Bacterial Genetics Flashcards

1
Q

T/F Bacteria are adaptable.

A

True

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2
Q

What does the bacterial genome consist of?

A

An organisms complete set of DNA:

  • chromosome- essential and nonessential proteins
  • plasmids
  • bacteriophage- prophage
  • IS elements, transposons, PAI’s (GEI’s)
  • integrons
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3
Q

Bacterial chromosome? shape?

A
  • one, circular, dsDNA (majority), some have more than one, some are linear
  • no histones or introns
  • encodes for essential and non essential genes, better fit to survive in environment
  • not housed in a membrane bound nucleus, but nucleiod, a region of the cell where the chromosome resides
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4
Q

Are bacteria haploid or diploid?

A

haploid -one copy of each gene, mutations are expressed from mother to daughter

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5
Q

Bacterial gene expression? essential vs nonessential?

A
  • genes required for basic survival are constitutively expressed (DNA, cell wall, RNA, translation)
  • expression of non essential genes can be positively (inducers) and negatively (repressors) regulated, usually at the level of transcription, some genes are present on DNA as operons
  • operons
  • polycistronic mRNA
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6
Q

What are operons?

A

sequence of DNA that contains multiple genes to produce multiple proteins for a single purpose (not in eukaryotic cells), multiple genes coordinately expressed

-multiple genes with single promoter

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7
Q

Polycistronic mRNA?

A

mRNA that has information for more than one gene or protein product

-there are sites where ribosome can bind to get independent proteins

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8
Q

What do bacteria adapt to?

A

they quickly adapt to environmental changes for survival by modulating gene expression

  • availability of sugars
  • iron concentration
  • presence of an antibiotic
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9
Q

what is an example of regulation for survival in bacteria?

A

the Lac operon

  • when glucose is available the lac operon encodes genes that allows for metabolism of lactose
  • using regulators and repressors, allosteric changes
  • positive and negative regulation
  • adapts to environmental changes to survive
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10
Q

What is gene regulation by quorum sensing? low vs high density

A
  • organism can change its phenotype based on density of bacteria
  • low density- signal molecules for harmless type
  • high density- signals bind receptors that bind upstream of genes to make organism more pathogenic by making biofilm of special toxins
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11
Q

The expression of many virulence genes are under regulation at the level of ______.

A

transcription

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12
Q

What are the mechanisms of mutations in bacteria?

A
  • base substitution or point mutation (transition or transversion), G->A, G->C
  • deletion or addition of nucleotides
  • insertional mutation- disruption of a gene by a transposon (jumping gene)- makes organism more pathogenic
  • recombination
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13
Q

Results of mutations?

A
  • missense mutation- changes in amino acids sequence of protein product
  • frameshift mutation- shift in reading frame of gene
  • inversion mutation- segment of DNA is removed and reinserted in reverse direction
  • inactivation of gene
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14
Q

Clinical significance of mutations?

A
  • changes in amino acids of bacterial structures can result in resistance to antibiotics
  • non resistant bacteria multiply, some develop mutation, non resistant bacteria die from antibiotic, drug resistant mutations thrive
  • base mutations, frameshift and gene arrangements can cause antigenic and phase variation of major surface components
  • antigenic variation
  • phase variation
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15
Q

antigenic variation?

A
  • changes in composition or structure of a molecule
  • pilli on organism is changed because amino acids look different, antibodies used need to be different
  • population- shift back and forth
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16
Q

phase variation?

A
  • turning on or off of the expression of a molecule
  • capsule is expressed, then it changes to be not expressed
  • some without variation can bind those that can in order to be protected from antibodies
17
Q

What structures can undergo phase and antigenic variation?

A
  • capsule
  • flagella
  • pilli
  • lipid A cannot because it is part of cell wall, O antigen can undergo variation
18
Q

When do these genetic changes normally take place? what are the consequences?

A

DNA synthesis

  • polymerase makes error
  • changes expression
  • organism looks different on surface
  • immune system struggles to recognize
  • antibiotics may not work
19
Q

What are mobile genetic elements (MGEs)?

A
  • elements that can move in and out of the genome
  • organisms that can share
  • elements that are responsible for bacteria becoming more resistant to antibiotics
  • plasmids
  • bacteriophage
  • insertion sequences
20
Q

What are plasmids?

A
  • small circular supercoiled DNA, extra chromosomal DNA
  • 1 to 5 copies/cell, large plasmids, 10 to 20 copies/cell small plasmids
  • replicate independently of the chromosome, inherited by daughter cells
  • conjugative plasmids (large) encode transfer enzymes, and sex pili for transfer to other cells
  • can carry genes that confer phenotypic advantages to bacteria
  • can allow organisms to share DNA, confers a survival advantage
  • can piggyback
21
Q

What is the clinical significance of plasmids?

A
  • plasmids may carry genes that provide resistance to antibiotics (R-plasmids) or that make proteins that act as toxins or other pathogenic factors
  • R plasmids may carry resistance to multiple antibiotics
  • use of antibiotics has applied a strong selective pressure for bacteria that can resist them
22
Q

Bacteriophage? structure? genome?

A

viruses that infect bacteria:

-specific, used to subtype bacteria (phage typing)

structure:

  • protein capsid that houses genome
  • may have base and tail
  • no membrane envelope

Genome:

  • DNA or RNA
  • single or double strand
  • linear or circular
23
Q

Life cycles of bacteriophage?

A

Lytic (virulent):

  • after binding -> rapid replication
  • 20 mins from infection to lysis, leads to cell death and production of new (progeny) phage, takes over machinery, can treat diseases

Lysogenic (temperate):

  • infection leads to cell lysis, or integration of phage DNA into chromosome or the formation of a plasmid (prophage-piece of DNA)
  • inject genome into chromosome and repress expression of their genes and stably replicate their genome prophage can encode for toxins to make organism more pathogenic
24
Q

lysogenic conversion of bacteriophage?

A
  • prophage conversion may increase virulence of bacteria
  • diptheria toxin is encoded on a prophage, only those with prophage can cause disease
25
Q

What are insertion sequences?

A

IS- the smallest and most simple transposable elements

  • jumping genes- go from one place to another
  • they have machinery to excise themselves, replicate genome, and move to another place (genes for transposition)
26
Q

What are transposons?

A
  • more complex insertion sequences, transposable elements that contain genes for transposition in addition to genes that encode for antibiotic resistance and other virulence properties
  • encode for toxins, fimbriae, increase virulence
27
Q

What are genomic or pathogenicity islands?

A
  • large segments of DNA that contain mobile genetic sequences
  • they can encode for genes that enhance the virulence of a pathogen
  • really large transposons
  • in S. aureus there are 12 PAIs that encode for a variety of super antigen toxins
28
Q

What is horizontal gene transfer?

A
  • lateral gene transfer (LGT)
  • tranformation
  • conjugation
  • transduction
29
Q

Transformation?

A

donor -> cell lysis: release DNA fragments -> DNA enters recipient cell and integrates into DNA

  • uptake of naked DNA by bacteria in state of competency
  • under right conditions, the DNA can be incorporated into genome of recipient and result in change in phenotype
  • naturally competent DNA have the ability to take up exogenous DNA across membrane without manipulation (strep, neisseria, gonorrhoeae)
30
Q

Conjugation?

A
  • intimate association with two individuals, cell contact
  • male (F+) and female (F-) cells come together
  • conjugative plasmid makes copy of itself and shares it with F-
  • after reaction, there are two F+ cells
  • conjugative transfer of plasmids with resistance genes is an important cause of spread of antibiotic resistance
  • Gram - use pili and Gram + use other systems
  • some transposons are conjugative
31
Q

Transduction?

A
  • transfer of genetic info from one bacteria to another by bacteriophage
  • prophage- DNA incorporated into chromosome
  • lysogenic conversion
  • donor organism goes through lytic phase with temperate phage
  • takes up DNA from donor and its own DNA to make progeny
  • infects another organism, DNA from donor will recombine with genome of recipient
  • transduction and conjugative play important role in antibiotic resistance
32
Q

Clinical significance of transfer mechanisms?

A
  1. evolution of new pathogens
    - non pathogenic strain of E coli aquires foreign DNA to produce E coli strains that cause diarrhea or UTI
  2. spread of antibiotic resistance
    - VRE and MRSA share info to make them resistant to vancomycin (MVRSA)
33
Q

Mechanisms of antibiotic resistance?

A
  1. decreased permeability
    - mutation of porin
  2. alteration of target
    - new PBP that does not bind penicillin
  3. inactivation of antibiotic
    - secretion of beta lactamases
34
Q

Beta lactams examples? method of actions? bacteria method of resistance?

A

-penicillin, methicillin, oxacillin, nafcillin, cephalosporins

MOA:

-bind transpeptidases (PBP), preventing peptidoglycan cross linking which leads to cell death

MOR:

  • cleavage of beta lactam ring by beta lactamases
  • modification of PBP (ex. MRSA)
  • spontaneous mutations of porins in Gram -
35
Q

Vancomycin method of action? bacteria method of resistance to it?

A

MOA:

-interacts with D-alanine, D-alanine termini, prevents cross linkage of peptidoglycan layers

MOR:

  • change of binding site to D-alanine, D-lac
  • thickening of cell wall that traps vancomycin