Midterm Exam Flashcards
(197 cards)
1
Q
How many americans die from sepsis?
A
210,000
2
Q
How many americans are affected with sepsis every year?
A
700,000
3
Q
What is requred for RNA polymerase to begin transcribing DNA?
A
Sigma subunit
4
Q
where does sigma subunit bind?
A
promoter sequence
5
Q
Sigma subunit leaves RNA polymerase at what point?
A
When polymerase begins transcribing
6
Q
Amino acids attach to the ____ end of a tRNA
A
3’
7
Q
what is the modified amino acid corresponding to the start codon in bacteria?
A
f-MET (formyl methionine)
8
Q
the first tRNA in translation binds in the ___ site of the ribosome
A
P site
9
Q
what form of energy is used for translation?
A
GTP (hydrolysis)
10
Q
Infection-
A
Colonization of the body by an organism
capable of causing disease
11
Q
Disease-
A
infection that causes symptoms
12
Q
Colonization
A
: A bacterium occupies and multiplies in the human body
13
Q
carrier
A
infected but asymptomatic
14
Q
Pathogenecity
A
Capacity of a bacterium to cause disease
15
Q
virulence
A
Often used interchangeably with
pathogenicity. Can also refer to the degree of
disease a bacterium has the capacity to cause
(e.g., highly virulent)
16
Q
Virulence (pathogenicity) factor
A
A component of a
bacterium that is required for disease
17
Q
Who studied anthrax?
A
Robert Koch
18
Q
What is Koch’s first postulate?
A
The microbe must be associated with symptoms of the disease and must be present at the site of infection
19
Q
What is Koch’s second postulate?
A
The microbe must be isolated from the lesions of disease and grown as pure culture
20
Q
What is Koch’s third postulate?
A
a pure culture of the microbe, when inoculated into a susceptible host, must reproduce the disease in the experimental host
21
Q
What is Koch’s fourth postulate?
A
the microbe must be reisolated in pure culture from the experimentally infected host
22
Q
What is the proposed fifth postulate for Koch?
A
Elimination of the disease-causing microbe from the infected host or prevention of exposure of the host to the microbe should eliminate or prevent disease.
23
Q
Molecular Koch’s first postulate
A
The gene (or its product) should be found
only in strains of a bacterium that cause
disease and not in strains that are avirulent
24
Q
Molecular Koch’s second postulate
A
The gene should be isolating by cloning
25
Molecular Koch's third postulate (a and b)
3a. Disrupting the gene in a virulent strain should reduce (attenuate) its virulence.
3b. Introducting the cloned gene into an
avirulent strain should render the strain
virulent.
26
What approaches are used to identify new virulence factors?
Biochemical
| Molecular genetics
27
What does the Biochemical approach to identifying new virulence factors entail?
purify the factor (e.g., a toxin) and demonstrate that it can reproduce disease symptoms.
28
What four ways can you identify new virulence factors using the molecular genetics approach?
a. Clone genes from pathogen into avirulent host (e.g., Escherichia coli) and show that the resulting strain is now virulent.
b. Mutagenize pathogen with a transposon and screen the resulting random insertion mutants for loss of virulence.
c. Measure virulence gene regulation using gene fusions. ( Fuse the promoter region of a given gene (or operon) to a reporter gene, which can be used to more easily measure gene expression)
d. Identify genes that are required for survival in the host.
29
Transposons experimentally introduced into cells often have _______ genes in order to isolate colonies with the transposon.
antibiotic resistance genes (selectable marker)
30
Transposon mutagenesis is a straightforward method to create a library of ________ of a strain of bacteria.
random insertion mutants
31
Transposon mutagenesis is only useful for studying ________ genes, because ___________
non-essential
| insertion into a gene usually inactivates it
32
transposon Insertions may be polar, meaning they ______________
knock out expression of downstream genes in an operon
33
location of a transposon may be determined with certain types of _____
PCR
34
B-galactosidase is an example of a reporter gene product that can be useful for measuring gene expression. B-galactosidase cleaves 3 things: ________
B- galactosides, galactopyranoside (X-gal), and ONPG
35
B-galactosidase cleaves X-gal to form a _______colored product
blue
36
B-galactosidase cleaves ____ to create a yellow product. This technique is especially useful in that it helps ____________
quantify the amount of gene expression occurring, rather than simply telling you the gene is being expressed. (it is quantified on a spectrophotometer)
37
When B-galactosidase is fused to a virulence gene, it is regulated the same way/a different way as the virulence gene?
the same way
38
Gene fusions can be constructed:
i. _______
ii. ________
i. Using cloned promoter region sequence of gene of interest.
ii. In the pathogen using a transposon derivative that contains a reporter gene (note: this creates a mutant and a gene fusion simultaneously).
39
Strains containing gene fusions can be further mutagenized to _____________
isolate regulatory mutants
40
Signature-tagged mutagenesis combines _______ with ______ using an animal model of infection to screen for mutants that _______.
Signature-tagged mutagenesis (STM)
combines transposon mutagenesis with an in vivo selection using an animal model of infection to screen for mutants that do not grow in the host.
41
instead of using a single transposon to generate a library of mutants, STM uses ________.
a mixture of transposon variants generated from a single transposon.
42
In STM, each transposon variant has its own unique "_______" or "______"
"tag" or "barcode"
43
Endotoxins-
toxic integral bacterial membrane components, including lipopolysaccharide (LPS), lipotechoic acid (LTA) and phosphatidylglycerol (PG), that are released into the host environment typically upon cell lysis.
44
LPS contains 3 structural regions:
O-specific chain, core, and Lipid A
45
LPS comes from _______ in bacteria
the outer cell membrane
46
Sepsis results from ________
septicemia
47
Septicemia-
systemic disease in which bacteria multiply in the blood or are continuously seeded into the bloodstream
48
The stages of sepsis in order are:
SIRS, sepsis, severe sepsis, septic shock, MODS
49
When septicemia occurs, circulating bacteria release ______, which triggers the _________ that leads to sepsis
endotoxin
| systemic immune response
50
The innate immune system consists of _____
Cells and proteins that are always present
and ready to respond to foreign invaders,
including bacteria.
51
The cells of the innate immune system include:
Phagocytes, Natural killer cells, Mast cells
52
Define Phagocytes-
cells that ingest and kill
| bacteria
53
Name the 4 phagocytic types of cells of the innate immune system:
1. polymorphonuclear leukocytes (aka PMNs, neutrophils)
2. monocytes
3. macrophages
4. dendritic cells (DCs).
54
Which two phagocytes migrate constantly throughout the bloodstream?
PMN's and monocytes
55
Dendritic cells localize to _______
tissues that are in contact with the external environment or the bloodstream
56
When monocytes leave the bloodstream to enter a tissue, they differentiate into _______
macrophages (more phagocytic)
57
Define Natural Killer cells-
kill host cells containing intracellular bacteria
58
Where do mast cells accumulate?
around blood vessels
59
What is the purpose of a mast cell?
when a foreign invader is detected, mast cells release histamine (vasodilator that makes blood vessels leaky) in order to facilitate the exit of PMNs and monocytes from the bloodstream to the site of infection
60
The three classes of proteins in the innate immune system are the:
cytokines, chemokines, and complement proteins
61
define cytokines and provide 4 examples
glycoproteins produced by a number of cell types including macrophages
1. TNF-alpha
2. IL-1
3. IFN- gamma
4. IL-8
62
how big is a cytokine in kDal?
8-30 kDal
63
define chemokines-
peptides produced by same cells as cytokines, but are smaller than cytokines
64
The binding of cytokines and chemokines to surface receptors on target cells initiates __________
a signal transduction cascade that modifies the function of the target cells
65
define complement proteins-
a set of proteins produced
by the liver that circulate in blood and have
the capability to enter tissue
66
complement proteins become active through ______
proteolytic cleavage
67
what are the 3 functions complement proteins are involved in?
a. Enhancing phagocytosis of invaders.
b. Chemotaxis of macrophages, PMNs.
c. Rupturing membranes of invaders
68
what are the 3 pathways involved in complement activation?
mannose-binding lectin pathway, classical pathway, and alternative pathway
69
define the mannose-binding lectin pathway
mannose-binding lectins are produced in the liver and bind specifically to mannose residues
on the surface of bacteria.
70
define the classical pathway
involves antibodies attached to bacteria.
71
define the alternative pathway
involves binding of bacterial surface components such as LPS and teichoic acids by complement component C3b.
72
the act of sticking stuff to a bacterial cell to make it less slippery and easier for a WBC to catch is called:
opsonization
73
when a phagocyte ingests a bacteria, it endocytizes it into a vesicle called a _______, which it then fuses with a ______ to destroy the bacteria. this fused vesicle is called a ______
phagosome
lysosome
phagolysosome
74
creation of a phagosome involves the rearrangement of __________
the actin cytoskeleton
75
The phagocyte engulfs bacteria by extending ______
pseudopods
76
a lysosome contains 7 things:
lysozyme, proteases, nucleases, anti-microbial peptides, membrane permeabilizing proteins, phospholipases, myeloperoxidase
77
as a result of the oxidative burst in a phagolysosome, these 4 products are formed:
peroxide, superoxide, hypochlorous acid, nitric oxide
78
The enzyme _____ is present in the phagosome membrane, and converts oxygen and NADPH into superoxide. ______ then converts the superoxide into _______, which is then converted into hydroxide radicals in the ________ reaction or hypochlorous acid by the enzyme _______ (present in the lysosome).
The enzyme NADPH oxidase is present in the phagosome membrane, and converts oxygen and NADPH into superoxide. Superoxide dismutase then converts the superoxide into H2O2, which is then converted into hydroxide radicals in the Fenton reaction or hypochlorous acid by the enzyme Myeloperoxidase (present in the lysosome).
79
Phagocytes become activated (produce _______) when what happens?
(cytokines and chemokines) when they recognize certain conserved structural components of bacteria
80
Name 4 conserved structural components of bacteria that phagocytes illicit a response to. What are they known as collectively?
LPS, lipotechoic acid, flagella, and CpG-rich DNA. They are collectively known as PAMPs (pathogen-associated molecular patterns)
81
how do PAMPs trigger cytokine/chemokine release?
Toll like receptors on host cell membranes recognize these PAMPs and subsequently initiate cytokine/chemokine release via signal transduction.
82
Toll was first identified as a _________ required for development and immune function in Drosophila
transmembrane receptor protein
83
We must know cyto/chemokine release pathway for the Lipid A receptor. Fill in the blanks below: When LPS dissociates from a bacterium such as E. coli, _____ will bind to it and transfer the LPS to ______ on the cell membrane, which then transfers LPS to ______, also on the cell membrane. Via signal transduction, ______ is activated and translocated to the nucleus, where it induces _____ and ______ genes.
We must know cyto/chemokine release pathway for the Lipid A receptor. Fill in the blanks below: When LPS dissociates from a bacterium such as E. coli, LBP will bind to it and transfer the LPS to CD14 on the cell membrane, which then transfers LPS to TLR-4, also on the cell membrane. Via signal transduction, NF-kB is activated and translocated to the nucleus, where it induces inflammatory and immune response genes.
84
NF-kB is important in regulating cellular responses because it belongs to the category of "________" ___________ i.e. transcription factors that are present in cells in an inactive state and do not require new protein synthesis to be activated (think about c-Jun, Fos, etc. These are in the same category) This fact allows NF-kB to be a first responder to ________
"rapid acting" primary transcription factors
| harmful cellular stimuli
85
Phagocytes become activated (produce _______) when what happens?
(cytokines and chemokines) when they recognize certain conserved structural components of bacteria
86
Name 4 conserved structural components of bacteria that phagocytes illicit a response to. What are they known as collectively?
LPS, lipotechoic acid, flagella, and CpG-rich DNA. They are collectively known as PAMPs (pathogen-associated molecular patterns)
87
how do PAMPs trigger cytokine/chemokine release?
Toll like receptors on host cell membranes recognize these PAMPs and subsequently initiate cytokine/chemokine release via signal transduction.
88
Toll was first identified as a _________ required for development and immune function in Drosophila
transmembrane receptor protein
89
We must know cyto/chemokine release pathway for the Lipid A receptor. Fill in the blanks below: When LPS dissociates from a bacterium such as E. coli, _____ will bind to it and transfer the LPS to ______ on the cell membrane, which then transfers LPS to ______, also on the cell membrane. Via signal transduction, ______ is activated and translocated to the nucleus, where it induces _____ and ______ genes.
We must know cyto/chemokine release pathway for the Lipid A receptor. Fill in the blanks below: When LPS dissociates from a bacterium such as E. coli, LBP will bind to it and transfer the LPS to CD14 on the cell membrane, which then transfers LPS to TLR-4, also on the cell membrane. Via signal transduction, NF-kB is activated and translocated to the nucleus, where it induces inflammatory and immune response genes.
90
NF-kB is important in regulating cellular responses because it belongs to the category of "________" ___________ i.e. transcription factors that are present in cells in an inactive state and do not require new protein synthesis to be activated (think about c-Jun, Fos, etc. These are in the same category) This fact allows NF-kB to be a first responder to ________
"rapid acting" primary transcription factors
| harmful cellular stimuli
91
Cytokines and chemokines fully activate killing capacity of _____ upon entrance into tissue, and cause ______ to differentiate into ______.
PMNs
| monocytes into macrophages
92
inflammation is characterized by 4 things
redness, swelling, pain, heat
93
What 5 cytokines recruit phagocytes, thus initiating the inflammatory response?
TNF-a, IL-1, IL-8, PAF, IL-6 (they are produced at the site of infection)
94
_____ induces mast cells to produce vasoactive compounds at site of infection, increasing vascular permeability.
PAF
95
Increased permeability of blood vessels at site of infection results in increased blood flow to infected area, causing ____ and ____, as well as leakage of fluid into tissue, causing ______.
redness and heat
| swelling
96
During killing of bacteria at site of infection, what is released from phagocytes.
some lysosomal enzymes (even more are released as phagocytes die)
97
The lysozymes released into tissues at sites of infection will _________
damage and kill surrounding tissue cells
| this occurrence is possibly an attempt to kill hidden bacterial cells
98
The pro-inflammatory response is down regulated by _______
anti-inflammatory cytokines
99
Name 4 anti-inflammatory cytokines
IL-1 receptor antagonist, IL-4, IL-10, IL-13
100
anti-inflammatory cytokines reduce production of _________, and reduce killing capacity of __________
inflammatory cytokines
| phagocytes
101
Exotoxins-
Protein toxins produced by bacteria that are usually released into the host environment during growth
101
Effector proteins (exoenzymes)-
bacterial toxins delivered directly into host cells by bacterial secretion systems
101
Superantigens (type I toxins)-
peptide
toxins that cause T cells (part of adaptive
immune response) to become overstimulated and release large of amounts of cytokines.
101
Membrane-disrupting toxins (type II toxins)-
lyse host cells (or compartment within host cell) by disrupting the integrity of their plasma membranes
101
What are the two types of membrane disrupting toxins (type 2 toxins)?
Proteins that form channels (pores) in the
plasma membrane and Enzymes that compromise the integrity of
the plasma membrane phospholipids.
101
What are the two classes of exotoxins?
Superantigens and membrane-disrupting toxins
101
alpha hemolysin is what kind of toxin?
a type 2 pore forming exotoxin
101
If pore forming proteins are one class of type II exotoxins, then what would the other class be?
phospholipases
102
Type III toxins are also called:
A-B toxins
103
Type III toxins-
Consist of two
functional subunits. The A subunit has enzymatic (toxin) function, while the B subunit binds to a receptor on host cells.
104
Single-chain A-B toxins have
one A subunit and one B subunit.
105
What type does diptheria toxin fall under?
Type III
106
Diptheria toxin is a ______ chain A-B toxin
single
107
Diptheria toxin receptor on cell membrane is:
HB-EGF (heparin binding epidermal growth factor)
108
The biological activity of the diptheria toxin is:
ADP-ribosyltransferase
109
Diptheria toxin:
- Outside the cell, how are the two subunits associated?
- Once they are endocytized, the reducing environment causes what to happen?
- they are joined by a disulfide bond
| - The disulfide bond breaks, and the B subunit acts as a pore for the A subunit to enter the cytosol
110
Diptheria toxin: once the A subunit has entered the cytosol, what reaction does it catalyze?
the formation of ADP-ribose from NAD+ and transfers it to a target protein.
111
What is the target protein for diptheria toxin?
| binds ADP-ribose to target protein
EF-2
112
- Diptheria bacteria do not produce the toxin unless what happens?
- If they do produce the toxin, it is under what conditions?
- a bacteriophage containing the toxin gene undergoes the lysogenic cycle in the bacteria
- low-iron conditions
113
Cholera toxin is a ______ subunit A-B toxin
multi
114
Cholera causes _____ deaths per year
100,000-200,000
115
What is the ratio of subunits in a multi-subunit A-B toxin?
one A subunit and multiple B subunits. The B units may or may not be identical
116
The B subunits of Cholera toxin bind to what receptor?
GM1 gangliosides
117
The target protein of Cholera toxin is:
Gs protein
118
What does cholera toxin do that fucks with you?
It prevents hydrolysis of GTP from the Gs protein, causing excessive cAMP production
119
Anthrax toxin is a _____ subunit ______ toxin
- multi
| - A-B
120
Humans and animals are susceptible upon infection by B. anthracis spores.
3 forms of infection depending on route of
infection-
subcutaneous, gastrointestinal,
| and inhalation anthrax.
121
Anthrax toxin
Consists of 3 plasmid-encoded proteins:
```
Lethal factor (LF)
Edema factor (EF)
Protective antigen (PA)
```
122
Lethal factor (LF)-
a protease that inactivates MAP kinase kinases.
123
Edema factor (EF)-
a calmodulin-dependent adenylate cyclase.
124
Protective antigen (PA)-
delivers LF and EF to the cytosol.
125
First anthrax vaccine was developed by who when?
Louis Pasteur in 1881
126
Sec system secreted proteins are synthesized in ______ form with a signal (leader) sequence at the _____
- precursor
| - N-terminus
127
Signal sequence is cleaved by a _____ during transport across the
cytoplasmic membrane.
-leader peptidase
128
Gram positive/negative. Is sec system found in one (which one) or both?
both
129
____ brings a Sec dependent protein to _____. ______ uses ATP hydrolysis to undergo a conformational change to push the protein through ______. ______ stabilizes this process.
- Sec B
- Sec A
- Sec A
- SecYEG
- SecDF-YajC
130
Integral membrane (IM) proteins inserted into the cytoplasmic membrane via ________.
- the Sec system
131
SRP is/is not necessary for the Sec system?
is not
132
As IM proteins begin to exit the ribosome their signal sequence is recognized by________
the signal recognition particle.
133
Secretion of IM protein occurs _______ (as it is being synthesized)
co-translationally.
134
TAT stands for:
Twin-arginine transport
135
TAT transports proteins that are ______
already folded
136
Proteins have N-terminal twin-arginine
signal sequence, which includes the
motif _____
-SRRXFLK.
137
SRP, attached to signal recognition sequence is recognized by _____, which somehow transfers the protein to ____
- FtsY
| - SecA
138
In the TAT system, the TAT signal sequence on the protein binds to ______. ______ is recruited to the complex, inducing transport of the protein across the membrane, also resulting in _______.
- TatBC
- TatA
- cleavage of the signal sequence
139
Does TAT system involve ATP hydrolysis?
no
140
What secretion systems are Sec-dependent?
T2SS and T5SS
141
What secretion systems are specific to gram negative bacteria?
T1,2,3,4,5,6 secretion systems
142
T2SS proteins are secreted across the outer membrane through:
a pore consisting of 12-14 proteins.
143
Proteins secreted via T5SS export themselves, they are also called ________
autotransporters
144
The ____ domain of a T5SS inserts itself in the outer membrane, forming a pore for the rest of the protein to be secreted through
Beta
145
T5SS uses __________ to cross the inner membrane, then ______ forms a pore for the rest of the protein to cross the outer membrane. Then, the protein undergoes ______ to release the _______ from ______
- general Sec dependent system
- beta domain
- autoproteolytic cleavage
- alpha domain (mature protein)
- the beta domain (pore)
146
Which types of gram-negative secretion systems are Sec-independent?
T1,3,4,6 secretion system
147
Type 1 secretion system (T1SS) involves a complex of ______ that span
_________________.
- 3 proteins
| - the cytoplasmic membrane, periplasm and outer membrane.
148
Type 1 secretion system (T1SS) secreted proteins have a _____ signal
sequence containing the _____-rich
motif _____ repeated many times. This signal sequence is/is not cleaved during export?
- C-terminal
- glycine
- GGXGXD
- is not
149
The E. coli hemolysin a T1SS system consists of a IM spanning _______ transporter, a periplasmic connecting protein ______, and an OM spanning pore protein called _____
- ABC transporter (HlyB)
- accessory factor HlyD
- TolC
150
Type 3 secretion system (T3SS) has a contact-dependent mechanism
involving an elaborate complex of over
20 proteins that forms a ________
delivery apparatus (injectisome).
151
Is ATP required for T3SS involving an injectisome?
yes
152
What kind of proteins are secreted in T3SS?
Effector proteins, because they are directly injected into the host cell
153
What genus species uses T3SS?
Pseudomonas aeruginosa
154
What toxins are secreted by P. aeruginosa?
ExoS,T,U,Y
155
What activity do ExoS and T have?
ADP-ribosyltransferase and Rho GTPase-activating protein domain
-ADPRT and GAP
156
What activity does ExoU have?
Phospholipase A2
157
What activity does ExoY have?
Adenylate cyclase
158
What does the injectisome resemble?
flagella
159
P. aeruginosa is a pathogen of:
humans, animals and plants
160
Pseudomonas aeruginosa survives on:
a variety of surfaces including on skin.
161
Pseudomonas aeruginosa is an __________ pathogen, which is capable of causing infections in ______(4 places)
- opportunistic and nosocomial
| - the pulmonary tract, urinary tract, and burn and wound sites.
162
A type 3 secretion system can be divided
| into five components:
```
Effector proteins
Chaperones
Translocation apparatus
Regulatory proteins
Needle complex and other proteins
```
163
```
Many pathogenic bacteria
use type 3 secretion, often
with distinct specific effects
on host cells. The specific effects are due
to the ____________
```
particular secreted effectors.
164
the injectisome consists of what components?
the translocation apparatus and the needle complex with other proteins
165
GAP activity-
promotes GTP hydrolysis of small G proteins.
166
G proteins targeted by ExoS and T GAP activity are:
| -What do these G proteins regulate?
-Rho, Rac, and Cdc42.
-These regulate a variety of cellular
processes including cytoskeletal
structuring.
167
Activated Rho stimulates ___________
contractile actin-
| myosin filament assembly.
168
Activated Rac triggers:
actin-rich surface protrusions (lamellipodia)
169
Activated Cdc42 triggers:
finger-like projections (filopodia)
170
Inactivation of the various G proteins by ExoS and T results in _____________
dramatic changes in cell shape.
171
An endothelial cell with active Rac is round, but one without activated Rac looks like ______
sharp, sickle shaped cells
172
Upon injection, a number of host cell
| proteins are targeted for __________
ADP-ribosylation
173
ExoS-mediated ADP ribosylation results in
| _____________(4 things)
actin cytoskeleton disruption, inhibition of
DNA synthesis, vesicular trafficking and
endocytosis, and eventually cell death.
174
ExoT-mediated ADP ribosylation results in
| _____________(4 things)
actin cytoskeleton disruption, and inhibition
| of cell migration, adhesion, and proliferation.
175
ExoU's phospholipase domain is also called _______ and has _______ activity
- Patatin-like domain
| - PLA2
176
ExoU-
A potent phospholipase that can cause cell death rapidly.
177
ExoU substrates include: (3 things)
phospholipids, lysophospholipids, and neutral lipids.
178
T3SS chaperones maintains newly synthesized effector proteins in a _________ state in the cytosol and guides them to ______
- translocation-competent (unfolded)
| - the injectisome.
179
SpcS is the chaperone for ________
SpcU is the chaperone for _________
No chaperone yet identified for _______
- ExoS and ExoT.
- ExoU.
- ExoY.
180
_____ is the chaperone for ExoS and ExoT
_____ is the chaperone for ExoU
_____ is the chaperone for ExoY
- SpcS
- SpcU
- none identified
181
where do chaperones bind to the effector proteins ExoS,T,U?
on the CBD (chaperone binding domain)
182
Does ExoY have a CBD?
No
183
Type 3 secretion in P. aeruginosa is regulated at 2 levels:
The 2 levels are _____.
1) transcription of type III secretion genes.
2) initiation of the secretion process itself.
- linked.
184
Normally the T3SS is turned off until what happens?
contact with host cell
185
T3SS
Upon contact with host cell ____ begins to be secreted into host cell, depleting it in the bacteria, which leaves ____ unbound. It may now bind ___, which is inhibiting ___.
- ExsE
- ExsC
- ExsD
- ExsA
186
Once ExsD is bound to C, ExsA can act as a _____________
-transcription activator of T3SS secretions.
187
For reasons that are not clear, nearly all aeruginosa strains have either the ____ or the ____ gene but not both
- exoS
| - exoU
188
exoU gets ______ in host cells, but the effect is unknown
ubiquitylated
189
The T3SS of aeruginosa is most closely related to that of _____
Yersinia.
190
The aeruginosa T3SS most likely evolved for ______ instead of for _______
- defense against predators
| - invasion of a host
