrial chromosome in the mitochondria and being inserted into eukaryotic chromosomes in the nucleus.
Horizontal Gene Transfer and aphid carotenoid biosynthesis
aphids feed off plant phloem (sap)
need to camouflage themselves by making carotenoids -
brightly colored molecules that plants make.
3. They do not simply get carotenoids from plants , they make their own (if you grow red aphids on green plants, they are still red).
No other animal can synthesize carotenoids
Evidence that aphids got the genes necessary for carotenoid
biosynthesis through Horizontal gene transfer from a fungus.
are viruses alive?
viruses can't replicate their own genome or make their own proteins
Viruses don't have their own ribosomes
they use the ribosomes of the host cell to make the viral proteins
All living organisms have ribosomes
Simplified viral replicative cycle
Virus bind to the surface of a cell
Viral genome gets inserted into a host cell and takes over the transcriptional and translational machinery of the infected cell
infected cell becomes a virus factory, producing tons of viruses.
Thus, viruses rely completely on their host cell for replication
No metabolic activity on their own (can't make ATP), no ribosomes
Structure of Viruses
-very diverse genomes
-some viruses have either double stranded and single stranded DNA
some viruses have either double stranded RNA
some viruses have single stranded RNA
single stranded RNA genome in the + strand orientation (+ RNA
strand is the same orientation as the mRNA)
single stranded RNA in the - strand orientation
this is the complement of the mRNA strand. The - strand RNA needs to be copied in order to make the + RNA strand that will function as an mRNA
have to reverse transcribe their genome (make DNA from an RNA template) at some point in their replication cycle
the most well known retrovirus is HIV has an RNA genome
Strangely some retroviruses have a DNA genome that gets made
into an RNA and then gets made back into a double stranded DNA
A protein coat the surrounds the genetic material of the virus
made up of proteins called capsomeres
iii. Usually a capsid is made up of repeating units of a small number of capsomeres
Example: Tobacco mosaic virus - one capsomere repeated thousands of times - forms a helical structure
Example 2: adenovirus - one main capsomere with a few minor capsomeres
C. Viral Envelopes (page 398 - 399)
many viruses have a phosolipid bilayer membrane outside of the capsid called a viral envelope
viral envelope comes from the host cell plasma membrane.
Have proteins in them that aid attachment to the host cell
Both HIV and influenza viruses have viral envelopes surrounding their
Evolutionary Origin of Viruses
-Huge diversity in genes, genome sizes, types of proteins etc. In fact, there are no genes that can be found in every virus - thus you can't actually do a phylogeny of viruses (no homologous genes)
-suggests that viruses have probably evolved multiple times independently, probably using different mechanisms.
One of the most common theories is that viruses are cellular pieces of self-repicating DNA that have gained the ability to escape the cell and move to another cell and replicate itself.
One possible way to do this would be to have a transposable element (retro-transposon) evolve a mechanism of moving outside of the cell
Interestingly, some retrotransposons make a capsid structure inside the cell that helps protect them from the cytoplasm of the host.
It's easy to imagine a retrotransposon evolving a way to jump between cells and becoming a retrovirus.
Viruses were initially living cells that became parasites of other
We know that most cellular parasites, especially intracellular
parasites, become highly reduced (look at the genome sizes of cellular parasites - parasites have smaller genomes) because they
favor fast growth and rely on the host for many of their cellular
processes - viruses might be an extreme example of this3. Eventually lost various components of ribosome, metabolism, etc.
and become completely dependent on their host.
Viral Attachment to Host Cell
proteins in the capsid or the viral envelope bind to molecules on the surface of
This viral protein binding to a molecule on the surface of the cell
attaches viruses to the outside of the host cell
The molecule on the surface of the host cell is called the "viral receptor"
lock and key fit. - highly specific
specificity of viral attachment is usually why most viruses have a
narrow host range and usually a narrow range of cell types that they can infect - For example, influenza usually only infects a single species and a single type of cell (cells of our lungs).
Entry of viral genome into host cell
(injection, fusion, endocytosis)
Some viruses directly insert their genome into the host cell (like an injection
needle) - bacteriophage do this.
Some viruses cause the host cell to bring them inside by endocytosis - our cells
will endocytose things that are stuck onto the outside of their plasma
membrane. - Influenza does this (as we will see on Friday)
Some viruses fuse their viral envelopes with the host cell membrane (HIV does
this as we will see on Friday)
Discovery of Bacteriophages
plaques on lawns
bacteriophages that replicate by lytic cycle and kill their host cells- example t4
overview-- lytic cycle
-virus injects DNA
-viral DNA begins to be immediately transcribed and translated tomake viral proteins
-host cell DNA is almost immediately degraded (one of the first
-viral enzymes to be transcribed and translated is an enzyme which digests the host DNA)
-Copies of the viral DNA is made by DNA polymerase
-Viral proteins assemble into a phage and the viral DNA is packaged into the virus
-Virus expresses lysozyme late in the infection
-lysozyme is an enzyme which digests the bacterial cell wall the cell bursts openlots of bacteriophage are released
come on between 1 and 3 minutes after initiation
function to inactivate the host genes (prevent the
host from defending itself) and induce expression
of the middle genes [and turn off the early genes]
come on between 5 and 8 minutes after the initiation of infection
important for replication of viral DNA and for inducing the expression of the late genes [and turn off the middle genes]
Come on between 15-20 minutes after the
initiation of infection
important for making the capsid and lysing the
bacterial cell to allow for release
Quick and simple description of normal bacterial
bacterial RNA polymerase can't bind to bacterial
promoters without the help of a protein called
sigma factor (σ)
Sigma factor + RNA polymerase can bind to
bacterial promoters and initiate transcription
The early genes (simplified)
Turning on the early genes
The early genes are transcribed using the
host RNA polymerase and host sigma factor
(the normal bacteria proteins).
Thus, transcription of early genes occurs really fast (phage doesn't need to modify
anything inside the cell to initiate
Example of early genes that get turned on
cuts up the host's bacterial DNA
inactivates the host genome (important
because the host is trying to beat the virus - it's a race against time to determine who wins)
2. anti-sigma factor (AsiA)a. b.
binds the host sigma factor and alters it's activity.blocks the ability of the host sigma factor to bring host RNA polymerase over to the regular host promoters (inactivate host transcription)
also is necessary to get transcription of
the middle genes. 3. MotA
transcription factor that binds to the middle gene promotersMotA is essential for the transcription of the middle genes
Turning on the middle genes
MotA binds to the middle gene promoters
Anti-sigma factor (AsiA)
Examples of middle genes that get turned on
T4 DNA polymerase - initiates replication of
the viral DNA
Viral sigma factor (Viral σ) - binds to the host
RNA polymerase and activates expression of
AsiA + Sigma Factor + RNA polymerase WILL bind to promoters that have MotA on them (i.e. the middle gene promoters). This induces transcription of the middle genes
binds the host sigma factor and alters it's activity.blocks the ability of the host sigma factor to bring host RNA polymerase over to the regular host promoters (inactivate host transcription)
also is necessary to get transcription of
the middle genes. 3. MotA
transcription factor that binds to the middle gene promotersMotA is essential for the transcription of the middle genes
binds to the host RNA sigma factor and changes the activity of the host sigma factor.The AsiA / Sigma factor complex binds to RNA polymerase and blocks binding of RNA polymerase to all bacterial promoters (host transcription gets shut down) and early gene promoters (early genes get turned off)
the late genes.
Turning on the late genes
Viral sigma + RNA polymerase binds to the
host RNA polymerase and blocks AsiA + host
sigma factor from binding
thus, middle genes are turned off.
Viral sigma + host RNA polymerase can bind
to the late gene promoters and activate transcriptionExample of late genes
Capsomere coding genes - makes the capsid
(head, tail, etc).
lysozyme - enzyme that will cut the bacterial
cell wall and cause Lysis
This tightly coordinated expression of these genes swiftly turns the host into a phage factoryThis is very efficient. Virulent bacteriophage can rapidly "chew through"
Temperate phages can incorporate their DNA into the host chromosomes and have the host cell replicate it without killing the bacteria (lysogenic phase of infection) or kill the host (lytic phase).
phage injects DNA
DNA circularizes inside the cell
In a lysogenic cycle the virus makes the enzyme integrase that cuts
the bacterial chromosome and inserts the viral DNA into the
bacterial DNA. The viral DNA is now called a prophage.
Viral DNA gets replicated along with the bacterial DNA during
bacterial cell replication.
transcription of most viral genes is kept off by one viral protein
(lambda (λ) C1 - This is essentially the only viral protein being
made during lysogeny
1. Sometimes the phage can perform a lytic phase2. phage injects DNA3. DNA circularizes inside the cell4. early, middle and late genes get turned on (similar to what we just
saw with T4) and the bacteria will be destroyed5. A temperate phage in a lysogenic cycle can also switch to a lytic
cycle if the cell becomes unhealthy
The CI protein binds to the Cro promoter and blocks RNA polymerase binding - inhibits Cro expression
Also binds to it's own promoter and activates it's own expression (positive feedback loop) - I will discuss this and the importance of this on Friday.
high levels of CI will cause the phage to perform a lysogenic phaseλ Cro
functions to inhibit λ CI expression
binds the λ CI promoter and blocks RNA polymerase binding
high levels of CRO will cause the phage to perform a lytic phase (early genes will get turned on)
(multiple= lysogenic, single= lytic)
well fed cell
Host protease require ATP to function, so they
efficiently cut up CII
proteases are active and the CII protein gets degraded
Lytic cycle is promoted
Adaptive advantage: Lots of resources are present that
will allow the bacteriophage to make lots of copies of
itself - lytic phase is favored
Less ATP aroundHost cell proteases can't degrade CII as efficiently because there isn't as much ATP around
CII is stabilized in starved cells (not degraded)
This tells the phage to go into a lysogenic phase
Adaptive advantage: Limited resources are present (not
very many ribosomes, etc). Therefore, not very many copies of the virus would be made by lysis. The virus will "decide" to go to the lysogenic phase and wait until things get better.
UV light cause DNA damage in the bacteria.This will turn on the bacteria's DNA damage response pathwaythe CI repressor is actively degraded by enzymes that are part of the bacteria's DNA damage response
λ Cro levels will increase as λ CI repressor levels fallλ CI repressor will eventually turn offThe Prophage DNA will pop out of the bacterial chromosome and make a circular piece of DNA again
Early genes will be transcribed and the virus will
enter the lytic phase
-Cholera is a disease caused by infection of the large intestine by the bacteria Vibrio cholerae.
-Bacteria secrete a toxin (called Cholera Toxin) that gets into the cells of our large intestine
-It's thought that the toxin is advantageous to the bacteria because the diarrhea helps the bacteria get transferred to a new host.
-There is strong evidence that the Cholera toxin comes from a temperate phage
-Vibrio Cholerae has both avirulent (non-disease causing and virulent (disease causing) strains.
a.Turns out that the virulent cholera strain has the cholera toxin gene is in the middle of a prophage that is inserted into the Vibrio Cholerae genome.
b.the avirulent strains (do not cause diseases) do not have this prophage.
-Scientists found that if they UV irradiated virulent Vibrio cholerae they could get bacteriophage capsids appearing in the sample (a lytic phase was initiated)
bacteriophage therapy (phage therapy)
-1. The Idea of phage therapy = treating people with bacteriophage to stop life-threatening bacterial infections.
-This is a possible solution to the antibiotic resistance crisis, since phage are known to be able to kill bacteria.
-We know that this will work in mice - treating mice with a bacteriophage 1 day after injecting a lethal bacteria into them allows 60% of mice to survive (100% of mice die that weren't given the bacteriophage)
Phage therapy is currently being tested on patients in multiple clinical trials - some have been successful, while others haven't and some are still in progress
Problems with phage therapy
-Bacteriophage are high specific in the type of bacteria they
-you need to find just the right bacteriophage which
will kill the specific bacteria each patient is infected by
This is time-consuming and expensive.
-This will prevent pharmaceutical companies from developing bacteriophage as a "drug" that they can sell (each bacteriophage drug will be expensive to make and have limited use - only useful on a few patients)
-Bacteria have evolved with bacteriophage for billions of years - so bacteria have evolved sophisticated mechanisms to deal with bacteriophage (as we will discuss in a week or so).
Human Gene Therapy- retroviruses
-Most retroviruses insert the DNA version of the viral genome into a
-Genetically alter a harmless retrovirus (not HIV) to carry the normal copy of the adult beta-globin gene
take stem cells out of the bone marrow
these stem cells have the potential to give rise
to all red blood cells of the patient
-Grow up tons of stems cells in the lab [cultured
-Infect these stem cells with genetically modified retrovirus
-retrovirus will insert the normal beta-globin gene into the genome of the stem cell by reverse transcription and
-the normal copy of the gene will get inserted into a random position (mostly) in one of the patient's chromosomes (retroviruses work like temperate bacteriophage and insert their genome into our chromosomes)
-Grow these genetically altered stem cells in culture
-Inject lots of these stem cells back into the bone marrow of the patient - will start making red blood cells with normal beta-globin levels and anemia will be cured.
Problems with retrovirus gene therapy
-The exact place in our genome where viral DNA integarates is random - the provirus may disrupt a gene that is needed for regulation of the cell cycle - leukemia could arise if you destroy the function of a tumor suppressor
-ew normal version of the gene might not be expressed properly
too high expression if the gene lands in part the chromosome that is highly expressed
too low expression if the gene lands in a part of a chromosome that is actively being turned off
-virus could come alive and infect
the infection with Herpes virus can
ramp up the immune system in such a way that individuals with an existing Herpes infection are more resistant to other infections (including HIV)
placental formation in mammals
the formation of the mammalian placenta relies on a gene that initially came into the genome of our ancestors from a retrovirus that infected the ancestor of all mammals.The viral protein is made by the growing embryonic placenta allows the embryonic portion of the placenta to "invade" into mom's uterus
a protein in the membrane of the viral envelope
important for fusion of the viral envelope with
the host cell plasma membrane.
GP41 has two transmembrane domains (a
transmembrane domain is a part of a protein that has a bunch of really hydrophobic amino acids that can become inserted into the hydrophobic center of a phospholipid bilayer)
One transmembrane domain is inside the viral envelope (anchors the GP41/GP120 complex on the outside of the virus)
The other transmembrane domain is hidden inside GP120. This transmembrane domain willeventually be inserted into the plasma
membrane of the host cell to induce fusion.
protein that attaches to gp41sits on the outside of the virusimportant for attachment of the virus to the
outside of the T-helper cell.
gp120, gp41, capsid, 2 + RNA strands
THREE VIRAL ENZYMES
envelope on virus bind to CD4 and CCR5 on cell surface of white blood cells
virus fuses with the cell and empties contents into the cytoplasm
reverse transcriptase copies the ssRNA viral genome into dsDNA (usually make mutations/genetic diversity)
Integrase (viral enzyme) inserts the dsDNA into the host genome
can go back into viral ssRNA to make more viruses in the cytoplasm
bud off once by the cytoplasm
HIV protease enzyme modifies protein chains, enabling particles/virions to mature into a form that is ready to infect a new host cell
MATURATION- proteases cut up GAG-Polto generate the various individual viral proteins (capsid proteins, RNA associated proteins, Reverse Transcriptase, integrase, etc) and activates them.
initial infection [Acute HIV syndrome]
HIV destroys lots of CD4 carrying T-helper cells
Virus is replicating rapidly and patient is highly
During this initial phase of the infection, the patient
likely feels mildly sick (cold like symptoms)
Clinical Latency (no symptoms)
Eventually, our body catches up and kills most of the virus.
However, The virus stays with us, because the HIV genome is sitting inside the chromosomes of T-helper cells. If the virus is not actively being replicated inside a T-cell our immune system can't attack it.
Some virus will continue to replicate and infect new T- cells (and cells of some other organs).
Viral loads stay low during this period (immune system is still actively fighting the infection
During this period the patient has no discernable symptoms
The HIV virus will over time deplete the CD4 carrying T-helper cells (many infected T-cells actually kill themselves by apoptosis)
Development of AIDS
i. T-helper cells are absolutely critical for the function of
our immune system as we will see in a few months. ii. After a few years the individual loses so many T-
helper cells that they becomes immunocompromised and develops the disease AIDS (Acquired ImmunoDeficiency Syndrome)
iii. People die from AIDS due to secondary infections / cancers that are normally prevented through the function of our immune system.
iv. Note: it appears that some HIV patients might never progress to AIDS (or at least some patients haven't progressed to AIDS yet, even without medical intervention) it's not clear exactly why.
Structure of Influenza
8 viral (-) RNAs
together comprise the viral genome
complementary to the mRNA (+)
these 8 viral RNAs are 8 different chromosomes that carry different genes (unlike HIV where both viral RNAs are identical)
viral RNA polymerase
Every year the sequence of NA and HA changes a
little bit as the virus mutates in people. Gives rise
to multiple strains of influenza.
influenza has a very high mutation rate (like all
Many times, these changes inhibit the ability of
people's pre-existing antibodies to bind fully to HA
Thus, people get sick for a while before their
immune system can fully adapt to the new virus.
This generally causes very mild disease
most people in the population have partial
immunity due to partial or weak binding of pre-
2 types infect mutual host
General Features of Prokaryotes
No nucleus (this is the defining characteristic)
Circular Chromosomes (not packaged into chromatin)
No membrane bound organelles
No chromatin (histones) surrounding their DNA in their chromosomes
shapes of bacteria
cocci, bacilli, spiral
Bacterial Cell Wall
made of peptidoglycan- glycosidic linkages of NAG and NAM (modified forms of glucose - this is the glycan part)
a small polypeptide (amino acid chain) is attached to NAM (this is the peptido part).
Peptidoglycan strands are held together by covalent linkages between the amino acid chains attached to NAM
The covalent linkages that attach the amino acid chains together is created by the bacterial enzyme transpeptidase
i. large peptidoglycan layer ii. no outer membrane
thin peptidoglycan layer
outer membrane - called the LPS layer because it has a membrane with a lot of lipopolysaccharides (LPS) in it
Medically important to distinguish between Gram + and Gram -
Gram negative more resistance to antibiotics (especially those that attack transpeptidase)
Gram negative more likely to cause sepsis (fever / shock) because some lipopolysaccharides make our immune system freak out.
Gram negative bacteria are often difficult for our immune system to attack effectively
A polysaccharide structure that forms a mucous-like coat
around a bacteria.
Very tightly associated with virulence (ability to cause
-Protects bacteria against the host immune system
-Aids in attachment to host cells
-Protects against dehydration.
Transformation of streptococcus pneumoniae experiment
Smooth strain of streptococcus = virulent (capsule on it evades the mammalian immune system)
Rough strain of streptococcus = nonvirulent (no capsule)
Heat killed smooth + rough = virulent (mouse dies because the rough strain was transformed into a smooth strain)
Mechanism rough strain is transformed into a smooth strain by the DNA that contains genes for the capsule coming from the dead smooth cells and getting incorporated into the rough strains chromosome. Rough is now smooth
Shorter than pili
Used to attach the bacteria to substrate or host cells
during an infection
longer and less numerous hairs off the cell
can be used for motility (Type IV) or conjugation
1. tight adhesive collections of bacteria on a
surface or inside our bodies2. secrete extracellular matrix materials that
make them all stick together
bacteria use their pili / fimbriae to help them attach
to the surface and to each other
biofilms are a major medical problem
Bacteria in a biofilm are more resistant to anti- microbial compounds (outside the body) and our immune system (inside our body)
the ability to form biofilms allows bacteria to infect us more effectively.
In hospitals bacteria can make biofilms on a catheter or other surfaces. This makes it very hard to disinfect surfaces and it easy for the bacteria in a biofilm to get into your body.
Bacterial flagellar structure / function
motor embedded in membrane /cell wall turns and makes the connected filament spin like a propeller.
This drives the bacteria forward
The Filament (the extracellular part of a Flagella) is made
up of a complex of Flagellin proteins all bound together.
force that makes the motor turn
motor rotation is driven by an movement of H+ protons through the motor and into the cell
2. Bacteria pumps H+ protons out of the cell3. Channels in the motor allow H+ to diffuse back into the cell 4. The movement of H+ protons through the motor makes it
turn.5. similar to the mechanism by which ATPsynthase in our
inner mitochondrial membrane turns and make ATP
Swimming Behavior and Flagella Rotation
Most bacteria have multiple flagella
When flagella are rotating counter-clockwise all the flagella fit
together and the bacteria moves forward in a straight line (run).
When flagella are rotating clockwise the flagella all come apart and
the bacteria tumbles (turns randomly)
Flagella will periodically switch back and forth between these two
situations at a random interval.
In a homogenous solution the bacteria will move randomly back and
forth between tumbling and running - don't really go anywhere -
called a "random walk
we use a pair of receptors (two ears) that are separated by a set
distance (your head).
We can determine direction of sound by determining the
difference in signal reception in each ear.
walk around randomly and periodically sample the environment.
If you are getting closer you will receive a stronger signal, if you
are getting farther away you will receive a weaker signal.
if you are moving toward the signal (smell is stronger) you will
keep moving straight in that direction.
If the smell is weaker you will randomly turn and start in a
Transmembrane receptors located in the plasma membrane of the cell.
bind to chemicals activates a signal transduction pathway that alters the direction of flagella spinning.
no binding= clockwise
binding= counter clockwise
-MCP receptors will eventually become methylated (a methyl
group (CH3) is added to amino acids in the part of the MCP receptor that is inside the cell) when they are bound to the attractant.
-methylation blocks clockwise(running)
Biased random walk
If moving away from attractant
No chemoreceptors activated CW rotation favored
Random tumblingfrequent change of direction
If moving toward chemical
Chemoreceptors activated and inhibit the CW rotation
Straight run - keeps moving in one direction
If a bacteria is staying at a constant concentration of attractant the chemosensory adaptation step will occur.
The chemoreeptors will be methylated
CW rotation will become more predominant again
They will start randomly turnin more freuntly
This helps them find higher concentrations
Bacterial Type IV pili and twitching motility
Twitching motility is a different form of locomotion that allows bacteria to
spread over the surface of a solid substrate
helps bacteria spread and colonize a solid surface (like a catheter in a
Important for creating "biofilms" - masses of bacteria on a surface.
this is a major concern in hospitals for obvious reasons.
The ability to perform twitching motility is closely associated with the
ability to make biofilms and therefore, the ability to infect patients in hospitals.
the cell division process in bacteria
Circular chromosomes replicate and each new chromosome sticks to a different pole of the cell
Cell splits in two
Very rapid - some bacteria can get one generation every ~20-30 minutes
caused by errors in DNA replication that happen randomly (spontaneously).
a test that you can use to measure mutations rates
Start with a bacterial strain that has a mutation in a gene that
encodes an enzyme that makes the amino acid Histidine - thus, this bacteria will not be able to grow on a plate that lacks Histidine.
"Revertant" or 2nd mutation
Two wrongs can make a right somtimes - a revertant is a
second mutation in a mutant allele of a gene that makes the
gene work again.
Second mutations that causes the His synthesis gene to start
working again - the example I gave in class was if the first mutation was the deletion of one extra nucleotide in a gene (frameshift mutation) then a second deletion of two nucleotides would make the reading frame correct again.
Bacteria that have picked up this second mutation will be able to grow on plates that lack Histidine because they will now make a functional protein that will synthesize Histidine
Spontaneous mutations and the AMES test
Grow bacteria in a culture in media that has the amino acid
Histidine in it - mutant bacteria will grow fine because they
don't need to make their own histidine (you're giving it to them).
You will get some spontaneous revertant mutations occuring
that make the His synthesis gene work again in a small number
If you plate these Salmonella cells on a plate that doesn't have
Histidine in it, you see that some bacteria picked up a
spontaneous revertant mutation
spontaneous mutation - in a population of bacteria there is huge
genetic variation due to spontaneous mutations.
The AMES test can be used to measure the spontaneous
mutation rate using this procedure
Mutations occurring spontaneously in any gene is very rare, but
combined with rapid replication you get a lot of genetic variation in the population. Basically every gene will have a a few different alleles present in a large population
AMES test can be used to identify chemicals that increase mutation rates
Add a chemical you want to test to the growing bacteria that have a mutant allele of Histidine synthesis.
You will get spontaneous mutations occurring
However, if the chemical increases the mutation rate (is a
mutagen) then you will generate many more revertant
mutations in the His synthesis gene
IF the chemical induces mutations to form - then you will get
many more colonies on a plate that lacks Histidine (more cells will create a second mutation in His synthesis gene that makes it function)
This chemical would be potentially cancer causing in humans, since any chemical that creates mutations is likely to cause cancer
Most chemicals in our food have been tested by the FDA in an AMES test to make sure they don't cause mutations.
In bacteria, the direct transfer of DNA between two cells that are temporarily joined.
a collection of genes required for formation of the sex pilus and
Bacterial cells that have the F-factor genes are "fertile" and can
mate with other cells
F factor (fertility factor)
A plasmid found in the donor cell during conjugation and transfers from F+ to F-
A small ring of DNA that carries accessory genes separate from those of the bacterial chromosome
F-factor can also be integrated into the bacterial chromosome
ells that carry an integrated F-factor are called Hfr cells - high
frequency of recombination
Can cause changes in alleles in the recipient strain since some the
chromosomal DNA from the donor strain comes over with the F-factor
Caused by an accident that happens during a bacteriophage infection Review virulent bacteriophage infections of bacteria
remember that one of the first enzymes made by the phage is the endonuclease which will digest the bacterial chromosomal DNA.
bacteria becomes a little phage factory.
Inadvertent transfer of genomic DNA from a different bacterial cell due to improper packaging of DNA into viral head.
phage mistakenly puts some bacterial DNA into the capsid, instead of the phage DNA
bacterial DNA will be inserted into the bacterial cell that the phage infects
This process can change genotype of the recipient bacteria due to homologous recombination / crossing over between the incoming DNA and the bacterial chromosomal DNA
movement of strand of DNA from a dead bacterial cell to a living cell.Note: This was how the genes that are necessary for the capsid production were able to jump from the heat-killed smooth (capsule containing) streptococcus cells over to the rough streptococcus cells in Griffith's experiment.Long thought that this was a random rare process that occurs by mistake We now know that bacterial cells actively bring DNA into them to increase genetic diversity
The Type IV pilus machinery can be used to bind DNA floating around and actively transport it into the cell through the outer membrane, peptidoglycan cell wall and cell membrane.
This increases genetic variation and may bring in genes that help the bacteria become better adapted
any carries genes needed to make a sex pilus (F-factor), so the can be spread by conjugation A bacterial plasmid carrying genes that confer resistance to certain antibiotics.
Prokaryotes vs. bacteriophage (phage)
red queen hypothesis, keep evolving and running to stay the same
cut DNA in specific sequences
Use of restriction enzymes by bacteria to protect against phage infections
bacteria make restriction enzymes - these float around inside the cell
If a phage has the restriction site in it's genome the phage DNA will be cut and the infection will fail
bacterial DNA is masked (methylated) so it is not cut even if the restriction site is present in the bacterial DNA
Note: phage have ways to evade the restriction enzymes - restriction enzymes are not perfect (for example, the phage can get their DNA methylated as well. Thus, the restriction enzymes won't work)
Structure of CRISPR locus (Clusters of Regularly Interspaced Short
Spacers - ~20-35 nucleotides long - DNA that came from phage
Repeats - ~20-35 nucleotides long - DNA that will get processed
out following transcription (sort of like an intron)
Mechanism of how CRISPR protects bacteria
1. Making crRNAs
CRISPR region gets transcribed as one big precursor RNA called a pre-crRNA
pre-crRNA get processed, the repeat sequences get removed (mostly) and the spacers are made into small little pieces of RNA called crRNAs (Crisper RNAs).
bacterial cells express these crRNAS all the time, just waiting for a phage to "get up in their grill and start something" / infect them.
Function of the CRISPR RNAs (crRNA)
inactivate bacteriophage DNA by binding of crRNA to phage
crRNA binds to phage DNA by standard basepairing
(A-T and C-G)
if it is an exact match the CAS9 enzyme will come
and cut the phage DNA
This occurs only if the bacterial cell is a descendant of a
bacterial cell that has already beaten this phage. (inherited
a spacer that was specific for the bacteriophage)
This is a form of "Immunological memory", which was
thought to only be present in vertebrate animals.
problems- retrovirus gene therapy
Does not replace the original defective gene - DNA is
inserted into our genome randomly.
New inserted normal allele can be under or over expressed
(regulation not correct) depending on where it lands
Can disrupt other essential genes if it lands inside them.
How CRISPR / CAS genome editing works
CRISPR/ CAS can make a cut in one specific place in the genome (any
genome, of any organism)
Make a synthetic "guide RNA" (basically a crRNA that you design)
that is complementary to a part of a gene that you want to edit.
Insert the guide RNA along with CAS9 enzyme into the cell (a
human stem cell if this is gene therapy).
CAS9 will cut the DNA only in the region where the guide RNA
This will make a double-stranded break in the chromosome
The cell will need to repair this break - this repair process gives
you an opportunity to change the gene that you just cut.
Non-homologous end joining
A quick-and-dirty mechanism for repairing double-strand breaks in DNA that involves quickly bringing together, trimming, and rejoining the two broken ends; results in a loss of information at the site of repair.
Homology Directed Repair
the cellular DNA repair pathway that uses homologous DNA sequence to precisely repair across a DNA break. The source of the homologous sequence is (1) the homologous chromosome, (2) a sister chromatid if the cell is dividing, or (3) an experimenter supplied template, often called a 'donor' template.
Destruction of the HIV genome inside infected T-cells
Put a guide RNA that binds to the HIV genome and CAS9 into infected T cells
Let non-homologous end joining occur
You should get deletions and insertions that will destroy the
function of the HIV viruses
Problem - if a mutation is made that doesn't block viral
replication, the guide RNA will not be able to bind to that position anymore (typically the match has to be perfect) and the virus will be able to escape the CRISPR treatment
The host organism + all the other prokaryotic organisms living with it
ecological relationships with two species living in close contact
A relationship between two species in which both species benefit
A relationship between two organisms in which one organism benefits and the other is unaffected
The lack of interaction between two species
A relationship in which one organism lives on or in a host and harms it.
Exotoxins and Endotoxins
poisons actively made by the cell and secreted by bacteria cells.
example - cholera toxin
toxins found on the surface of bacterial cells that are part of the structure of the cell (not proteins that are actively secreted by the cell)example: The LPS layer of gram negative bacteria can function as a powerful endotoxin in our bodies (makes our immune system freak out and can cause sepsis)
example #1 of a Pathogenic prokaryote - vibrio cholerae and
Vibrio cholerae bacteria get into our large intestine through
drinking fecal contaminated water.
Bacteria colonizes our large intestine and secretes the cholera
an exotoxin that is released by bacteria in the intestine
causes diarrhea and can lead to massive dehydration very
g- protein switch
G-protein bound to GTP = on
G-protein bound to GDP = off
Turning G-proteins on
Guanine Exchange Factor (GEF) turn G- proteins on
GEFs bind to G-protein and makes them drop GDP and bind to GTP
Turning G- proteins off
GTPase Activating Protein (GAP) turn G-
Bind to G-proteins and turns on the GTPase
activity of the G-protein (the ability to
hydrolyze GTP to GDP + P)
Under the influence of the GAP, the G-
protein will hydrolyzes GTP to GDP and P
and is now bound to GDP (off form)
Cholera toxin inhibits the GTPase activity of the G-protein.
GTPase turns g proteins off. G protein stuck ON
Therefore, the cholera toxin creates a high
concentration of cAMP in our cells
cAMP is an important signaling molecule in our
cAMP binds to and activates the Protein Kinase A protein
In the cells lining our intestines, Protein Kinase A
phosphorylates (and activates) a protein called CFTR viii. CFTR
a protein in the membrane of our cells that line our large intestines that actively pumps Cl- ions out of the cell into the lumen of the large intestine.
Protein Kinase A phosphorylates CFTR, which turns CFTR on.
Activated CFTR pumps chloride ions into the lumen of the large intestine
cl- into intestine, water follows ions
closely associated with eukaryotic hosts
makes enzyme for n2-n3, nitrogen fixation. root cells provide nutrition, rhizobium bacteria provides fixed nitrogen
to the plant
a kind of microorganism that is between a virus and a bacterium; parasitic within the cells of insects and ticksThe fact that our mitochondria is closely related to living alpha-proteobacteria like Rickettsia raises the distinct possibility that the mitochondria was initially a parasite that was taken into the cell by phagocytosis / endocytosis
This ancient alpha-proteobacteria then escaped and entered into the cytoplasm where it eventually developed a mutualistic relationship with the host cell. It is now the organelle we call the mitochondria
utilize plant like photosynthesis
cells from this lineage likely gave rise to chloroplasts in
eukaryotic plants by endosymbiosis (similar to what
happened with the mitochondria).
parasitic pathogenic bacteriaspiral shapeHas a flagella that lies between the peptidoglycan layer and the outer LPS layer (these bacteria are gram (-)). Flagella rotation makes the bacteria "corkscrew" through the liquid. This is a really good way to move through highly viscous liquids, like we have in our joints.
nitially causes a skin level infection (bulls-eye rash)
Can get into bloodstream and cause a more general
infection (fevers, flu-like symptoms)
Eventually it gets into our joints and causes arthritis
(inflammation in the joints)
Treatable with antibiotics.
If infection is not caught until late in the game (when
it's in our joints) you can get "chronic lyme disease". In this situation the symptoms persist even after the bacteria has been cleared through the use of antibiotics.
causes tuberculosis (as you might have guessed from the name).hid by macrophages, lungs isolate by making granulomas, decreasing lung function
Bacteria in the gut
asymbiotic bacteria that lives inside our digestive tract.
helps us break down nutrients
sends out signals to increase vascularization in small
We provide the bacteria with nutrients and a place to live
and also produce antimicrobial chemicals that reduce
Note: this is mostly mutualistic, but sometimes this bacteria
can become parasitic and cause infections like meningitis (infection of central nervous system) if the bacteria gets out of our intestines and into our central nervous system.
A toxic component of the outer membrane of certain gram-negative bacteria that is released only when the bacteria die.
secreted and cause disease even if the prokaryotes that produce them are not present
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