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Genetics > microbiology exam 2 chapter 8 part 2 > Flashcards

microbiology exam 2 chapter 8 part 2 Flashcards

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1
Q

What is Anabaena?

A

Anabaena is a filamentous cyanobacterium that is an oxygenic phototroph, producing oxygen and fixing nitrogen.

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2
Q

What is nitrogen fixation?

A

Nitrogen fixation is the reduction of nitrogen gas to ammonia, which is energy-demanding and catalyzed by nitrogenase.

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3
Q

Why is nitrogenase oxygen-sensitive?

A

Nitrogenase is extremely sensitive to oxygen, which can inhibit its function.

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4
Q

What are heterocysts in cyanobacteria?

A

Heterocysts are specialized cells in Anabaena and Nostoc dedicated to nitrogen fixation.

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5
Q

Why do heterocysts lack a photosystem?

A

Heterocysts lack a photosystem, making them anoxic, which provides a suitable environment for nitrogenase.

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6
Q

What is the role of heterocysts in nitrogen fixation?

A

Heterocysts provide a hospitable environment for nitrogenase to fix nitrogen.

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7
Q

How do heterocysts form in Anabaena?

A

Heterocysts arise from the differentiation of phototrophic vegetative cells and typically form in a pattern along the filament.

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8
Q

Why is the patterning of heterocysts important?

A

The patterning separates incompatible metabolic processes while allowing nutrient exchange and growth.

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9
Q

What regulates heterocyst formation in Anabaena?

A

It is regulated by a network of systems sensing external conditions and intracellular signaling molecules.

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10
Q

What happens to the cell wall during heterocyst formation?

A

The cell wall thickens to prevent the diffusion of oxygen into the cell.

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11
Q

What happens to the photosystem in heterocysts?

A

The photosystem is inactivated in heterocysts.

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12
Q

What is expressed during heterocyst formation?

A

Nitrogenase is expressed in heterocysts for nitrogen fixation.

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13
Q

How does heterocyst differentiation occur along the filament?

A

Heterocyst differentiation follows a specific pattern along the filament to optimize function.

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14
Q

What are the four basic stages of biofilm formation?

A

Attachment, colonization, development, and dispersal.

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15
Q

What accounts for the initial attachment in biofilm formation?

A

Random collision.

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16
Q

What structures help facilitate attachment in biofilm formation?

A

Flagella, pili, and cell surface proteins.

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17
Q

What happens after attachment in biofilm formation?

A

Attachment signals the expression of biofilm-specific genes, including those for intercellular signaling molecules and extracellular polysaccharides.

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18
Q

What happens to cells once they commit to biofilm formation?

A

Cells lose their flagella and become nonmotile.

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19
Q

How are cells released from a biofilm?

A

Through active dispersal.

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20
Q

What triggers the switch to biofilm growth in bacteria?

A

The accumulation of cyclic di-guanosine monophosphate (c-di-GMP).

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21
Q

What does c-di-GMP signal in biofilm formation?

A

It signals the transition from planktonic growth to life in a semisolid matrix.

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22
Q

How does c-di-GMP affect bacterial movement?

A

It binds proteins that reduce flagellar motor activity.

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23
Q

What role does c-di-GMP play in attachment during biofilm formation?

A

It regulates attachment proteins.

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24
Q

How does c-di-GMP affect the extracellular matrix?

A

It mediates the biosynthesis of extracellular matrix polysaccharides.

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25
What is a characteristic of Pseudomonas aeruginosa biofilms?
It forms a tenacious biofilm containing polysaccharides that increase pathogenicity and prevent antibiotic penetration.
26
What type of pathogen is Pseudomonas aeruginosa?
it is a classic opportunistic pathogen.
27
Where is the primary reservoir of Pseudomonas aeruginosa?
The primary reservoir is soil.
28
What types of infections can Pseudomonas aeruginosa cause?
It infects blood, lungs, urinary tract, ears, skin, and other tissues.
29
how does Pseudomonas aeruginosa affect people with cystic fibrosis?
It causes thick biofilms in the lungs, contributing to cystic fibrosis symptoms.
30
Is Pseudomonas aeruginosa a significant hospital pathogen?
Yes, it is a significant nosocomial (hospital-acquired) pathogen.
31
What role does quorum sensing play in Pseudomonas aeruginosa biofilm formation?
Quorum sensing is critical for biofilm development and maintenance through intercellular communication.
32
What molecule accumulates to signal biofilm growth in Pseudomonas aeruginosa?
Acyl homoserine lactones (AHLs) accumulate to signal that the population is growing.
33
What do AHLs trigger in Pseudomonas aeruginosa?
AHLs trigger genes for extracellular polysaccharide and c-di-GMP synthesis.
34
What happens when c-di-GMP levels are elevated in Pseudomonas aeruginosa?
elevated c-di-GMP initiates extracellular polysaccharide production and reduces flagellar function.
35
How does DNA release promote biofilm formation in Pseudomonas aeruginosa?
DNA release from lysed cells promotes biofilm formation.
36
What causes the "explosive death" of a subpopulation in Pseudomonas aeruginosa?
Lysis protein expression by inactive prophage in response to stress causes "explosive death."
37
Why does antibiotic treatment enhance biofilm formation in Pseudomonas aeruginosa?
Antibiotic treatment induces cell lysis, releasing DNA and promoting biofilm formation, which thwarts the effectiveness of antibiotics.
38
What are antibiotics?
Antibiotics are antimicrobials naturally produced by microbes that kill or inhibit bacterial growth.
39
What do antibiotics target in bacteria?
Antibiotics target essential molecular processes in bacteria.
40
What molecular processes do many antibiotics target?
Many antibiotics target DNA replication, RNA synthesis, and translation.
41
What do quinolones target in bacteria?
Quinolones target DNA gyrase and topoisomerase, interfering with DNA unwinding and replication.
42
How do rifampin and actinomycin inhibit RNA synthesis?
Rifampin and actinomycin block the RNA polymerase active site or RNA elongation.
43
How do antibiotics inhibit protein synthesis in bacteria?
By targeting the 70S ribosome in bacteria, which differs from the 80S ribosome in eukaryotes.
44
How does puromycin inhibit protein synthesis?
Puromycin binds to the A site in the 70S ribosome, inducing chain termination and inhibiting protein synthesis.
45
How do aminoglycoside antibiotics (e.g., streptomycin) work?
They target the 16S rRNA of the 30S ribosome, leading to error-filled proteins that inhibit bacterial growth.
46
How does daptomycin affect bacterial cells?
Daptomycin binds to phosphatidylglycerol residues in the bacterial cytoplasmic membrane, leading to pore formation, depolarization, and cell death.
47
what is the action of polymyxins on bacterial cells?
Polymyxins are cyclic peptides with long hydrophobic tails that target the LPS layer, disrupting the membrane and causing leakage and cell death.
48
49
How do β-lactams (e.g., penicillin, cephalosporins) affect bacteria?
β-lactams interfere with transpeptidation, preventing the formation of cross-links between muramic acid residues in peptidoglycan.
50
What is the action of vancomycin in peptidoglycan synthesis?
Vancomycin binds to the pentapeptide precursor and prevents interbridge formation in peptidoglycan.
51
How does bacitracin inhibit peptidoglycan synthesis?
Bacitracin binds to bactoprenol and prevents new peptidoglycan precursors from reaching the site of synthesis.
52
What are the four classes of antibiotic resistance mechanisms
1) Modification of drug target 2) Enzymatic inactivation 3) Removal via efflux pumps 4) Metabolic bypasses
53
How do random chromosomal mutations contribute to antibiotic resistance
Random mutations can lead to resistance, such as spontaneous mutants resistant to rifampin, selected by exposure to the drug.
54
How can resistance genes spread in bacterial populations?
Resistance genes can exist on mobile genetic elements and be transferred by horizontal gene flow.
55
What role do enzymes play in antibiotic resistance?
Many mobile resistance genes encode enzymes that inactivate antibiotics, e.g., β-lactamase cleaves a ring structure, and acetylating enzymes add acetyl groups to chloramphenicol.
56
How does biofilm growth affect antibiotic resistance?
Biofilm growth increases resistance, making infections harder to treat, and some efflux pump genes are upregulated when cells enter biofilm growth mode.
57
How do efflux pumps contribute to multidrug resistance?
Many efflux pumps are promiscuous and can transport different classes of antibiotics, contributing to resistance against multiple drugs.
58
what do efflux pumps do in antibiotic resistance?
Efflux pumps transport various molecules, including antibiotics, out of the cell, lowering intracellular concentration and allowing survival at higher external concentrations.
59
What is persistence in bacterial populations?
Persistence is when antibiotic-sensitive bacteria produce rare, transiently tolerant cells.
60
What are persisters?
Persisters are dormant, genetically identical cells that are viable but do not grow, avoiding antibiotic killing.
61
How do persisters contribute to recurring infections?
Persisters can emerge from dormancy after treatment stops, causing recurring infections like tuberculosis and cystic fibrosis.
62
What mechanisms are involved in persistence?
Toxin-antitoxin modules, stringent response, and phenotypic heterogeneity.
63
What are Toxin-Antitoxin (TA) modules?
TA modules consist of a toxin that inhibits cell growth and an antitoxin that counteracts the toxin.
64
Where are TA modules found?
TA modules are found in almost all bacteria and many archaea.
65
What is the role of TA modules in bacteria?
They promote cellular adaptation by slowing growth, helping cells survive stress.
66
What triggers the stringent response pathway?
Stalling of translation triggers the stringent response, reducing rRNA and tRNA synthesis.
67
What does the stringent response lead to?
It inhibits protein synthesis, DNA replication, and cell division, causing cells to become dormant.
68
How does antibiotic treatment affect persisters?
Antibiotic treatment selects for and enriches multidrug-tolerant persisters.
69
what happens when antibiotic exposure ends?
Persisters exit the stringent response, produce antitoxin, and resume protein synthesis and growth.

Genetics (20 decks)

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