Virulence

Question 1

To survive the journey through the stomach and small intestine, a pathogen must rapidly express a variety of gene products, including:

Answer 1

• proteins that help tolerate low pH of stomach
• flagella and chemotaxis proteins for migration to suitable niche
• adhesins that permit colonization
• toxins and invasins to elicit diseaes
• siderophores to scavenge for iron

Question 2

Most virulence factors are __________.

Answer 2

genes encoding metabolic enzymes

Question 3

What are examples of virulence factors?

Answer 3

• polysaccharide capsule
• adhesins
• acid tolerance factors (ASPs)
• enzymes that synthesize unavailable nutrients

Question 4

What is a virulence gene?

Answer 4

any gene that encodes a virulence factor

Question 5

Where are virulence genes located?

Answer 5

on mobile genetic elements (plasmids or phage) or in pathogenicity islands

Question 6

What is the relationship b/t glucose and cAMP?

Answer 6

more glucose entry into cell = decreased adenylyl cyclase activity = decreased cAMP

Question 7

Where does a repressor bind in an operon?

Answer 7

It binds the operator, thus reducing RNAP binding affinity (steric hindrance).

Question 8

How does the lac operon function when glucose is present and cAMP is absent?

Answer 8

repression (repressor binds to operator and prevents RNAP from binding; therefore, no transcription of lac genes)

Question 9

What is lacR?

Answer 9

it is the lac regulator, or the gene that encodes the repressor for the lac operon; it displays constitutive transcription (always on, only binding of an inducer can prevent it from blocking transcription)

Question 10

How does the lac operon function when glucose is absent and cAMP is present?

Answer 10

This would be a situation where lactose is present and acts as an inducer that binds the repressor, making it incapable of binding to the operon. With cAMP present, CRP (an activator) binds tightly to cAMP, allowing the CRP-cAMP complex to bind tightly to the promoter sequence. This helps RNAP bind to the promoter, allowing for a lot of transcription.

Question 11

What is the activator and co-activator in the lac operon?

Answer 11

• activator=CRP

- co-activator=cAMP

Question 12

What is a regulon?

Answer 12

a gene network (set of operons) regulated by a single repressor

Question 13

What is an operon?

Answer 13

a unit of DNA containing a cluster of genes under the control of a single promoter (genes are transcribed and translated together; genes on an operon are expressed together or not at all)

Question 14

What are some of the key features of the causative agent of cholera?

Answer 14

V. cholerae:

• extracellular pathogen
• highly motile
• uniflagellated
• gram (-) curved rod

Question 15

V. cholerae synthesizes virulence factors that help it do what?

Answer 15

reach, adhere to, and colonize intestinal epithelial layer

Question 16

What is the main virulence factor of V. cholerae?

Answer 16

cholera toxin (very potent)

Question 17

What is the CTX phage?

Answer 17

It is a prophage incorporated into the chromosomes of a V. cholerae lysogen and gives the bacterium its toxinogenicity. Once inside the bacterium, CTX phage integrates into the chromosome, and the lysogen expresses cholera toxin (composed of 2 subunits - CtxA and CtxB)

Question 18

True or false: Flagellar genes and toxin genes of V. cholerae are expressed at the same time.

Answer 18

False - flagellar genes are expressed when toxin genes are not. Motility is used to reach the site of colonization, then motility genes are turned off because the bacterium is where it needs to be; then, colonization and toxigenic genes are turned on.

Question 19

What are the virulence factors involved in V. cholerae colonization?

Answer 19

TCP (toxin colonization pilus) and ACF (accessory colonization factors)

Question 20

What permits V. cholerae to synthesize virulence factors?

Answer 20

activation of ToxR regulon

Question 21

Are ToxR and ToxS transcribed outside of the host or inside?

Answer 21

They are transcribed outside of the host at low temperatures; once the host ingests vibrio, ToxR and ToxS are no longer transcribed, but they are stable.

Question 22

What does it take to turn on the ToxR regulon?

Answer 22

a stimulus received by ToxR and ToxS from the lumen of the small intestine

Question 23

What are the member genes of the ToxR regulon?

Answer 23

ToxT, tcp, acf, ctxAB