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BIOL-M 250 > Exam 4 New > Flashcards

Exam 4 New Flashcards

1
Q

Replication: Initiation

A

DnaA binds to origin and recruits DNA Polymerase III to begin bilateral replication

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2
Q

Replication: Elongation

A

Starts to expand

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3
Q

Replication: Termination

A

Stop at 180 degrees. Tus binds to things like is own

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4
Q

Replication: Decatenation

A

Topo IV then splits these two circles apart.

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5
Q

Plasmids

A

Often able to be shared among bacteria. Contain non-essential genes. Copy number varies from 1-1000 per cell.

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6
Q

What do Plasmids often encode?

A

Often encode environmental advantages. Catabolic genes for new compounds. Toxicity genes for pathogens. Antibiotic resistance.

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7
Q

Plasmic Replication

A

Some plasmids replicate by Theta Replication. Bi-directional replication with double stranded synthesis. Others replicate by “rolling circle replication”; a uni-directional replication of single strand synthesis

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8
Q

Plasmid Segregation - High Copy Number

A

High copy number plasmids (~100/cell) segregate by chance.

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9
Q

Plasmid Segregation - Low Copy Number

A

Low copy number palsmids (~1/cell) have partitioning systems to ensure inheritance

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10
Q

Translation Error

A

Errors in translation affect ONE protein. This can be dramatic. This can cause protein to misfold.

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11
Q

Transcription Error

A

Errors in transcription affect a subset of proteins translated from the transcript with error. Everything originating from the wrong information will cause the sub protein to fail but the overall protein will still function.

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12
Q

Replication Error (Mutation)

A

Mutations alter ALL proteins encoded by that gene.

Mutation alter ALL proteins of ALL descendants of the mutant strain. The generation will suffer from this as well.

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13
Q

Replication Forks

A

When DNA being synthesized, we have a replication fork. One DNA strand is synthesized in short bursts because of the 5’>3’ synthesis of DNA

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14
Q

What is DNA Polymerase III?

A

It is the primary replicating polymerase.

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15
Q

Genetics

A

The study of heritable changes in the DNA sequence (Mutation + Inheritance)

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16
Q

Error 1 in Replication: Mismatch

A

Sometimes, DNa polymerase makes a mistake. A mismatch. An example would be “g” pairing with “a”.

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17
Q

Error 2 in Replication: Slipped Strand Mispairing

A

When DNA polmerase tracks over a repetitive sequence, it can “slip” forward or reverse. Happens at a higher frequency than mismatch but requires repetitive site.

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18
Q

Mutagens

A

Environmental factors that damage DNA.

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19
Q

What can go wrong with Benzopyrene?

A

It can slip into a double strand of DNA. When this happens, it causes disortion of the backbone. It can then cause a misreading of the backbone. dsDNA intercalating agents distorting double helix.

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20
Q

What can go wrong with Methyl-Nitrosoguanidine?

A

It chemically modifies the bases so it can’t react. T forms a base pair with G, which should not happen. Chemical modification of a base.

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21
Q

What cna go wrong with UV light?

A

Base Crosslinking can occur

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22
Q

What can go wrong with Ionizing Radiation?

A

Base Elimination. Oxygen attacks connection between the base and sugar. The information is then permanently gone.

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23
Q

Mutation

A

A change in the DNA sequence. If unrepaired, it is passed to the next generation.

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24
Q

Mutant

A

A cell line that has inherited a particular mutation.

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25
Q

Genotype

A

The DNA sequence of a gene/chromosome

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26
Q

Phenotype

A

The measurable/observable trait conferred by a gene, mediated by proteins.

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27
Q

Allele

A

A version of a gene.

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28
Q

Wild Type Allele

A

An arbitrarily defined sequence. Relative, not absolute.

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29
Q

Mutant Allele

A

A change in DNA sequence relative to the wild type.

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30
Q

Changes in protein sequence…

A

change protein shape and change proetin function

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31
Q

A random mutation will either…

A

do nothing, or result in protein loss-of function

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32
Q

very very rarely, …

A

gain-of-function mutation will arise that increases o changes protein activity.

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33
Q

Types of Point Mutations: Missense Mutation

A

Single base pair change that changes the codon to a different amino acid.

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34
Q

Types of Point Mutations: Nonsense Mutation

A

Single base pair change that changes the codon to a premature stop codon

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35
Q

Types of Point Mutations: Silent Mutation

A

Changes the codon but codes for the same amino acid due to degeneracy. “Silent” in protein sequence, but may have phenotype

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36
Q

Types of Point Mutations: Frameshift Mutation

A

Insertion or deletion of base pairs in amounts not divisible by 3. Completely alters subsequent amino acid sequence.

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37
Q

Polarity

A

A side effect of mutations within operons. Mutations early in a operon decrease or abolish expression of downstream genes. Rho can bind and terminate transcription inappropriately. Muation creates a premature translation stop.

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38
Q

Mutation Frequencies

A

10^-3 - Mutagent (Many events per genome
10^-6 - Slipped strand mspairing (1 per genome)
10^-8 - Missense loss of function (1 in 100 genomes)
10^-10 - Missense gain-of-function (1 in 1,000,000 genomes)

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39
Q

Steps in DNA Repair System

A
  1. DNA Polymerase 3’ –> 5’ Proofreading
  2. Methyl-directed mismatch repair
  3. SOS response and excision repair
  4. Recombination Repair
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40
Q

DNA Polymerase III repair function

A

DNA Polymerase III has a 3’ –> 5’ exonuclease activity when mismatch is detected. Backs up one base and excises it. It then proceeds with replication

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41
Q

What happens if DNA Polymerase III misses?

A

If it fails to recognize the mismatch and continues on, the mismatched base does not base pair correctly and causes a distortion.

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42
Q

MutS

A

REcognizes and binds to DNa Distortion

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43
Q

MutL

A

“Linker Protein” - Recruits MutH to Muts

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44
Q

MutH

A

Endonuclease, nicks DNA near damaged base.

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45
Q

Metyl-Directed Mismatch Repair

A

Damaged DNa is excised. The repair polymerase DNA polymerase I loads, fills in the gap.

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46
Q

How do repair recognize which base is the “wrong” mutated base

A

Older, original DNa strand is modified by methyalation. Newer strands lack metyl groups. MutHSL cuts out distortion on unmethylated DNA strand.

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47
Q

Base Methyalation

A

After replication the DNa is full methylalated by an enzyme: DNA Methyltranserase

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48
Q

Short window of “hemi-methylation”

A

MutSLH can only catch mismatches in a brief window behind Pol III

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49
Q

SOS System (1)

A

Begins with a protein called Rec A. RecA binds to damaged base and becomes activated to RecA*

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50
Q

SOS System (2)

A

LexA is a transcriptional repressor DNA binding protein that inhibits SOS genes. RecA* causes cleavage of LExA and de-repression of SOS genes.

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51
Q

SulA

A

An inhibitor of FtsZ

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52
Q

UvrABC

A

DNA excision Repair; chemically detects damaged base. DNA Polymerase fills in gap.

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53
Q

Pol IV

A

Error Prone Polymerase

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54
Q

SulA job

A

SulA inhibits cell divsion. Interacts with FtsZ and blocks Z-wring formation until DNA damage has been resolved. SOS system makes sure that DNA damage has been repaired before proceeding with cell divison

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55
Q

Error Prone of Polymerase?

A

DNA Polymerase III cannot replicate through damaged bases. Causes a replication jam.

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56
Q

What is the last resort of Error Prone PolymerasE?

A

DNA Polymerase IV is switched into replication fork. Can polymerize past severe damage but creates many mismatches.

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57
Q

First DNA Repair System

A

DNA Polymerase III has the ability to back up and excise a mismatched base.

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58
Q

Second DNA Repair System

A

Methyl Directed Mismatch REpair. MutSLH can excise mismatches

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59
Q

Third DNA Repair System

A

SOS!

Excision Repair UveABC can excise damaged nucleotides.

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60
Q

Fourth DNA Repair System

A

SOS! Error prone DNA Polymerase IV copies over the top of damaged nucleotides.

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61
Q

What do you do in the case of large deletions?

A

The only way to repair a deletion is to bring in a fresh copy of the genetic sequence with all missing information. Recombination and Gene Replacement

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62
Q

DNA Uptake

A

Cell needed DNA from an External Source. DNA can either be destroyed by restriction or recombined into chromosome.

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63
Q

Restriction

A

Restriction enzymes recognize patterns on dsDNA and cut the incoming DNA into pieces. Defense against forein DNA

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64
Q

EroRI

A

Enzyme from E. Coli that cuts DNa at the pattern “GAATTC”

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65
Q

When foregin DNA is wanted in the body..

A

DNA Methyltransferase methylates “GAATTC” soEcoRi cannot bind

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66
Q

If incoming DNA strand is similar to chromosome…

A

it ma replace old sequence. Sequences must base pair over some of their length for replacement. Mediated by the RecA protein.

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67
Q

Vertical Transfer

A

Requires cell divison

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68
Q

Horizontal Transfers

A

requires two cells. A Donor –> Recipient

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69
Q

Horizontal Gene Transfer: Mechanism 1

A

Transformation:

Uptake of free DNA directly from the einvornment. “Com machinery”

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70
Q

Horizontal Gene Transfer: Mechanism 2

A

Conjugation - Export of DNa from one cell into another. “Tra machinery”

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71
Q

Horizontal Gene Transfer: Mechanism 3

A

Transduction - Transfer of genetic material between two bacteria by means of Bacteriophage. Generalized v Specialized.

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72
Q

Transformation

A

Uptake of DNA found free in the environment. Cells die and release genetic material. Other cells can then take up free DNA.

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73
Q

COM Machinery

A

Similar to Type IV Pilus.

1. Pilus Binds dsDNA (One strand destroyed, one strand imported) and then recombine into chromosome.

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74
Q

Benefit of competence, taking free DNA from environment where cell didn’t survive?

A
  1. Maybe bacteria sample the genetic environment for beneficial genes?
  2. Repair of damaged gene sequences?
  3. Maybe competence is a way of “Eating” DNA?
    REal reason unclear.
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75
Q

Conjugation

A

Cell Interaction faciliatated by a sex pilus. Donor cells have a F Factor, which is a plasmid.

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76
Q

What is encoded on the F Factor?

A

Sex Pilus (Retractile Pilus)
Tra Machinery for DNA Transfer
Independent Origin of Replication

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77
Q

Sex Pilus and Mating Steps

A
  1. Pilus Extends
  2. REcognizes, and binds to a receptor on the surface of recipient
  3. Pilus retracts.
  4. Plasmid is replicated beginning at OriT via the rolling circle mechanism and transfered through Tra machinery.
  5. Recipient gains a cop of F factor plasmid and can now be a donor.
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78
Q

Side Effect of F Factor?

A

F Factor can spontaneously integrate into the chromocome and create a HFR Strain”
High Frequency Recombination

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79
Q

What can a HFR Strain do?

A

During mating, it will now copy and transfer the chromosome instead of the F Factor plasmid.

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80
Q

Transfuction

A

A phage accidently packages bacterial chromosomal DNA and transfers this DNA to another bacterium

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81
Q

Generalized Transducion

A

Mispackaged bacterial DNA can come from any location on the bacterial chromosome.

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82
Q

Specialized Transduction

A

Mispackaged bacerial DNA can only come from teh part of the bacterial chromosome that is adjacent to the prophage interaction site.

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83
Q

Bacteriophage

A

Viruses that infect bacteria. Use a host to make copies of themselves. LAck ribosomes and cannot make their own energy

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84
Q

Lysogeny

A

When phage DNA is stably integrated into host chromosome and remains dormant as a prophage

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85
Q

Where does Phage DNa integrate?

A

At a specific DNA sequence in the host called the att site (attachment site)

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86
Q

Lysogen Maintenance

A

Phage Repressor Protein “c1” inhibits phage gene expression. Phage DNA “hides” inside of bacterial chromosome and is replicated as the bacterium grows.

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87
Q

Lysogenic to Lytic Transition

A

SOS response RecA* cleaves repressor C1. This activates phage lytic cycle. Phage excises, replicates, and releases through lysis.

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88
Q

Types of Bacterial Motility

A 
Swimming
Swarming
Twitching
Gliding
Floating
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89
Q

Swimming Motility

A

Takes place in liquid. Individual movement. Powered by rotating flagella.

90
Q

Flagella

A

Cell surface machines. Made of protein. Helical shape. Rotates at ver high speed to propel the cell body (200 rotations/ second)

91
Q

Flagellar number/arrangements…

A

differes for each species.

92
Q

Flagellum Componens

A

A massive molecular machine that spans the cell envelope. Built as a complex of more than 30 different proteins. Subunit assembly must be perfectly timed and accurately ordered

93
Q

Parts of the Flagellum

A

Filament - “Properller”
Hook - Flexible Universal Joint
Basal Body - Transits envelope. Secretion. Powers Rotation.

94
Q

How is the flagellum assembed?

A

From the inside-out. Basal Body –> Hook –> Filament

95
Q

What is at the core of the flagellum?

A

Type III Secretion. The only different between these is that only the flagellum rotates.

96
Q

Biofilms

A

Multicellular aggregates of baceria held together by an extracellular polsaccharide (EPS)

97
Q

Stages of Biofilm Development?

A
  1. Planktonic Cells - Attachment
  2. Biofilm Cells - Growh
    Planktonic Cells - Deatchment
98
Q

Motility to Biofilm Transition

A
  1. Flagella lands on EPS Capsule or Slime Layer
  2. GGDEF Proteins signals to form biofilms
  3. EPS helps cells stick to each other and to surfaces. Cells grow up in aggregates.
99
Q

Cross Section of Colony Meaning

A

Yellow - Sporulation Genes
Blue - Motility Genes
Green - Sporulation Genes
Red - Matrix Genes

100
Q

Advantages of Biofilms? (1)

A

Concentrate digestive enzymes. Many bacteria eating as one.

101
Q

Advantages of Biofilms? (2)

A

Persist in favorable environment. Prevent cells from being flushed out of environment.

102
Q

Advantages of Biofilms? (3)

A

Collaborative metabolism between different species. Anaerbobically respiring sugars to sulfur which produces sulfde that aerobically respires to oxygen

103
Q

Advantages of Biofilms? (4)

A

EPS provides for chemical and engulfment defense. Diffusion barrier to antibiotics.

104
Q

Advantages of Biofilms? (5)

A

Maintains high cell density to facilitate a variety of processes. This includes Quorum Sensing and Genetic Transfer

105
Q

Examples of Good Biofilms?

A

Rhizosphre (Growth on plant roots)
Cyanobacterial mats/blooms (“pond scum”)
Marine Snow
Normal Body Flora

106
Q

Examples of Bad Biofilms?

A 
Bathtub Scum
Clogged Pipelines
Grow on Hulls of Ships
Plaque
BioCorrosion
107
Q

Biocorosion

A

Biofilm metabolism makes acids and anaerobic respiration reduces metals. This is corrosive!

108
Q

Attenuation

A

the loss of pathogenicy by propagation

109
Q

Pathogenesis

A

A nutrtional strategy. To take nutrients away from other cells.

110
Q

Mutalism

A

When both partners benefit.

111
Q

Commensalism

A

One partner benefits while the other partner is unharmed.

112
Q

Parasitism

A

One partner benefits while one partner is harmed.

113
Q

Mutalism - Ruminants

A

Animals with a rumen, an organ containing bacteria that degrade cellulose. Bacteria eat cellulose. Cow eats fermentation acids left over from the bacteria.

114
Q

Mutalism - Gut Microbiome

A

25% of the energy we eat is consumed by gut bacteria. Bacteria then feed us fermentation products. Short chain acids. Occupy niche and out compete pathogens.

115
Q

Parasitism

A

Pathogens infect the body and kill our cells.

116
Q

Virulence Factors - First One

A

Genes can change randomly. This includes E. Coli, Cholera, and Whooping Cough. Also Opporunistic infections. If the body’s immune system is compromised, commensal bacteria can become pathogens.

117
Q

Koch’s Postulates

A
  1. Isolate organism from infected individual
  2. Culture organism in lab
  3. Re-infect new individual and reproduce disease
  4. Re-isolate organism
118
Q

General Disease Ccle

A

Reservoir –> Invasion –> Colonization –> Growth –> Toxicity –> Death

119
Q

Infective Dose (ID50)

A

Number of bacteria that results in infections in 50% of hosts.

120
Q

Lethal Dose (LD50)

A

Number of bacteria that results in lethality in 50% of hosts.

121
Q

What do Antibacteral Enzymes do?

A

Lysozyme in tears destroys peptidoglycan. Salva and stomach acid have suites of digestive enzymes.

122
Q

Defense - Iron Sequestration

A

Iron is a scarce micronurient. Body sequesters iron with proteins to starve bacteria. Has Lactoferrin

123
Q

Lactoferrin

A

Proeins flaoting in blood and tissue that can give iron to blood and tissues tat need it . It also makes it difficulty for bacteria to rip the iron away from their ability to grow.

124
Q

Defense - Macrophages

A

Macrophages are one type of white blood cell that protects the body. Macrophages secrete hydrogen peroxide and engulf bacteria.

125
Q

Defense - Antibodies

A

Antibodies are proteins made by the immune system that bind to antigens. Aid Phagocytosis. Anitgens are specific patterns found on bacterial surfaces.

126
Q

O Antigen

A

Unique Sugar pattern on LPS of each Gram Neg

127
Q

H - Antigen

128
Q

K - Antigen

129
Q

Virulence Factors

A

Properties of the bacterium that enhance either invasiveness or toxicity

130
Q

Invasiveness

A

The ability to enter and survive in the body

131
Q

Toxicity

A

The ability to damage cells and obtain nutrients.

132
Q

Genes Encode Virulence Factors (4)

A
  1. Gene should be found in strains that cause disease and absent in strains that do not.
  2. Mutation of the gen ehsould result in a reduction in virulence
  3. Introduction of the gene should increase virulence
  4. Immune response to gene product should protect against infection
133
Q

Virulence Factor - Moility

A

Tissue Tropism - Some bacteria infect particular parts of the body. Motility can aid in tropism (migration) to target tissues.

134
Q

Swarming Example?

A

Through Viscous Mucus

135
Q

Twitching Example?

A

Over Surfaces

136
Q

Endoflagella example?

A

Between body cells.

137
Q

Virulence Factor - Adhesion

A

Attachment at the site of infection. Resists. flushing. This includes Pili, Adhesins, and Capsule.

138
Q

Pili

A

Proteinaceous fibers that stick to surfaces

139
Q

ADhesins

A

Bacterial proteins that bind to sugar patterns on the eukarotic cell. The host decorates its surface proteins with sugars to distinguish itself from invaders. Adhesins bind to these sugars.

140
Q

Capsule

A

Extracellular polsaccharide coat. Sticky substance to attach to host.

141
Q

OOTW - Streptococcus Penumoniae

A

Gram positive diplococci
• Infects the lung.
• Most deaths from flu virus come fromsecondary infection by S. pneumoniae.
• Natural transformation system:makes Com machinery.
• Antigenic variation, 90 different capsule structures in species.

142
Q

Griffith Transformation Experiment 1928 (No Capsule)

143
Q

Griffith Transformation Experiment 1928 (With Capsule)

A

Dead, Virulent.

144
Q

Griffith Transformation Experiment 1928 (Dead, with Capsule)

145
Q

Griffith Transformation Experiment 1928 (Dead capsule strain mixed with Live capsuleless strain)

A

Dead, Virulent.

146
Q

Conclusion from Griffith Transformation Experiment 1928?

A

Capsule is required for virulence. CApsule genes transferred to avirulent strisn during co-infection by natural competence. (transformation)

147
Q

Antigenic Variation: Promoter Inversion

A

Site specific recombination causes promoter to flip.

148
Q

Virulence Factors - Siderophores

A

High affinity ion sequestration systems. Can rip iron away from Lactoferrin.

149
Q

Exotoxins

A

Secreted enzymes that disrupt host cell structure or processes

150
Q

Endotoxin

A

Structures released from dead baceria that hyperstimulate the immune system .

151
Q

Exotoxin - Hemolysins

A

Proteins secreted by bacteria. Creates holes in host cell membranes. Host cells then burst.

152
Q

Exotoxin - Phospholipase

A

Phospholipase lets bacteria escape from endocytic vesicle. Cells grow inside host cell. Hidden from immune system.

153
Q

Exotoxin - IgA Protease

A

IgA protease degrades antibodies and prevents them from targeting bacteria.

154
Q

Exotoxin - A/B Toxins

A

A self injecting secreted toxin complex. A subunit is the toxin and the B Subunit is the delivery vehicle. Toxin typically overrides host signaling systems.

155
Q

A/B Example - Choler aToxin

A

Modifies host signaling proteins. Overrides normal regulation of iron transporters. Causes massive water efflux and severe diarrhea.

156
Q

A/B Example - Shiga Toxin

A

Destroys eukaryotic ribosomes to kill host cell.

157
Q

OOTW - Yersinia Pestis

A

Causes Bubonic plague
.• Black Death 1347-1351 killed ~30% of European population
• Carried between rodents and people by fleas.
• Wide variety of virulence factors encoded on plasmids.
• Injects toxins directly

158
Q

Y. pestis: virulence plasmids

A

Virulence Factors encoded on three different plasmids.
pMT1 - Encodes Pili
PPCP1 - Encodes Protease
pCD1 - Enodes toxins and type III secretion machine
HPI - Island of genes on chromosome codes for biofilm formation

159
Q

Y. pestis: infects fleas

A

Biofilm blocks flea digestive tract. Flea starves and bites more for food. Flea cannot eat and regurgitates pathogen into host.

160
Q

Y. pestis:needle complex

A

Type III Secretion System
~10 Toxins are directly injected into host cells. Minimizes diffusion of toxins and toxins are in the same space as their target. Antigens on toxins are never exposed to immune system .

161
Q

How do endotoxins work?

A

If gram negative bacteria gets into the blood, some of them will be killed by the immune system . The baceria release fragments of their cell wall. “Endotoxin” because it is normally part of the bacterial cell structure

162
Q

Immune sysem recognizes Lipid A

A

Lipid A binding protein (LBP) is secreted by white blood cell.
LBP binds to Lipid A and docks with a TOLL Receptor on white blood cell.
TOLL instructs the white blood cell to secrete massive amounts of cytokines.

163
Q

What do cytokines cause

A

They cause inflammation of blood vessels. Immune system is sensitive to lipid A so too many cytokines are released. Blood pressure crashes. This leads to “Toxic Shock Syndrome”

164
Q

How was Penicillin discovered?

A

A fungus (penicillium) inhibited the growth of a bacterium

165
Q

Antibiotic vs Antibodies

A

Antibiotics are small chemical “secondar metabolites”. Antibodies are proteins.

166
Q

Antibiotic Properties

A

“Static” - Suspend growth while antibiotic present
“Cidal” - Actually kill the bacteria
Assay - Lawn of Bacteria.

167
Q

MIC

A

The lowest concentration of antibiotic required to inhibit an organism.

168
Q

To be useful, what must antibiotics have?

A

Selective Toxicity. It must prevent the growth of some organisms (bacteria) but permit the growth of others (humans) The antibiotic must target specialized functions in a cell.

169
Q

Anti-Bacterial Targets

A

Target systems bacteria require to grow
Target pathways humans do not use
Target enzymes for which humans have a similar but substantially different variation
Complex multi-step processes provide many targets

170
Q

What does Penicillin inhibit?

A

Crosslinking

171
Q

What does Vancomycin inhibit?

A

Inhibits polymerization

172
Q

What does Bacitracin inhibit?

A

Inhibits activation of membrane carrier.

173
Q

Translation Inhibitor - Tetracycline

A

Blocks amino acyl tRNA entr

174
Q

Translation Inhibitor - Chloramphenicol

A

Blocks peptide bond formation

175
Q

Translation Inhibitor - Erythromycin

A

Blocks ribosome translocation

176
Q

OOTW - Streptomyces Coelicolor

A 
mistaken for a eukaryotic fungus
•  Gram positive soil bacterium
•  hyphal growth, cell division is rare
•  linear chromosome
•  multiple chromosomes per cell
•  developmental cycle
•  sporulation
•  polyketide antibiotics
177
Q

Streptomyces Coeicolor Basic Function

A
  1. Grows Into Substrate
  2. During starvation, it secretes antibiotics and hydrophobin
  3. Grows into the air and forms chains of spores.
178
Q

Streptomyces Coelicolor - Problems with Linear Chromosome

A

Discontinuous strand must continuously re-prime. No template DNA to re-prime the termini.

179
Q

Streptomyces Coelicolor - End Replication

A

Eukaryotes use Telomerase to extend the 3’ termini. They have TPG “terminal proteins” covalently fuxed to ends of chromsomes. These proteins somehow fill in the DNA gap.

180
Q

75% of the worlds antibiotics come from

A

Streptomyces

181
Q

Streptomyces specialize in polyketide antibiotics

A

Polyketides look very complex but are actually varations on one anothe. Related to fatty acid biosynthesis.

182
Q

Polyketide Biosynthesis

A

Genes are in “islands” on the chromsome. All related genes grouped together. Synthase genes are huge.

183
Q

Genetic Regulators

A

Control production of polyketide synthase

184
Q

Polyketide Synthase

A

Synthase is a series of enzmes fused together. Rearranging domains on synthase can produce new antibiotic structures.

185
Q

Resistance Genes

A

Provide resistance for the polyketide antibiotic that is being made.

186
Q

Antibiotic Resistance Strategies - Exclusion

A
  1. Prevent antibiotic from entering passive. Example is the gram negative outer membrane.
  2. Actively pump antibiotic out. Transporter genes. Example is “TetA” Tetracycline Exporter
187
Q

Antibiotic Resistance Strategies - Inactivation

A
  1. Enzymatically destroy antibiotic. Enzyme Genes. Example: B-Lactamase and Penicillin
  2. Enzymatically modify antibiotic. Enzyme Genes. Example is Chloramphenicol Acetyltransferase.
188
Q

Antibiotic Resistance Strategies - Immunit

A
  1. Modify cellular target. Spontaneous mutations in target. Example is sreptomcin binds directly to ribosomes and certain mutations in ribosome prevent Streptomycin binding.
189
Q

The more we use antibiotics,

A

the more resistance increases

190
Q

Vaccines

A

A deliberaely introduced antigen to raise antibodies prior to actual infection.

191
Q

Common Vaccines

A

MMR - Measels, Mumps, Rubella (Viruses)
DTP - Diptheria, Tetanus, Pertussis (Bacteria)
TB - Tuberci;psos

192
Q

Probiotic

A

A living organism which when ingested, may confer increased resistant to infection.

  1. They may add to or enhance native flora to prevent infection, c
  2. Create a low grade immune response to rime the body against infection
  3. not do anything.
193
Q

Biocontrol Agents

A

Probiotics for Plants. They reduce disease and pesticide use.

  1. Form biofilm on roots
  2. Enhance general resistance pathways
  3. Do noting
194
Q

Three Primary Groups of Archaea

A

Hyperthermophiles >100 Degrees Celscius
Exremee Halophiles
Metanogens

195
Q

“Pseudo”peptidoglycan

A

Chemically different from peptidoglycan.

  1. No N-Acetyl Muramic Acid
  2. Uses N-Acetltalosaminuronic Acid Instead
  3. Uses L-Amino Acids rather than D Amino Acids
196
Q

S-Layer Protein Shell - Archaea

A

A crystalline shell of glcoproteins (proteins with decorated with sugars. Provides strucutal integrity.

197
Q

Lipid Linkages

A

Bacterial Lipids rely on “Ester” linked lipids.

Archaeal Lipids rely on “Ether” linked lipids

198
Q

Branching

A

Bacterial has single branch at end. Means increase of molecular space in membrane. Archaeal has extensive branching. Decreases molecular space in membrane. Elongation during lipid snthesis must be different

199
Q

FtsZ in Archaea?

A

None. Instead they have CdvA, CdvB, and CdvC.

They resemble ESCRT vescle traficking system f Eukaryotes.

200
Q

Archael Motility

A

Archael rotates as a propeller and related to type IV pilus with ~ 10 proteins. Bacterial flagellum rotates as a propeller and related to TYPE III needle ~ 30 proteins.

201
Q

OOTW - Methanococcus Jannascii

A 
•  isolated from 1.6 mile deep vent
•  grows at 200 atm pressure, 85°C
•  strict anaerobe
•  no pseudopeptidoglycan
plasma membrane with an S-layer
•  contains cyclic lipids
•  chemolithoautotroph
•  methanogenOrganism

Anaerobically respires H2 to CO2

202
Q

The Volta Experiment

A

The discovery of Methane that was trapped on the surface of liquids. Methanogens reduce CO2 to CH4 in multiple steps. They use Strange Metals.

203
Q

Methanococcus - autotrophy

A

Archaea do not use RuBisCO for Carbon Fixation. They use Reverse TCA.

204
Q

The Korachaeota

A

A newly discovered Archaea. They occupy the deepest branch on the phylogenetic tree but none have been cultured.

205
Q

Flagellum Power

A

When protons flow through the Stator, it changes conformation to push on the Rotor

206
Q

MotA

A

Protein in the stator that changes shape

207
Q

MotA interacts with..

A

the rotor protein FliG

208
Q

OOTW - Borrelia Burgdorferi

A 
causative agent of Lyme disease
•  tick-borne human-pathogen
•  spirochete
•  endo-flagellum
•  rotates cell body to push         through viscous environment
•  requires no iron!
•  has linear chromosome!
209
Q

Swarming Motility

A 
Surface Motility
Social or Group Behavior
Requires Flagella
Requires a surfactant to reduce surface tension
Cells become hyperflagellate
210
Q

Common Features of swarming motility

A

Some become filamentous, division failure
Some become a multinucleoid
Some have two different flagella systems
Swarming thought to be triggered by surface contact

211
Q

Twitching Motility

A

Surface Motility
Type IV Pilus Mediated
Pilus Extends and Attaches
Pilus Retracts and Pulls cells

212
Q

PilA

A

Polymerized at the base of pilus. Pilus extends and binds to a surface.

213
Q

PilT

A

Motor binds to base, burns ATP and pulls PilA subunits into the membrane. Cell is then pulled forward as pilus retracts

214
Q

Gliding Motility

A

REquires slime or surfactant
No visible surface structures
Mechanism of propulsion is poorly understood
Often slow, follow trails, and can reverse directions

215
Q

Focal Adhesion Complexes

A

There must be something that moves on the cell surface. The focal adhesion complex that binds to surface and moves. Leaves latex beds behind.

216
Q

What is required for gliding?

A

AglZ. It’s part of the focal adhesion complex. Cells move relative to stationary foci of AlgZ

217
Q

Possible Gliding Method: Tread

A

Focal adhesion complexes bind surface. Internal helical track moves relative to adhesion complex

218
Q

More Information of Gliding Motility

A

Focal adhesion complexes explain lack of visible external motors. Cell body moves relative to adheasion sites like a tank tread

219
Q

Floating

A

Gas Vesicles

Inflate to rise, deflate to sink. Often found in photosynthetic bacteria.

220
Q

Floating Behavior during Day?

A

Recieve energy from photosynthesis causing it to rise.

221
Q

Floating Behavior during Night?

A

Carbohydrates synthesized and accumulate. Increase in turgor pressure in cell cause it to sink.

BIOL-M 250 (11 decks)

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