Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bacterial Diseases > Midterm Exam > Flashcards

Midterm Exam Flashcards

1
Q

How many americans die from sepsis?

A

210,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How many americans are affected with sepsis every year?

A

700,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is requred for RNA polymerase to begin transcribing DNA?

A

Sigma subunit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

where does sigma subunit bind?

A

promoter sequence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sigma subunit leaves RNA polymerase at what point?

A

When polymerase begins transcribing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Amino acids attach to the ____ end of a tRNA

A

3’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the modified amino acid corresponding to the start codon in bacteria?

A

f-MET (formyl methionine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

the first tRNA in translation binds in the ___ site of the ribosome

A

P site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what form of energy is used for translation?

A

GTP (hydrolysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Infection-

A

Colonization of the body by an organism

capable of causing disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Disease-

A

infection that causes symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Colonization

A

: A bacterium occupies and multiplies in the human body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

carrier

A

infected but asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pathogenecity

A

Capacity of a bacterium to cause disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Virulence (pathogenicity) factor

A

A component of a

bacterium that is required for disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Who studied anthrax?

A

Robert Koch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Koch’s second postulate?

A

The microbe must be isolated from the lesions of disease and grown as pure culture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is Koch’s fourth postulate?

A

the microbe must be reisolated in pure culture from the experimentally infected host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Molecular Koch’s second postulate

A

The gene should be isolating by cloning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Molecular Koch’s third postulate (a and b)

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What approaches are used to identify new virulence factors?

A

Biochemical

Molecular genetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does the Biochemical approach to identifying new virulence factors entail?

A

purify the factor (e.g., a toxin) and demonstrate that it can reproduce disease symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What four ways can you identify new virulence factors using the molecular genetics approach?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Transposons experimentally introduced into cells often have _______ genes in order to isolate colonies with the transposon.

A

antibiotic resistance genes (selectable marker)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Transposon mutagenesis is a straightforward method to create a library of ________ of a strain of bacteria.

A

random insertion mutants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Transposon mutagenesis is only useful for studying ________ genes, because ___________

A

non-essential

insertion into a gene usually inactivates it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

transposon Insertions may be polar, meaning they ______________

A

knock out expression of downstream genes in an operon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

location of a transposon may be determined with certain types of _____

A

PCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

B-galactosidase is an example of a reporter gene product that can be useful for measuring gene expression. B-galactosidase cleaves 3 things: ________

A

B- galactosides, galactopyranoside (X-gal), and ONPG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

B-galactosidase cleaves X-gal to form a _______colored product

A

blue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

B-galactosidase cleaves ____ to create a yellow product. This technique is especially useful in that it helps ____________

A

quantify the amount of gene expression occurring, rather than simply telling you the gene is being expressed. (it is quantified on a spectrophotometer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

When B-galactosidase is fused to a virulence gene, it is regulated the same way/a different way as the virulence gene?

A

the same way

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Gene fusions can be constructed:

i. _______
ii. ________

A

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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Strains containing gene fusions can be further mutagenized to _____________

A

isolate regulatory mutants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Signature-tagged mutagenesis combines _______ with ______ using an animal model of infection to screen for mutants that _______.

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

instead of using a single transposon to generate a library of mutants, STM uses ________.

A

a mixture of transposon variants generated from a single transposon.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

In STM, each transposon variant has its own unique “_______” or “______”

A

“tag” or “barcode”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Endotoxins-

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

LPS contains 3 structural regions:

A

O-specific chain, core, and Lipid A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

LPS comes from _______ in bacteria

A

the outer cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Sepsis results from ________

A

septicemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Septicemia-

A

systemic disease in which bacteria multiply in the blood or are continuously seeded into the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

The stages of sepsis in order are:

A

SIRS, sepsis, severe sepsis, septic shock, MODS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

When septicemia occurs, circulating bacteria release ______, which triggers the _________ that leads to sepsis

A

endotoxin

systemic immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

The innate immune system consists of _____

A

Cells and proteins that are always present
and ready to respond to foreign invaders,
including bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

The cells of the innate immune system include:

A

Phagocytes, Natural killer cells, Mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Define Phagocytes-

A

cells that ingest and kill

bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Name the 4 phagocytic types of cells of the innate immune system:

A
  1. polymorphonuclear leukocytes (aka PMNs, neutrophils)
  2. monocytes
  3. macrophages
  4. dendritic cells (DCs).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Which two phagocytes migrate constantly throughout the bloodstream?

A

PMN’s and monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Dendritic cells localize to _______

A

tissues that are in contact with the external environment or the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

When monocytes leave the bloodstream to enter a tissue, they differentiate into _______

A

macrophages (more phagocytic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Define Natural Killer cells-

A

kill host cells containing intracellular bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Where do mast cells accumulate?

A

around blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the purpose of a mast cell?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

The three classes of proteins in the innate immune system are the:

A

cytokines, chemokines, and complement proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

define cytokines and provide 4 examples

A

glycoproteins produced by a number of cell types including macrophages

  1. TNF-alpha
  2. IL-1
  3. IFN- gamma
  4. IL-8
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

how big is a cytokine in kDal?

A

8-30 kDal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

define chemokines-

A

peptides produced by same cells as cytokines, but are smaller than cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

The binding of cytokines and chemokines to surface receptors on target cells initiates __________

A

a signal transduction cascade that modifies the function of the target cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

define complement proteins-

A

a set of proteins produced
by the liver that circulate in blood and have
the capability to enter tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

complement proteins become active through ______

A

proteolytic cleavage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what are the 3 functions complement proteins are involved in?

A

a. Enhancing phagocytosis of invaders.
b. Chemotaxis of macrophages, PMNs.
c. Rupturing membranes of invaders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what are the 3 pathways involved in complement activation?

A

mannose-binding lectin pathway, classical pathway, and alternative pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

define the mannose-binding lectin pathway

A

mannose-binding lectins are produced in the liver and bind specifically to mannose residues
on the surface of bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

define the classical pathway

A

involves antibodies attached to bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

define the alternative pathway

A

involves binding of bacterial surface components such as LPS and teichoic acids by complement component C3b.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

the act of sticking stuff to a bacterial cell to make it less slippery and easier for a WBC to catch is called:

A

opsonization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

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 ______

A

phagosome
lysosome
phagolysosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

creation of a phagosome involves the rearrangement of __________

A

the actin cytoskeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

The phagocyte engulfs bacteria by extending ______

A

pseudopods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

a lysosome contains 7 things:

A

lysozyme, proteases, nucleases, anti-microbial peptides, membrane permeabilizing proteins, phospholipases, myeloperoxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

as a result of the oxidative burst in a phagolysosome, these 4 products are formed:

A

peroxide, superoxide, hypochlorous acid, nitric oxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

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).

A

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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Phagocytes become activated (produce _______) when what happens?

A

(cytokines and chemokines) when they recognize certain conserved structural components of bacteria

80
Q

Name 4 conserved structural components of bacteria that phagocytes illicit a response to. What are they known as collectively?

A

LPS, lipotechoic acid, flagella, and CpG-rich DNA. They are collectively known as PAMPs (pathogen-associated molecular patterns)

81
Q

how do PAMPs trigger cytokine/chemokine release?

A

Toll like receptors on host cell membranes recognize these PAMPs and subsequently initiate cytokine/chemokine release via signal transduction.

82
Q

Toll was first identified as a _________ required for development and immune function in Drosophila

A

transmembrane receptor protein

83
Q

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.

A

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
Q

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 ________

A

“rapid acting” primary transcription factors

harmful cellular stimuli

85
Q

Phagocytes become activated (produce _______) when what happens?

A

(cytokines and chemokines) when they recognize certain conserved structural components of bacteria

86
Q

Name 4 conserved structural components of bacteria that phagocytes illicit a response to. What are they known as collectively?

A

LPS, lipotechoic acid, flagella, and CpG-rich DNA. They are collectively known as PAMPs (pathogen-associated molecular patterns)

87
Q

how do PAMPs trigger cytokine/chemokine release?

A

Toll like receptors on host cell membranes recognize these PAMPs and subsequently initiate cytokine/chemokine release via signal transduction.

88
Q

Toll was first identified as a _________ required for development and immune function in Drosophila

A

transmembrane receptor protein

89
Q

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.

A

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
Q

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 ________

A

“rapid acting” primary transcription factors

harmful cellular stimuli

91
Q

Cytokines and chemokines fully activate killing capacity of _____ upon entrance into tissue, and cause ______ to differentiate into ______.

A

PMNs

monocytes into macrophages

92
Q

inflammation is characterized by 4 things

A

redness, swelling, pain, heat

93
Q

What 5 cytokines recruit phagocytes, thus initiating the inflammatory response?

A

TNF-a, IL-1, IL-8, PAF, IL-6 (they are produced at the site of infection)

94
Q

_____ induces mast cells to produce vasoactive compounds at site of infection, increasing vascular permeability.

A

PAF

95
Q

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 ______.

A

redness and heat

swelling

96
Q

During killing of bacteria at site of infection, what is released from phagocytes.

A

some lysosomal enzymes (even more are released as phagocytes die)

97
Q

The lysozymes released into tissues at sites of infection will _________

A

damage and kill surrounding tissue cells

this occurrence is possibly an attempt to kill hidden bacterial cells

98
Q

The pro-inflammatory response is down regulated by _______

A

anti-inflammatory cytokines

99
Q

Name 4 anti-inflammatory cytokines

A

IL-1 receptor antagonist, IL-4, IL-10, IL-13

100
Q

anti-inflammatory cytokines reduce production of _________, and reduce killing capacity of __________

A

inflammatory cytokines

phagocytes

101
Q

Exotoxins-

A

Protein toxins produced by bacteria that are usually released into the host environment during growth

101
Q

Effector proteins (exoenzymes)-

A

bacterial toxins delivered directly into host cells by bacterial secretion systems

101
Q

Superantigens (type I toxins)-

A

peptide
toxins that cause T cells (part of adaptive
immune response) to become overstimulated and release large of amounts of cytokines.

101
Q

Membrane-disrupting toxins (type II toxins)-

A

lyse host cells (or compartment within host cell) by disrupting the integrity of their plasma membranes

101
Q

What are the two types of membrane disrupting toxins (type 2 toxins)?

A

Proteins that form channels (pores) in the
plasma membrane and Enzymes that compromise the integrity of
the plasma membrane phospholipids.

101
Q

What are the two classes of exotoxins?

A

Superantigens and membrane-disrupting toxins

101
Q

alpha hemolysin is what kind of toxin?

A

a type 2 pore forming exotoxin

101
Q

If pore forming proteins are one class of type II exotoxins, then what would the other class be?

A

phospholipases

102
Q

Type III toxins are also called:

A

A-B toxins

103
Q

Type III toxins-

A

Consist of two
functional subunits. The A subunit has enzymatic (toxin) function, while the B subunit binds to a receptor on host cells.

104
Q

Single-chain A-B toxins have

A

one A subunit and one B subunit.

105
Q

What type does diptheria toxin fall under?

A

Type III

106
Q

Diptheria toxin is a ______ chain A-B toxin

A

single

107
Q

Diptheria toxin receptor on cell membrane is:

A

HB-EGF (heparin binding epidermal growth factor)

108
Q

The biological activity of the diptheria toxin is:

A

ADP-ribosyltransferase

109
Q

Diptheria toxin:

  • Outside the cell, how are the two subunits associated?
  • Once they are endocytized, the reducing environment causes what to happen?
A
  • 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
Q

Diptheria toxin: once the A subunit has entered the cytosol, what reaction does it catalyze?

A

the formation of ADP-ribose from NAD+ and transfers it to a target protein.

111
Q

What is the target protein for diptheria toxin?

binds ADP-ribose to target protein

A

EF-2

112
Q
  • Diptheria bacteria do not produce the toxin unless what happens?
  • If they do produce the toxin, it is under what conditions?
A
  • a bacteriophage containing the toxin gene undergoes the lysogenic cycle in the bacteria
  • low-iron conditions
113
Q

Cholera toxin is a ______ subunit A-B toxin

A

multi

114
Q

Cholera causes _____ deaths per year

A

100,000-200,000

115
Q

What is the ratio of subunits in a multi-subunit A-B toxin?

A

one A subunit and multiple B subunits. The B units may or may not be identical

116
Q

The B subunits of Cholera toxin bind to what receptor?

A

GM1 gangliosides

117
Q

The target protein of Cholera toxin is:

A

Gs protein

118
Q

What does cholera toxin do that fucks with you?

A

It prevents hydrolysis of GTP from the Gs protein, causing excessive cAMP production

119
Q

Anthrax toxin is a _____ subunit ______ toxin

A
  • multi

- A-B

120
Q

Humans and animals are susceptible upon infection by B. anthracis spores.
3 forms of infection depending on route of
infection-

A

subcutaneous, gastrointestinal,

and inhalation anthrax.

121
Q

Anthrax toxin

Consists of 3 plasmid-encoded proteins:

A 
Lethal factor (LF)
Edema factor (EF)
Protective antigen (PA)
122
Q

Lethal factor (LF)-

A

a protease that inactivates MAP kinase kinases.

123
Q

Edema factor (EF)-

A

a calmodulin-dependent adenylate cyclase.

124
Q

Protective antigen (PA)-

A

delivers LF and EF to the cytosol.

125
Q

First anthrax vaccine was developed by who when?

A

Louis Pasteur in 1881

126
Q

Sec system secreted proteins are synthesized in ______ form with a signal (leader) sequence at the _____

A
  • precursor

- N-terminus

127
Q

Signal sequence is cleaved by a _____ during transport across the
cytoplasmic membrane.

A

-leader peptidase

128
Q

Gram positive/negative. Is sec system found in one (which one) or both?

A

both

129
Q

____ brings a Sec dependent protein to _____. ______ uses ATP hydrolysis to undergo a conformational change to push the protein through ______. ______ stabilizes this process.

A
  • Sec B
  • Sec A
  • Sec A
  • SecYEG
  • SecDF-YajC
130
Q

Integral membrane (IM) proteins inserted into the cytoplasmic membrane via ________.

A
  • the Sec system
131
Q

SRP is/is not necessary for the Sec system?

A

is not

132
Q

As IM proteins begin to exit the ribosome their signal sequence is recognized by________

A

the signal recognition particle.

133
Q

Secretion of IM protein occurs _______ (as it is being synthesized)

A

co-translationally.

134
Q

TAT stands for:

A

Twin-arginine transport

135
Q

TAT transports proteins that are ______

A

already folded

136
Q

Proteins have N-terminal twin-arginine
signal sequence, which includes the
motif _____

A

-SRRXFLK.

137
Q

SRP, attached to signal recognition sequence is recognized by _____, which somehow transfers the protein to ____

A
  • FtsY

- SecA

138
Q

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 _______.

A
  • TatBC
  • TatA
  • cleavage of the signal sequence
139
Q

Does TAT system involve ATP hydrolysis?

A

no

140
Q

What secretion systems are Sec-dependent?

A

T2SS and T5SS

141
Q

What secretion systems are specific to gram negative bacteria?

A

T1,2,3,4,5,6 secretion systems

142
Q

T2SS proteins are secreted across the outer membrane through:

A

a pore consisting of 12-14 proteins.

143
Q

Proteins secreted via T5SS export themselves, they are also called ________

A

autotransporters

144
Q

The ____ domain of a T5SS inserts itself in the outer membrane, forming a pore for the rest of the protein to be secreted through

A

Beta

145
Q

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 ______

A
  • general Sec dependent system
  • beta domain
  • autoproteolytic cleavage
  • alpha domain (mature protein)
  • the beta domain (pore)
146
Q

Which types of gram-negative secretion systems are Sec-independent?

A

T1,3,4,6 secretion system

147
Q

Type 1 secretion system (T1SS) involves a complex of ______ that span
_________________.

A
  • 3 proteins

- the cytoplasmic membrane, periplasm and outer membrane.

148
Q

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?

A
  • C-terminal
  • glycine
  • GGXGXD
  • is not
149
Q

The E. coli hemolysin a T1SS system consists of a IM spanning _______ transporter, a periplasmic connecting protein ______, and an OM spanning pore protein called _____

A
  • ABC transporter (HlyB)
  • accessory factor HlyD
  • TolC
150
Q

Type 3 secretion system (T3SS) has a contact-dependent mechanism
involving an elaborate complex of over
20 proteins that forms a ________

A

delivery apparatus (injectisome).

151
Q

Is ATP required for T3SS involving an injectisome?

A

yes

152
Q

What kind of proteins are secreted in T3SS?

A

Effector proteins, because they are directly injected into the host cell

153
Q

What genus species uses T3SS?

A

Pseudomonas aeruginosa

154
Q

What toxins are secreted by P. aeruginosa?

A

ExoS,T,U,Y

155
Q

What activity do ExoS and T have?

A

ADP-ribosyltransferase and Rho GTPase-activating protein domain
-ADPRT and GAP

156
Q

What activity does ExoU have?

A

Phospholipase A2

157
Q

What activity does ExoY have?

A

Adenylate cyclase

158
Q

What does the injectisome resemble?

A

flagella

159
Q

P. aeruginosa is a pathogen of:

A

humans, animals and plants

160
Q

Pseudomonas aeruginosa survives on:

A

a variety of surfaces including on skin.

161
Q

Pseudomonas aeruginosa is an __________ pathogen, which is capable of causing infections in ______(4 places)

A
  • opportunistic and nosocomial

- the pulmonary tract, urinary tract, and burn and wound sites.

162
Q

A type 3 secretion system can be divided

into five components:

A 
Effector proteins
Chaperones
Translocation apparatus
Regulatory proteins
Needle complex and other proteins
163
Q 
Many pathogenic bacteria
use type 3 secretion, often
with distinct specific effects 
on host cells. The specific effects are due 
to the \_\_\_\_\_\_\_\_\_\_\_\_
A

particular secreted effectors.

164
Q

the injectisome consists of what components?

A

the translocation apparatus and the needle complex with other proteins

165
Q

GAP activity-

A

promotes GTP hydrolysis of small G proteins.

166
Q

G proteins targeted by ExoS and T GAP activity are:

-What do these G proteins regulate?

A

-Rho, Rac, and Cdc42.
-These regulate a variety of cellular
processes including cytoskeletal
structuring.

167
Q

Activated Rho stimulates ___________

A

contractile actin-

myosin filament assembly.

168
Q

Activated Rac triggers:

A

actin-rich surface protrusions (lamellipodia)

169
Q

Activated Cdc42 triggers:

A

finger-like projections (filopodia)

170
Q

Inactivation of the various G proteins by ExoS and T results in _____________

A

dramatic changes in cell shape.

171
Q

An endothelial cell with active Rac is round, but one without activated Rac looks like ______

A

sharp, sickle shaped cells

172
Q

Upon injection, a number of host cell

proteins are targeted for __________

A

ADP-ribosylation

173
Q

ExoS-mediated ADP ribosylation results in

_____________(4 things)

A

actin cytoskeleton disruption, inhibition of
DNA synthesis, vesicular trafficking and
endocytosis, and eventually cell death.

174
Q

ExoT-mediated ADP ribosylation results in

_____________(4 things)

A

actin cytoskeleton disruption, and inhibition

of cell migration, adhesion, and proliferation.

175
Q

ExoU’s phospholipase domain is also called _______ and has _______ activity

A
  • Patatin-like domain

- PLA2

176
Q

ExoU-

A

A potent phospholipase that can cause cell death rapidly.

177
Q

ExoU substrates include: (3 things)

A

phospholipids, lysophospholipids, and neutral lipids.

178
Q

T3SS chaperones maintains newly synthesized effector proteins in a _________ state in the cytosol and guides them to ______

A
  • translocation-competent (unfolded)

- the injectisome.

179
Q

SpcS is the chaperone for ________
SpcU is the chaperone for _________
No chaperone yet identified for _______

A
  • ExoS and ExoT.
  • ExoU.
  • ExoY.
180
Q

_____ is the chaperone for ExoS and ExoT
_____ is the chaperone for ExoU
_____ is the chaperone for ExoY

A
  • SpcS
  • SpcU
  • none identified
181
Q

where do chaperones bind to the effector proteins ExoS,T,U?

A

on the CBD (chaperone binding domain)

182
Q

Does ExoY have a CBD?

A

No

183
Q

Type 3 secretion in P. aeruginosa is regulated at 2 levels:

The 2 levels are _____.

A

1) transcription of type III secretion genes.
2) initiation of the secretion process itself.
- linked.

184
Q

Normally the T3SS is turned off until what happens?

A

contact with host cell

185
Q

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 ___.

A
  • ExsE
  • ExsC
  • ExsD
  • ExsA
186
Q

Once ExsD is bound to C, ExsA can act as a _____________

A

-transcription activator of T3SS secretions.

187
Q

For reasons that are not clear, nearly all aeruginosa strains have either the ____ or the ____ gene but not both

A
  • exoS

- exoU

188
Q

exoU gets ______ in host cells, but the effect is unknown

A

ubiquitylated

189
Q

The T3SS of aeruginosa is most closely related to that of _____

A

Yersinia.

190
Q

The aeruginosa T3SS most likely evolved for ______ instead of for _______

A
  • defense against predators

- invasion of a host

Bacterial Diseases (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions