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MICR 221 > Lecture 15 > Flashcards

Lecture 15 Flashcards

1
Q

What are some environmental conditions that bacteria can sense?

A

Bacteria can sense nutrient levels, antibiotics, pH levels, and other factors in their environment.

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2
Q

What do bacteria sense when interacting with host organisms?

A

Bacteria can sense host organisms, distinguishing between commensals (harmless) and pathogens (disease-causing).

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3
Q

What happens in the lac operon when lactose is present?

A

When lactose is present, it is converted into allolactose. Allolactose binds to the LacI repressor protein, preventing it from binding to the operator region.

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4
Q

How does the presence of allolactose affect the lac operon?

A

The presence of allolactose prevents the LacI repressor protein from binding to the operator region of the lac operon, allowing RNA polymerase to transcribe the genes involved in lactose metabolism.

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5
Q

What is the consequence of the direct interaction between allolactose and LacI in the lac operon?

A

The consequence of this interaction is the derepression of the lac operon, leading to increased transcription of genes involved in lactose metabolism in the presence of lactose.

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6
Q

How can bacteria sense and respond to external stimuli?

A

Bacteria can sense and respond to external stimuli through two-component signal transduction systems (TCSs), which involve separate proteins: sensor kinases and response regulators.

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7
Q

What are the main components of a two-component signal transduction system?

A

The main components are the sensor kinase, a membrane protein that detects the stimulus, and the response regulator, a cytoplasmic DNA-binding protein that carries out the cellular response.

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8
Q

What types of stimuli can be sensed by two-component signal transduction systems?

A

Two-component signal transduction systems can sense a variety of stimuli, including nutrients, antibiotics, and environmental factors such as host environment cues (e.g., hormones) and high osmolarity.

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9
Q

What happens when a stimulus activates the sensor kinase in a two-component signal transduction system?

A

When a stimulus activates the sensor kinase, its kinase domain undergoes autophosphorylation, leading to the transfer of a phosphate group to the response regulator.

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10
Q

What is the consequence of phosphorylation on the response regulator in a two-component signal transduction system?

A

Phosphorylation of the response regulator induces a conformational change in its structure, allowing it to bind to DNA.

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11
Q

How does the binding of phosphorylated response regulator to DNA affect transcription?

A

The binding of phosphorylated response regulator to DNA can either activate or repress transcription, depending on the specific regulatory elements involved.

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12
Q

What are some key characteristics of Enterococcus faecalis and Enterococcus faecium?

A
  • Common gut bacteria
  • Major nosocomial pathogens
  • Persist in hospital environments
  • Cause infections in immunosuppressed patients (e.g., bacteremia, endocarditis, urinary tract infections)
  • Some strains exhibit resistance to antibiotics like Vancomycin
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13
Q

What is a notable characteristic of Enterococcus faecalis and Enterococcus faecium in healthcare settings?

A

They are major nosocomial pathogens, meaning they are frequently associated with healthcare-associated infections acquired in hospitals.

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14
Q

How does the genome of Enterococci contribute to their antibiotic resistance?

A

Enterococci exhibit high genome plasticity, enabling them to easily acquire and incorporate new DNA, such as genomic islands.

This characteristic allows them to accumulate antibiotic resistance genes, including those against Vancomycin, used for resistant Gram-positive infections.

The prevalence of Vancomycin-resistant enterococci (VRE) is increasing due to their ability to acquire resistance genes.

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15
Q

How do changes in peptidoglycan (PG) structure confer vancomycin resistance in Enterococci?

A

Vancomycin resistance in Enterococci is conferred by changes in the peptidoglycan (PG) structure, specifically through the expression of van genes.
- alters the composition of PG, causing it to be made with D-lactate instead of D-alanine.
- however this change impairs bacterial growth.

Two-component systems (TCS) are used to regulate the expression of van genes, ensuring that PG is only made with D-lactate in the presence of vancomycin.

In the absence of vancomycin, PG reverts to its normal composition, and bacterial growth is not impaired.

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16
Q

What is the mechanism by which Agrobacterium tumefaciens causes disease in plants?

A
  • Agrobacterium tumefaciens is a plant pathogen that causes crown gall disease by forming tumor-like growths on plants.
  • Strains of A. tumefaciens that cause gall carry a tumour-inducing (Ti) plasmid.

These gall-causing strains transfer a portion of the Ti plasmid, known as T DNA, into plant cells. They are transcribed within the plant cell, leading to tumour formation.

Additionally, the genes in the T DNA encode enzymes that produce nutrients for the bacteria, further promoting bacterial growth.

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17
Q

How does Agrobacterium tumefaciens enter plants and initiate pathogenesis?

A
  • Agrobacterium tumefaciens enters plants through surface wounds.
  • It senses the presence of the plant using a two-component system (TCS), where the sensor kinase VirA detects phenolics, which are plant metabolites.
  • The response regulator VirG is phosphorylated in response.
  • This phosphorylation activates the transcription of virulence (vir) genes located on the Ti plasmid.
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18
Q

What role do vir genes play in Agrobacterium tumefaciens pathogenesis?

A
  • The vir genes encode a type IV secretion system (T4SS).
  • This T4SS is similar to the one used in bacterial conjugation.
  • The T4SS forms a bridge between the bacterium and the plant.
  • Vir proteins produced by the vir genes help to excise T DNA from the Ti plasmid.
  • The T DNA is then secreted into the plant by the T4SS.
19
Q

What happens after T DNA is secreted into the plant by Agrobacterium tumefaciens?

A
  • T DNA enters the plant nucleus.
    It integrates into the plant’s genome.
  • The plant cell starts producing enzymes encoded by T DNA.
  • These enzymes make phytohormones, promoting cell proliferation and tumor formation.
  • Additionally, T DNA enables the plant to produce opines, which serve as a nutrient source for Agrobacterium tumefaciens.
20
Q

How is Agrobacterium tumefaciens utilized in plant genetic engineering?

A

Agrobacterium tumefaciens is employed to genetically engineer plants in laboratory settings.

Researchers prepare a recombinant Ti plasmid in the lab.

The desired gene(s) are added to the Ti plasmid.

Tumor-inducing genes are removed from the Ti plasmid to ensure the plant does not develop tumors.

The modified Ti plasmid, containing the desired gene(s) but lacking tumor-inducing genes, is transferred to the plant.

This genetic modification alters the properties of the plant, such as conferring resistance to insects and viruses or enhancing nutritional content.

21
Q

What is a more complex version of Two-Component Systems (TCS)?

A

A more complex version of Two-Component Systems (TCS) involves a process called phosphorelays.

In phosphorelays, phosphate groups are transferred from one protein to another in a series of reactions.

Unlike traditional TCS, phosphorelays involve one or more intermediary proteins between the sensor kinase and response regulator.

This additional complexity allows for more opportunities for regulation and fine-tuning of cellular responses.

The presence of intermediary proteins enables modulation and amplification of signals, allowing cells to finely adjust their responses to various environmental stimuli.

22
Q

How is endospore formation in Bacillus spp. regulated?

A

Endospore formation in Bacillus spp. is highly regulated to ensure it occurs only when necessary.

The process involves a phosphorelay, where each step is controlled by different factors, including both positive and negative signals.

This regulation ensures that endospores are formed only under specific conditions.

The response regulator Spo0A plays a central role in this process, controlling over 500 genes involved in endospore formation.

Once the process of endospore formation is initiated, it is irreversible.

23
Q

Once the process of endospore formation is initiated, is it reversible?

A

No, it is irreversible

24
Q

How does sensing occur in bacterial chemotaxis?

A

Sensing in bacterial chemotaxis involves methyl-accepting chemotaxis proteins (MCPs).

MCPs detect various attractants and repellants in the environment.

However, sensing does not always lead to changes in transcription.

Instead, the response to sensing is a change in the rotation of the bacterial flagellum.

25
Q

How does Vibrio fischeri utilize quorum sensing?

A

Vibrio fischeri resides in the light organs of fish and squid.

At high density, V. fischeri emits light through bioluminescence.
Bioluminescence benefits both the host and the bacterium: it confuses predators and lures prey for the host, while providing a safe environment and nutrients for the bacterium.

At low density, V. fischeri does not emit light through bioluminescence. This is because producing light at low density would be inefficient and a waste of energy.

26
Q

What is quorum sensing and how does it work in bacteria?

A
  • Quorum sensing is a mechanism used by bacteria to communicate and coordinate behavior based on population density.
  • Bacteria produce signaling molecules called autoinducers (AIs), such as N-acylhomoserine lactones (AHLs).
  • The level of AIs in the environment is proportional to the number of bacterial cells present.
  • When AIs reach a certain threshold concentration, they impact gene expression in the bacterial population.
  • AIs can be sensed by transcriptional regulators and sensor kinases, including those involved in two-component systems (TCS).
27
Q

How does quorum sensing regulate luminescence in Vibrio fischeri?

A

Luminescence in Vibrio fischeri is regulated by the lux operon.

Proteins encoded by the lux operon produce light, with LuxAB being luciferase (makes light) and LuxCDEG being enzymes that synthesize luciferase substrate.

The lux operon is regulated by two key proteins:
- LuxI, which synthesizes autoinducers (AIs).
- LuxR, a transcriptional activator that responds to AIs.

As cell density increases and AIs accumulate, LuxR binds to AIs and activates transcription of the lux operon, leading to luminescence.

28
Q

How does high cell density trigger luminescence in Vibrio fischeri through quorum sensing?

A

At high cell density, there is a high concentration of autoinducers (AIs) produced by the bacteria.

AIs bind to LuxR, forming a complex.

The LuxR-AI complex then binds near the promoter region of the lux operon and recruits RNA polymerase (RNAP).

RNA polymerase initiates transcription of the lux operon, leading to the production of Lux proteins.

Lux proteins facilitate the bioluminescent reaction, causing the cells to emit light.

29
Q

How does low cell density affect luminescence in Vibrio fischeri through quorum sensing?

A

At low cell density, there is a low concentration of autoinducers (AIs) produced by the bacteria.

The low concentration of AIs is insufficient to bind to LuxR.

As a result, LuxR does not form a complex with AIs and does not bind near the promoter region of the lux operon.

Without LuxR binding to the promoter, RNA polymerase is not recruited, leading to no transcription of the lux operon.

Consequently, Lux proteins are not produced, and there is no bioluminescence emitted by the cells.

30
Q

How does quorum sensing relate to the virulence of Enterohemorrhagic E. coli (EHEC)?

A

Enterohemorrhagic E. coli (EHEC) causes illnesses like hemorrhagic colitis and hemolytic uremic syndrome.

EHEC produces virulence factors only when the cell density is sufficiently high.

Its genome contains a pathogenicity island that encodes a type 3 secretion system (T3SS) which is used to secrete proteins from bacterial cytoplasm to host cell cytoplasm.

The T3SS delivers effector proteins (T3SS effectors) into host cells, aiding infection.

Quorum sensing likely plays a role in regulating the expression of virulence factors in EHEC.

31
Q

How does the effector Tir contribute to the virulence of Enterohemorrhagic E. coli (EHEC)?

A

The effector protein Tir is secreted by EHEC into host epithelial cells.

Tir then binds to the intimin protein on the surface of EHEC.

This binding facilitates the attachment of EHEC to the host epithelial cells.

Tir remodels the host cell cytoskeleton, leading to the formation of pedestal-like structures known as “attaching-effacing lesions.”

These structures help EHEC to colonize the gut by enhancing its adherence to the host epithelium.

Additionally, EHEC releases Shiga toxin, contributing to its pathogenicity.

32
Q

What is Shiga toxin?

A

An AB toxin that targets ribosome function

33
Q

How are virulence factors in Enterohemorrhagic E. coli (EHEC) regulated by quorum sensing?

A

Quorum sensing (QS) in EHEC involves a two-component system (TCS).

The sensor kinase QseC detects autoinducers (AIs), signaling molecules produced by bacterial cells.

Upon sensing AIs, QseC activates the response regulator QseB.

QseB then upregulates the expression of genes associated with motility, toxin production, and lesion formation, enhancing virulence.

Interestingly, QseC can also recognize adrenaline, a host hormone, suggesting a connection between host signaling and bacterial virulence regulation.

34
Q

How can quorum sensing (QS) be targeted therapeutically in the context of Enterohemorrhagic E. coli (EHEC) infections?

A

Quorum sensing (QS) represents a potential therapeutic target for combating EHEC infections.

Unlike antimicrobials, which kill bacteria, antivirulence strategies aim to disrupt bacterial virulence mechanisms without harming the bacteria themselves.

Probiotics, such as certain strains of Lactobacillus spp., are commonly used as antivirulence agents.

For example, some strains of Lactobacillus acidophilus interfere with EHEC’s production of autoinducers (AIs), disrupting QS.

By disrupting QS, probiotics prevent EHEC from transcribing virulence factor genes, thereby inhibiting its ability to attach and colonize the gastrointestinal tract.

35
Q

What is dental plaque?

A

Dental plaque is a biofilm that forms on the surface of teeth.

36
Q

What covers the dental enamel initially?

A

The dental enamel is initially covered with a pellicle, consisting of mucin glycoproteins from saliva.

37
Q

How does the pellicle affect colonization?

A

The pellicle has a negative charge, which limits the colonization of bacteria. Despite the negative charge, commensal bacteria can still attach to the pellicle.

38
Q

What leads to the formation of dental plaque?

A

Pathogens can attach to commensal bacteria, leading to the formation of dental plaque.

39
Q

How do commensals like Streptococcus mitis attach to the pellicle?

A

Commensals like Streptococcus mitis have surface proteins that bind to mucins in the pellicle.

40
Q

What do initial colonizers release?

A

Initial colonizers release autoinducers (AIs).

41
Q

How do commensals respond to AIs?

A

Commensals can detect very low levels of AIs.

42
Q

What happens after commensals detect AIs?

A

After detecting AIs, commensals shift to the biofilm mode of growth.

43
Q

How do pathogens interact with commensals in the formation of dental plaque?

A
  • As the biofilm grows, the concentration of autoinducers (AIs) increases.
  • Pathogens can then detect and respond to AIs produced by commensals.
  • Although pathogens are less sensitive to AIs compared to commensals, they still respond to them.
  • This allows for interspecies communication within the biofilm.
  • Pathogens attach to commensals and become part of the biofilm.
44
Q

What are the consequences of biofilm formation in dental plaque?

A
  • Pathogens in dental plaque release insoluble extracellular polymeric substances (EPS).
  • This leads to the tooth surface becoming anoxic (no oxygen)
  • Pathogens ferment sugars and produce acids.
  • The plaque becomes impermeable, and saliva is unable to dilute the acid.
  • The acid demineralizes enamel, leading to dental caries (cavities).
  • Additionally, the biofilm causes inflammation, contributing to periodontal disease.

MICR 221 (12 decks)

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