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Molecular Microbiology > Virulence Factors and their genes > Flashcards

Virulence Factors and their genes Flashcards

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Biology 101 flashcards
1
Q

What are some challenges faced by bacteria in different microenvironments?

A 
external water requires different metabolic lifestyles in different environments where over half the organism genes change when environment changes.
In water:
-cold temperatures
-neutral pH
-oxygen
-respiratory metabolism
-free iron
-adhesions to stick to rocks

in human:

  • high temperature
  • high osmotic strength
  • low pH/high pH
  • low/no oxygen
  • fermentative metabolism
  • iron is bound to proteins
  • adhhesions stick to cells
  • exposed to bile salts
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2
Q

Why are survival proteins regulated?

A

proteins are made in one environment may not be useful in another environment.
In fact, they must be produced at the correct time so they are not recognised by the immune system before it can attack host.

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3
Q

In what ways can virulence genes be regulated?

A

1) Change number of transcripts through activators and repressors to switch genes on or off; the most common form of regulation
2) DNA rearrangements
3) Change in the number of proteins via change in rate RNA transcription/degradation rather than transcription.

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4
Q

What is DNA rearrangment

A

Involves surface structures which interact with the immune system.

Epigenetic changes also control genes where the DNA sequence is not changed but the methylation of cytosine which then changes repressor/activaor binding.

  • gene inversions
  • gene conversions
  • slipped-strand mispairing
  • excisions and insertions
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5
Q

What are regulators

A

Proteins that control transcription gene

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6
Q

Describe trancriptional control

A

promoter upstream of start of codon of the gene is bound by RNA polymerise. The operator sequence is close to promoter

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7
Q

What is an operon?

A

Several genes transcribed as part of a single transcript controlled by a single promoter; they are made on a single mRNA

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8
Q

What is a regulon

A

set of genes/operins all of which have a promoter region which responds to the same regulatory protein; lots of promoters with same regulation which may repress/activate

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9
Q

What is stimulon?

A

Set of genes that respond to same regulatory signal but respond in different ways

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10
Q

What is the operator sequence?

A

part of DNA recognised and bound by regulatory protein; different protein recognise different operator sequences

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11
Q

How do activators stimulate transcription

A
  • recruit RNA polymerase to promoter
  • help RNA polymerase open double helix so transcription can start.

They bind weakly to DNA, but with an inducer molecule/ligand joining onto activator conformation changes and it can bind very tightlly

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12
Q

Give an example of an activator protein

A

MalT protein which binds a sugar called maltose which activates genes to catabolise maltose

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13
Q

How do repressors stop translation?

A

-bind to DNA near promoter and so prevent RNA polymerase.

ligand binding to repressor also causes conformational change and tight binding; the ligand is needed for repression and therefore it is a co-repressor

or
-binds tightly to DNA without a ligand. Then ligand bind once it is on DNA, causing change in conformation and the repressor detaches so translation starts again

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14
Q

Give an example of a repressor and co-repressor

A

E.coli tryptophan repressor (TrpR) can only bind to DNA when bound to co-repressor tryptophan.

This provides a negative feedback system regulating the synthesis of tryptophan.

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15
Q

What is a aporepressor?

A

repressor in the absence of a co-repressor ligand that is inactive

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16
Q

Give an example a repressor that does not need a ligand to bind

A

Lactose repressor (LacI) which binds to promoter of lac operon. lactose binds to LacI releases repressor and starts expression of lac operon

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17
Q

What are 2 component systems?

A

It is very important that cells sense the external environment to regulate genes according to the outside conditions.

There is a protein inserted into the bacterial cytoplasmic membrane containing a site facing exterior so it can see external environment signal. This protein is a sensor kinase.

Signal from environment causes autophosphorylation of the protein where a phosphate is attached to a histidine. Phosphate then transferred to another intracellular protein (on to this second protein’s aspartic acid)

Second protein is called a response regulator (RR) which when phosphorylated binds to DNA and start/stops gene expression

The attached phosphate is eventually removed by a phosphatase to reset system.

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18
Q

What is the effects of Bordetella pertussis?

A

It is a respiratory pathogen causing whooping cough. It can be fatal in infants with underlying cardia/pulmonary disease. It can also cause neurological sequalae. Treatment: vaccination.

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19
Q

How does Bordetella pertussis work?

A
  • Very contagious to humans only
  • it is inhaled and enters at trachea and bronchi where it binds to lung epithelial cells and multiplies there
  • whooping cough after 3 weeks for around 2-3 months
  • damage in the body caused by toxins and other virulence factors
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20
Q

What are the virulence factors associated with Bordetella pertussis

A
  • filamentous haemagglutinin adhesion binds to sulphates on cilia of epithelial cels.
  • cytotoxin stops cilia beating so debris is not cleared and causes coughing
  • transmitted via coughing
  • pertussis toxin inhibits immune system; it inhibits G protein coupling that regulates adenylate cyclase-mediated conversion of ATP to cAMP: Too much cAMP alters cell signalling, prevents phagocytosis
  • Invasive Acase (CyaA) toxin
  • Tracheal cytotoxin
21
Q

What is tracheal cytotoxin (TCT)? in Bordetella pertussis

A

A soluble peptidoglycan fragment found in the cell wall of gram negative bacteria. The PGN-transporter protein known as AmpG keeps TCT in cell wall. but TCT can escape when there is no more PGN.
It is made of disaccharide and peptide chain.
This damages/extrudes cilliated cells and damages the ciliary escalator and host cannot remove debris (mucus/microbes)

22
Q

What causes paroxtsmal/whooping cough?

A

mucus build up due to cilliated tissue damage via toxins.

23
Q

Summarise Bordetella pertussis

A

1) inhalation
2) bacteria adhere to ciliated epithelial cells via Ptx, Fha adhesions.
3) it produces toxins which i) act on neurones via Ptx, Acase
ii) damage mucosal cells via Ptx, Acase, Tracheal cytotoxin
4) causes cough

OR

1) Ptx, Acase toxins inhibit phagocyte migration
2) Bacteria adhere to pahgocytes via Fha, Ptx
3) they are ingested
4) causes intracellular phase.

24
Q

In what way are the virulence factors of Bordetella pertussis regulated?

A

It is controlled by a Bvg two component system where the membrane bound sensor kinase is BvgS and the cytoplasmic response regulator is BvgA. In different temperatures swiches on/off genes.
fha, cycA, ptx express in high temps of 37C but are repressed at low temps.

25
Q

Describe the mechanism of Bordetella pertussis regulation

A

1) stimulated by temperature, or deactivation by magnesium/nicotinamide
2) phosphorylation of cytoplamsic domain BvgS via its histidine.
3) phosphate transferred to aspartic acid og BvgA,
4) BvgA can now bind and supress/activate DNA.

26
Q

What are the classes of promoters that the phosphorylated BvgA in Bordetella pertussis binds to?

A 
class 1-4
Class 1: activator. expresses ptx, cya at high concentration levels of BvgA-P

Class 2: activator: including adhesion Fha. intermediate levels of BvgA-P

Class 3: activator expressing BipA which encodes a protein with an unknown role at low levels of BvgA-P for the high affinity DNA site. However there is a low affinity site for binding at high levels of BvgA-P and thus stops transcription.

Class 4: repressor. These genes are vrg/virulence genes including flagellum/survival. low levels of BvgA-P

27
Q

In what way is BvgA-P a rheostat

A

different affinity binding sites mean it controls expression of different genes at different times of infection; ie switch on adhesions before toxin produced.

28
Q

What is noradrenaline?

A

It is a hormone and a neurotransmitter found in the gut which acts to modulate immune responses and peristalsis. This is needed in innate response to bacterial infections

29
Q

What is the effect of norepinephrine on bacteris

A

stimulates production of virulence factors to promote adhesion; E.coli EHEC adheres to mucosa in intestines.

Shown using a confocal laser scanning micrograph

30
Q

How does E.coli sense hormone?

A

Through 2 components systems:

1) OseC/QseB system
2) OseE/F system

31
Q

How does the QseC/B system work?

A

OseC has two transmembrane domains with a periplasmic loop that interacts with the hormone gland. There are other domains which allow other signals too. hormone binds to QseC which is then autophosphorylates. The phoshate transsfers to QseB which is response regulator. B modulates flagella regulation, potassium uptake and osmolarity

32
Q

How does the QseE/F 2 component system work?

A

E is senor kinase but contains a different binding site; it phosphorylates which phosphorylates F which expresses Ler gene (activating LEE) and espF protein leading to actin polymerisation.

C can also phosphorylate F; there is cross communication between 2 systems

33
Q

How are cholera regulated?

A

toxin (gene on phophage region) and the Toxin co-regulated pilus (TCP: genes on PAI) are both needed and they are regulated together.

TCP is type 4 pilus needed for colonisation of intestines.

They are not regulated by a classical 2 component system

34
Q

Describe the regulation of cholera toxin

A

Tox S and ToxR are both proteins in cytoplasmic membrane,
However, S has no cytoplasmic domain but has a periplasmic domain which recieves hormone signal. R has cytoplasmic and periplasmic domains; R ans S form a complex in membrane in order to regulate genes.
R activates transcription of toxT and partially activates ctxAB.
ToxT fully activates ctxAB

35
Q

What is ToxT

A

a transcription factor targeted by ToxR which is needed for full activation of toxins A and B/ controls production of major virulence factors.

It binds to bile in intestine. ToxT binding means cholera has infected.

ToxT and bile activate transcriptional factor, leading to

i) more expression of toxin genes
ii) coregulates pilus genes
iii) it own ToxT gene on vibrio pathogenicity island

36
Q

How is ToxT activateD?

A

ToxS/R senses and partially activate cholera toxin genes. ToxR bind to ToxT promoter bu it requires TcpP and TcpH (another 2 component system)

ToxT activated when both ToxR and TcpP bind

37
Q

Describe the TcpP and TcpH system

A

There is no phosphorylation where H complexes with P. P is stablised by H, without H P would be degraded

38
Q

What regulates TcpP/TcpH and TcpA-F (the pilus genes)?

A

AphA and AphB, proteins in cytoplasm that need to bind to the promoter for transcription of TcpP/H.

AphA influenced by cell density; density of bacteria and making virulence factors are linked

39
Q

Describe the evolution of pandemic strains

A

Ancestral strain non-pathogenic organism

  • aquires PAI encoding TCP pili via horizontal transfer.
  • TCP is receptor for ctx phage
  • leads to a pandemic strain secreting toxin.
40
Q

What is phase variation

A

This deals with changing environments without requiring mutations.
It randomly varies protein expression frequently in different parts of a bacterial population and therefore changes phenotype much faster than normal mutation rates. Reversible

The DNA around promoter/downstream of start codon is altered so gene is ON or OFF.

41
Q

What is antigenic variation?

A

expression of various alternative forms of antigen on cell surface where DNA rearrangement/change of DNA sequence of proteins

42
Q

What are the benefits of phase/antigenic variation?

A
  • increased fitness
  • evasion strategies to prolong infection
  • adaption to environment.
43
Q

What is neisseria gonorrhoeae?

A
  • Gram negative diplococi
  • non-motile
  • specific for humans
  • causes pelvic inflammatory disease (PID)
  • shows both phase and antigenic variation
  • shows drug resistance
44
Q

How does neisseria gonorrhoeae infect?

A

Through sexual contact causing urogenital tract infection.

i) cellular invasion
ii) transcytosis through cell layer
iii) inflammation
iv) polymorphonuclear leukocye (PMN) influx
v) where there is systemic infection , it causes arthritis.

45
Q

What are the virulence factors of neisseria gonorrhoeae?

A

Phase varied:
-type 4 pili bind to CD46 on epithelial cells mediating primary adherence. The pili is glycosylates with 2 sugars
-Opa proteins in the membrane also mediate adhesion and cell selectivity
Antigenic variation:
-Porin (PorB)

46
Q

What is PorinB

A

GTP binding protein which forms a voltage gated channel that translocates from the outer membrane of bacteria to the host membrane; it inserts into outer membrane of mitochondria. This causes cell apoptotsis via signalling.

It helps adhere C4BP from complement

47
Q

What are Opa proteins

A

outer membrane proteins that adhere to host cells and evade neutrophil engulfment. They allow bacteria to reside in different cell types sepending on the type of Opa.

Bacteria with no Opa are not engulfe.

There a 11 types of OPA proteins with their own genes. They contain repeated sequence CTCTT at 5’ end.

Expression is turned on/off by the loss/gain of repeats. Loss/gain occurs due to mispairing in DNA replication

48
Q

What is slipped strand mispairing?

A

In DNA replication. One strand slips and pairs with the wrong repeat on opposite strand.

If new strand

Molecular Microbiology (4 decks)

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