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MMI 351 > Midterm #1 > Flashcards

Midterm #1 Flashcards

1
Q

What is the miasmas?

A
  • “black cloud” or foul vapours that are inhaled into the body to cause illness
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2
Q

Antonie Van Leeqenhook (1632-1723)

A
  • Observed the first microb
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3
Q

Louis Pasteur (1800s)

A
  • realized that microbs were source of decay
  • ruled out spontaneous generation by swan flask experiment
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4
Q

Describe Louis Pastuers swan neck flask experiment.

A
  1. Place nutrient rich fluid in 2 different swan neck flasks and sterilize fluid with heat
  2. break the swan neck off of one of the flasks and then leave both to sit for a period of time

You will find that after a period of time the flask wth the neck will exhibit no growth but the neckless flask will be turbid with microbial growth

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5
Q

Ignaz Semmelweis (1800s)

A
  • Showed that handwashing by medical proffesionals prevented infection (realization that microbial contamination leads to disease)
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6
Q

Joseph Lister (1800s)

A
  • developed antiseptics that reduced microbial contamination of surgical instruments
  • realized that killing microbs could prevent disease
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7
Q

Do all microbes cause the same disease?

A

NO

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8
Q

Robert Koch (1800s)

A
  • developed Koch’s postulates
  • developed a way in which we can determine what bacteria are causative agents for a specific disease
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9
Q

What are Koch’s postulates?

A

One germ = One disease (not always true)
1. The same organism must be present in every case of the disease
2. The organism must be grown in pure culture from a diseased animal or human
3. The organism must then cause the same disease if inoculated into a heathy human or animal
4. The same organism must be found from samples of the inoculated population

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10
Q

What are limitations to Koch’s postulates?

A
  • Some bacteria can colonize without causing any symptomatic disease
  • Disease does not entirely depend on one specific bacterium
  • Some bacteria cannot be cultured
  • Bacteria of one genus are not all the same (Staph species)
  • Disease may be to severe to test in humans and will not occur in an animal
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11
Q

Microbial dysbiosis

A

Animbalance of normal flora

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12
Q

Keystone pathogens

A
  • predict that the return to normal microbiota will resolve disease
  • An agent that remodels the commensal microbiota into a dysbiotic state by causing disruption of host homeostasis
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13
Q

What is an example of a keystone pathogen? Describe what it does.

A
  • Porphyromonas gingivalis
  • The P. gingivalis is introduced to the normal oral flora and it releases the protease Gingipain. The Gingipain cuases the C5 protein to be cleaved into the C5a protein which induces an inflammatory response and impairs leukocyte killing. Both of these factors cuase dysbiosis or the oral microbiota (overgrowth of normal flora)
  • The overall effect of P. gingivalis is complement dependent inflammation and bone loss
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14
Q

What are the molecular Koch’s postulates?

A
  1. The phenotype should be associated with pathogenic members of a genus or pathogenic strains ofa species
  2. Specific inactivation of the gene associated with the suspected virulence trait should lead to a measurable loss in pathogenicity or virulence (deletion)
    - Deletion of virulent gene should result in loss of phenotype
    3.Reversion or allelic replacement of the mutated gene should lead to resoration of pathogenicity (complemention)
    - Restoration of virulent gene with restore phenotype
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15
Q

What are the limitations of Molecular Koch’s postulates?

A
  • need percise information about all of the virulence genes (structural, biochemical, regulatory)
  • Requires a relevant model for studying pathogenicity
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16
Q

What is a primary (A) tissue culture models?

A
  • Derived from the tissue of intrest
  • More reproducable but not durable
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17
Q

What is a immortalized (B) tissue culture model?

A
  • Routine cells used in lab (HEK or HeLa)
  • Robust but genetically variable
  • Usually oncoprotein- mediated
  • Surface antigens can be variable
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18
Q

Organoid cell model

A
  • Compramised of multiple cell types
  • Maintains sme architectural features of an organ
    **Cell culture made of many cell types that maintains the structure of the original cell
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19
Q

Microfluidic cell model

A
  • “organ on a chip”
  • Scalable (very small and can use a limited amount of reagents)
  • High precision
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20
Q

ID50

A
  • Amount of bacteria needed to infect 50% of population/ hosts
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21
Q

LD50

A

Amount of bacteria needed to kill 50% of population/ hosts

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22
Q

What does a low ID50 or LD50 mean?

A

the organism is more pathogenic.

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23
Q

Competitive index

A
  • comparison of wild type and mutant
    CI= [output ratio (CFU mutant/ CFU WT)]/ input ratio (CFU mutant/ CFU WT)]
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24
Q

Gentamicin protection assay

A
  • Used to measure bacterial virulence
  • Distinguishes between adherant and invasive pathogens
  • +Gent means that there is invasion by pathogen
  • -Gent means that there is attachment/ adherance by pathogen to cell
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25
Q

Plaque assay

A
  • Used to measure bacterial virulence
  • Assesses cell-to-cell spread capabilities of pathogens
  • The plate has infected cells covered with soft agar and +Gent and it is incubated to see if bacterial growth disappears throughout plate
  • Large plaques indicate that the bacteria is better at infecting adjacent cells
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26
Q

Infection

A

a colonization of the body by a bacterium capable of causeing disease

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27
Q

Disease

A

Infection that produces symptoms

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28
Q

Colonization

A

Bacterium occupies and multiplies in a particular area of the body

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29
Q

Asymptomatic carrier

A

an infected person who does not have symptoms and does nt know that they are infected

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30
Q

Symptoms

A

effects of bacterial infection apparent in an infected indivisual

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31
Q

Zoonosis

A

A disease carried by animals and accidentally transfered to humans

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32
Q

Virulence (pathogenicity)

A

ability of a bacterium to cause disease

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33
Q

Virulence factor

A

bacterial product or strategy that contributes to virulence (pathogenicity)

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34
Q

Opportunist

A

Bacteria that normally dont cause disease in healthy people but can cause disease in immunocomprimised people or if the bacterium gets into a niche where it does not belong

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35
Q

Pathogen

A

An organism known to cause an infctious diesease

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36
Q

Explain the advantages and limitations of illumina and oxford nanopore technologies sequencing plateforms.

A

Illumina
- advantage: highly accurate (base-by- base sequencing), can do many more reads than Nanopore, relatively cheap, short reads
- disadvantage: Cant see sequence until it is done, takes long time, only does DNA (not RNA)

Oxford Nanopore
- advantage: can see sequence as it is forming, forms sequences in longer chains than Illumina, portable, relatively cheap, can sequence RNA and DNA
- disadvantage: limited accuracey because of DNA translocation spead is not accurate, stuggles with homopolymers

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37
Q

What are the challenges in genome analysis?

A
  • there are many repeats of genetic sequences created in sequencing (long reads can span repeats)
  • sequencing errors
  • millions of short sequences or less accurate longer sequences
  • ploidy (copies of the same chromosome)
  • incomplete sequencing
  • requires powerful computers
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38
Q

What are the applications of sequencing/ genomics in microbiology?

A
  • survallience of pathogens that are causing a disease in a population
  • Cluster investigation (investigating for similar genes amoung different pathogens)- outbreaks
  • Diagnostics
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39
Q

Genome

A

total nucleic acid (DNA & RNA) content of an organism

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40
Q

Genomics

A

study of genomes

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41
Q

Metagenomics

A

The study of all genomes in a sample

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42
Q

What was the first genome sequenced? What was the first genome sequenced of a living organism?

A
  • bacteriophage x174
  • Haemophilus influenzae
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43
Q

How many genes doe all E. coli share with one another?

A
  • 50% (the other 50% of genes differ,explains how some strains of E. coli have different virulence factors)
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44
Q

Core genome vs Accessory genome. What do these make up together?

A
  • Core genome- the component of the genome that is constant/ shared amoung all organisms of the species
  • Accessory genome- the portion of the genome that is not shared amoung all the organisms in a species
  • The Pangenome
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45
Q

Depth vs Coverage

A

Depth: how often a base/ position is sequenced
Coverage: how much of the genome has depth
(coverage is not always even across a genome)

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46
Q

Why do we read short read assemblies over Long read assemblies?

A
  • they are more accurate and faster
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47
Q

Why do we use molecular approches for diagnosis/ detection? Drawbacks

A

Benifits:
- Faster
- Cheaper
- More objective
- Can detect organisms that cannot be cultivated
- Can define complex mixtures of bacteria through analysis of a single sample

Drawbacks:
- limited information (+ or - but no chance for follow up as with culture)

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48
Q

What are the goals of molecular typing?

A
  • identify the icrobial cause of disease
  • track strains during an outbreak
  • Identify phyogenic relationships between bacteria
  • characterize complex bacterial communities and how they change with changing conditions
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49
Q

Polymerase chain reaction (PCR)

A
  • simple method of selectively amplifying a segment of DNA
  • Requires that you know something about the sequence
  • Repeated cycling of degranulation, primer annealing and extension is used to amplify target DNA sequence
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50
Q

What do you nned to do PCR?

A
  • template DNA
  • primers
  • enzymes and dNTPs
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51
Q

How is DNA amplified in PCR? (rate of growth?)

A

exponecitial amplification of DNA

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52
Q

What is the critical piece of PCR?

A

The thermalstable enzyme (tac polymerase)

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53
Q

How can we identify a specific strain in PCR?

A
  • primers must have specificity (we need to know the sequence)
  • we use 16S rRNA gene (exists in all bacteria) which consists of conserved reigons and variable reigons
    **conserved reigons are homologous amoung al bacterial species
    **variable reigons have sequence signatures for different bacterial species
  • After we isolate the bacterial DNA in PCR we do next Gen sequencing where we compare the sequences of variable reigons to rDNA sequence database
54
Q

Do we preform a PCR specific to every known pathogen?

A

No

55
Q

What are the uses of 16S rDNA sequencing?

A
  • identify the types if microbs present (single or multiple bacterial species)
  • allows the studying of complex microbial populations (can determine what species are present and how they change under certain circumstances)
  • allows us to compare strains of bacteria
56
Q

What are the limitations of phylogenic trees?

A
  • Not quantitative (no information on relative abundance of bacteria)
  • Does not indicate variation in the composition of the bacterial communities between indivisuals
57
Q

How do you compare how closely species are related on phylogenic trees?

A
  • Looking at the branch lengths
  • To compare a species add branch lengths
58
Q

Principal component analysis (PCA)

A
  • method to reduce complexity of complex mixtures of bacteria to a 2D diagram
  • a statistical procedure that allows you to summarize the information content in large data tables by means of a smaller set of “summary indices” that can be more easily visualized and analyzed
  • similarity= clustering
  • The first principal component (PC1) accounts for the largest variation in the data, which is attributed to factor 1, and
    the second principal component (PC2) accounts for the second largest variation in the data, which is attributed to factor 2.
59
Q

Transposon mutagenesis

A
  • creates a collection of random mutations genome-wide usng transposons
  • need selectable marker and sequence identifier
60
Q

Transposon

A
  • “jumping genes”
  • they can excise themselves from one loci and insert themselves into another
  • transposase mediates the jumping
61
Q

What are the limitations of transposon mutagenesis?

A
  • can introduce transcriptional termination that dissrupts expression of downstream genes in an operon
  • insertions in genes essencial for growth on the selection medium are not recovered (lethal mutation)
  • laborious and time consuming
62
Q

Describe how the transposon mutagenesis works to examine gene function in an invasive bacterial cell. (hint: quinoline resistance)

A
  1. Transposon is introduced into chromosome of invasive bacterial cells
  2. Plate them on medium that selects for quinoline resistnace
  3. collection of qnr colonies are produced, each of which has transposon in different site of chromosome
  4. Then you screen the qrn colonies for their ability to invade tissue culture cells
  5. Sequence the clones to identify the disruted gene
  6. Clone gene interuppted by transposon
    a) use qnr as a marker to clone disrupted gene
    b) clone by complementation (restore invasivness/ phenotype) to confirm gene function
63
Q

High-throughput transposon sequencing (Tn-seq)

A
  • used to generate a comprehensive transposon insertion library of mutants in pathogen and monitor the loss of virulent traits
  • pools mutants together and there is selective pressure applied to determine gene function
  • Use next gen sequencing to identify location of Tns in the input (in virto) and output (in vivo) bacterial pools
  • The absence or decline of mutants indicates that the Tn- disrupted genes are important for growth
64
Q

Explain the process of High-throughput transposon sequencing (Tn-seq)

A
  1. Create a transposon library
  2. Pool high density transposon mutant library
  3. Grow transposon library under desired (selective) conditions
  4. Attach sequencing adaptors and amplify transposon junctions from library DNA
  5. High throughput sequencing of insertion sites in each library
65
Q

What are the limatations of High-throughput transposon sequencing (Tn-seq)?

A

Mostly produces loss-of -function mutations, thus does not identify genes that decrease fitness when expressed

66
Q

RNA- seq technology

A
  • next gen seq of cDNA generated from RNA
  • Purify total RNA, deplete, reverse transcribe into cDNA
  • Can determine the levels of every bacterial and host mRNA under a variety of conditions
67
Q

Describe the process of RNA- seq technology

A
  1. RNA extraction (can start with a mixture of DNA and RNA but get rid of DNA by digesting it with Dnase 1 treatment)
  2. rRNA/tRNA depletion
  3. RNA fragmentation
  4. cDNA synthesis from the RNA fragments via reverse transcriptase
  5. Adapter ligation
  6. Library amplification and sequencing
  7. Sequence read assessment, alignment and annotation (Next gen sequencing)
68
Q

Duel RNA-seq

A
  • host and pathogen transcriptomics
  • enrich infected cells
  • pooled host and pathogen RNA-seq
  • The transcritomes of host and pathogen can be seperated during sample preparation (wet lab) and data analysis (dry lab)
69
Q

Describe the process of Duel RNA-seq.

A
  1. Take a naive host cell culture and infect it with a bacterial pathogen that has a flourecent or some other marker in it
  2. sort the mied population of challenged host cells into homogenous populations of invaded host cells
  3. Take the total RNA from the infected host cells and complete RNA-seq for both host cell and bacteria
70
Q

Describe functional screening of recombinant genomic libraries.

A
  • take genes from virulent organism and clone them into a avirulent strain of E. coli
71
Q

What are the limitations of functional screening of recombinant genomic libraries?

A
  • Avirulent bacterial species needs to be closely related to virulent strains (must be capable of expressig exgenous genes)
  • Can only test small portions of a bacterial genome (30-40kb)
72
Q

Step by step of functional screening of recombinant genomic libraries

A
  1. Insertion of DNA fragments into cloning plasmids
  2. Introduction of cloning plasmid into bacterial cells
  3. Selection of clones carrying plasmid DNA
    4.Identification of clones containing gene of intrest (that formed plaques)
  4. Grow bacterial clones with plasmids containing gene of intrest
  5. Isolate plasmid DNA and sequence gene
73
Q

Transcriptional fusion

A

transcription of the reporter is driven by the promoter of the virulence gene

74
Q

Translational fusion

A
  • reporter is co translated with the virulence factor
  • useful when tracking the localization of the virulence factor is desired
  • can identify regulatory factors using Tn mutants carrying the pertinent reporter
  • mutagenize the strain that contains virulence gene reporter fusion (look for altered regulatory pattern) and the use next gen sequencing to identify where the associated mutations are located
75
Q

Reporter gene

A
  • an exogenous coding region joined to a promoter sequence or element in an expression vector that is introduced into cells to provide the means for measuring the promoter activity
  • produce a detectable phenotype, but are usually fused to an inducible promoter
  • common reporters are flourcent proteins (GFP) and enzymes (Beta galactosidase)
76
Q

Disinfectants

A
  • eradicates microbs from inanimate objects (largely driven by toxicity of compound)
  • strong agents used on inaminat objects (not for use on people)
  • usually have non-specific targets (general mechanism for killing)
  • includes bleach, phenolic compounds, quaternary ammonium compounds (QACs), and peroxides
77
Q

Antiseptics

A
  • eradicates microbs from skin but not internally (largely driven by toxicity of compound)
  • compounds applied to the skin but not internally
  • general mechanism for killing
  • Usually diluted concentrations of disinfectants
  • includes povidone iodine solutions (betadyne), ethanol, hydrogen peroxide, benzalkonium chloride, and hexachloraphene
78
Q

Antibiotics

A
  • eradicates microbs from inside the body (largely driven by toxicity of compound)
  • for internal use
  • specifically targets unique bacteria
  • can be broad or narrow spectrum
  • indiscriminate of pathogen or commensal
79
Q

What are the 2 main strategies for antibiotic discovery?

A
  • natural products: antibiotics produced by microbs as secondary metabolites (which implys inherent resistance mechanisms); need to purify/ identify the active componenet and the bacterial target; has been historically successful for identifying new classes of antibiotics
  • rational design: target specific reaction/ process (usually an enzyme); requires characterization and high resolution structural information for the target; has not been successful as expected for novel agents; optimize existing antibiotics (accounts for most recent antibiotics/ 2nd generation antibiotics)
80
Q

What are some new applications on natural product screening for antibiotics?

A
  • integrating genomics/ metagenomics (takes advantage of knowing microbial metabolism/ genetics
  • examine understudied populations (example of this is marine extracts, the antibiotics found in these would be very potent because of how dilute they are in the ocean)
81
Q

Why has antibiotic development been stalled?

A
  • defined treatment course with short duration
  • emergance of antimicrobial resistance (AMR)
  • restrictions on use (reserved for last line of treatment)
82
Q

Antibiotic properties

A
  • Selective for bacteria and not the host
  • Need desirable pharmacokinetics/ pharmacodynamics (must reach desired site of action, must accumulate to effective concentration and have sufficent stability, preferable to have oral route of administration, and must not be toxic)
83
Q

What are different cellular processes that are targeted by antibiotics in a bacterial cell?

A
  • metabolic enzymes
  • cell wall synthesis
  • ribosomes (70S)
  • cell membranes
  • DNA synthesis
84
Q

Bactericidal

A
  • effective independent of immune status (gives immune system time to act)
  • it kills bacteria
85
Q

Bacteriostatic

A
  • effective in immunocompetent patients
  • agent prevents the growth of bacteria (i.e., it keeps them in the stationary phase of growth)
86
Q

What does “influenced by bacterial growth state” mean?

A
  • metabolic reduction can cause switch from bacteriacidal to bacteriostatic
87
Q

Methodology examples

A
  • disk diffusion assay (solid medium)
  • liquid culture silution assay
88
Q

Minimal inhibitory concentration (MIC)

A

minimum concentration of a substance to stop bacterial growth (the more potent a substance the lower the MIC)

89
Q

Minimal bactericidal concentration (MBC)

A
  • relevant to bacteriostatic antibiotic
  • minimum concentration of a bacteriostatic to kill bacteria
90
Q

What is Halicin?

A
  • New lead antibiotic
  • Applied model to larger molecule library
  • Confirmed antibacterial activity of predictive hits and vis versa
91
Q

Tolerance

A
  • bacteria stop growing
  • does not require genetic change
  • reversible
  • L form (lacking cell wall) confers tolerance to cell wall inhibitors if osmoprotected
92
Q

Persistance

A
  • small populations that are dormant
  • can reproduce after antibiotic removal
  • contributes to tolerance
93
Q

Toxin

A
  • a stable protein or peptide that induces growth arrest
94
Q

Antitoxin

A
  • unstable protein or small RNA that acts as an immunity protein to the cognante toxin
  • 6 types based on mechanism of toxicity/ immunity
95
Q

How do toxin-antitoxin systems contribute to persistance?

A

contribute to persistance by inducing a metabolically inert state

96
Q

Type 1 TA (toxin-antitoxin) system

A
  • toxin causes membrane lysis
  • antitoxin is canceled out by toxin and degrated by RNases
97
Q

Type 2 TA (toxin-antitoxin) system

A
  • toxin inhibits translation and replication
  • cellula proteases break down antitoxin
98
Q

Type 3 TA (toxin-antitoxin) system

A
  • toxin inhibits translation
99
Q

Type 4 TA (toxin-antitoxin) system

A
  • toxin destabilizes bacterial filaments
  • antitoxin stabalizes bacterial filaments
100
Q

Type 5 TA (toxin-antitoxin) system

A
  • toxin causes membrane lysis
101
Q

Type 6 TA (toxin-antitoxin) system

A
  • Toxin inhibits replication
  • Antitoxin targets toxin for degradation by ClpXP
102
Q

How is tetracycline regulated?

A
  • Transcriptional repression
  • tetracycline repressor (TetR) binds operator sequences and prevents transcription of efflux pump (TetA)
  • tetracycline binds TetR preventing repression of TetA
103
Q

How is negative Beta-lactam regulated?

A
  • Transcriptional regulation
  • BlaZ expression repressed by BlaI
  • low level expression of blaRI (membrane sensor of beta-lactams)
104
Q

How is postive Beta-lactam regulated?

A
  • Transcriptional reguation
  • BlaRI covalently bind beta lactam
  • BlaR2 (protease) is released from the membrane and degrades BlaI
  • BlaZ cleaves the beta-lactam
105
Q

How is vancomycin regulated?

A
  • Transcriptional activation
  • Resistance is made by replacing D-ala-D-ala with D-ala-D-lyc
  • 2 regulatory componenets are VanS (membrane proetin; vancomysin sensor kinase) and VanR (response regulator; phosphorylated and activated by VanS)
  • VanRS controls the enzymes VanH (lactate dehydrogenase), VanA/B (D-ala-D-lac ligase), and VanX(D-ala-D-ala hydrolase)
  • only want this active when vancomycin is present because it is energenically coastly
106
Q

VanH

A
  • lactate dehydrogenase
  • produce D-lactate from pyruvate
107
Q

VanA/B

A
  • D-ala-D-lac ligase
  • Produces new terminal dipeptide
108
Q

VanX

A
  • D-ala-D-ala hydrolase
  • Cleaves vancomycin suseptible D-ala-D-ala (product of DdIA) to stop incorporation into cell wall
109
Q

VanY

A

can cleave terminal D-ala from preformed D-ala-D-ala pentapeptide

110
Q

How is Erythromycin regulated?

A
  • translational attenuation
  • resistance is encoded by RNA methylase (ErmC)
  • neg. Erm: stem loop is formed masking ermC start codon and leader sequence is translated
  • pos Erm: ribosome does not function allowing stem loop rearrangment (exposing start codon) - ribosome stalls
111
Q

How is chloramphenicol regulated?

A
  • translational attenuation
  • The leader sequence and stem loop upsteam of cat gene
  • CM binding alters ribsosome structure to bind stall sequence, relieving stem loop
  • allows another ribo to bind cat RBS and translate mRNA
112
Q

Transformation

A

uptake of linear DNA from enviroment (requires homologous recombinatation)

113
Q

Transduction

A

transfer of DNA by bacteriophages

114
Q

Conjugation

A

direct cell to cell transfer of DNA (via plasmids or transposons)

115
Q

Mobilized plasmids

A
  • mob gene: relaxes the nick and binds DNA
  • oriT: site of DNA nicking by relaxase
  • does not encode T4SS (relies on tra gene products in trans)
  • can be small
116
Q

Self-transmissible plasmids

A
  • tra genes- encodes T4SS
  • T4CP- ATPase to push DNA through T4SS
  • oriT- site of DNA nicking to mobilize ssDNA
  • Relaxase- nicks and covalently binds oriT
117
Q

Conjugative transposon

A
  • chromosomally encoded transposon
  • excises from donor
  • conjugated to recipient
  • integrated into chromosome
  • broader host range than plasmids
118
Q

Integrons

A
  • linear DNA
  • transposon like elements
  • integrase (int): enzyme that recombines circular DNA into integron
  • att: integration site and contains promoter to drive expression of integrated genes
  • likely cause of multiresistance plasmids
119
Q

SecB

A
  • chaperone (maintain unfolded)
120
Q

SecA

A

dimer,ATPase, binds SecYEG

121
Q

SecYEG

A

heterotrimer, channel

122
Q

SRP

A

Signal recodnition particle

123
Q

FtsY

A

SRP receptor

124
Q

T2SS

A
  • Sec dependent SS (proteins folded or unfolded are translocated throigh IM by Sec or TAT then through outer membrane via T2SS)
  • 4 components: IM platform, ATPase, OM complex (secretin), pseudopilus
  • substrates are folded in periplasm
  • Pseudopillus acts like a piston to push proteins through secretion channel
  • Examples: Cholera toxin and exotoxin A
125
Q

T5SS

A
  • Sec dependent SS (proteins folded or unfolded are translocated throigh IM by Sec or TAT then through outer membrane via T5SS)
  • dedicated porin translocates substrate
  • Autotransporters (porin and substrate part of same polypeptide)
  • 2 partner SS: porin encoded on seperate protein
  • Porin folding drives translocation across outer membrane
126
Q

T1SS

A
  • Sec independent SS (have continuous channel across periplasm)
  • Channel from IM to OM
  • has ABC protein (ATPase), membrane fusion protein, and outermembrane protein
  • unfolded proteins are not exposed to periplasm
127
Q

T3SS

A
  • Sec independent SS (have continuous channel across periplasm)
  • wide spread in gram neg pathogens
  • delivers effecors across vasicular or plasma membranes
  • highly conserved derivative of flagella
  • takes a substrate and transfers it from bacterial to host cell through hollow needle
  • substrates are bound by chaperones
128
Q

T4SS

A
  • Sec independent SS (have continuous channel across periplasm)
  • Transports proteins and/ or DN (bound to proteins)
129
Q

T6SS

A
  • Sec independent SS (have continuous channel across periplasm)
  • highly conserved
  • targeting eukaryotes (actin crosslinking)
  • target prokaryotes (requires antidote): petidoglycan degradation, pore forming, lipase activity
  • inverted T4 phage tail spike (molecular syringe)
  • multiple T6SS clusters in single organism
  • Sheath subunits in high energy confirmation (effector secretion doesnt require ATP hyrdolysis)
  • effectors loaded on sip of skipe (not hollow)
  • contraction fires the secretion and disassemply requires energy
130
Q
A

MMI 351 (4 decks)

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