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CMMB 343 > last section (after M2) > Flashcards

last section (after M2) Flashcards

1
Q

ORFs in ____ outnumber the amount of ORFs in the human genome

A

micribiome

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2
Q

95% of human microbiota live in the ?

A

GI tract

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3
Q

what organ is similar to a continuous culture system?

A

colon

we shed a LOT of cells every day from the colon

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4
Q

___ and _____ help digest complex carbs?

A
  • Bacteroidetes and Firmicutes help digest complex carbs
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5
Q

10 % of human nutrition is from ?

A

short-chain fatty acids that are produced by bacteria

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6
Q

how is the promotion of b-oxidation by microbes in the human gut beneficial to humans?

A

b-oxidation of fatty acids consumes O2 and releases CO2 which keeps Large intestine in anaerobic conditions, and helps prevent aerobic bacteria like E. coli from growing

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7
Q

IBD is likely the result of ?

A

improper development of gut in infancy and massive changes to diet + lifestyle

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8
Q

obese animals have more of what and less of what??

A

they have more firmicutes and methanogens

less bacteroidetes

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9
Q

High fat/low fiber diet results in

A

obese like microbiota

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10
Q

sec and tat

A

the 2 universal translocases involved in protein secretion

sec: general secretory system
tat: twin-arginine tranpsport

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11
Q

which processes (btw the diff sec and tat stuff) are mediated by PMF, ATP, GTP

A

remember GAP
Sec:
- co-translation of transmembrane proteins into cytoplasmic membrane = GTP mediated
- transportation of UNfolded proteins out of cytosol = ATP mediated

Tat:
- transport of FOLDED proteins out of cytosol = PMF mediated

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12
Q

2 step transport types

A

type II and V
(2 and 5)

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13
Q

1 step transport types

A

I, III, IV, VI
(1, 3, 4, 6)

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14
Q

T2SS

A
  • Protein is moved via Sec or Tat out of inner membrane
  • Proteins then attach to the T2 secretion pore and are pushed out of the outer membrane using ATP to power it
  • Common to remove AB toxins like ExoA or CT
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15
Q

T5SS

A
  • Sec moves autotransporter proteins out of inner membrane
  • Transporter part of protein forms the pore in the outer membrane used to move the passenger part of protein out of cell
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16
Q

autotransporter

A

a type of protein with 2 domains:
- amino end = transporter domain and forms the pore in the outer membrane to move out the passenger domain
- passenger domain is the other half that is secreted

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17
Q

what secretion system is commonly used to move exoenzymes, what are exoenzymes?

A

T5SS
exoenzymes are proteins that function outside of the cell

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18
Q

T1SS

A
  • ABC transporters move proteins across both membranes in ONE step
  • protein goes thru intermembrane transporter to a periplasmic fusion protein via ATP then pushed out outer membrane pore
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19
Q

which secretion systems tend to appear due to random mutations and are sometimes involved in biofilm mediation?

A

T1SS

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20
Q

T3SS

A
  • ONE step
  • Injectosomes: puncture adjacent cells (going thru 3 lipid bilayers)
  • Upon contact, tip fuses w host cell membrane
  • proteins transported via PMF
  • Does NOT move to stab the new host cell
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21
Q

T4SS

A
  • MOST COMMON
  • ONE STEP
  • ATP-mediated
  • conjugation system (HGT, F plasmids)
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22
Q

T6SS

A
  • ONE STEP
  • ATP-mediated
  • T4 phage-like injection
  • MOVING SHEATH / spike
  • microbial warfare
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23
Q

what is the most common SS type?

A

T4SS
(IV)

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24
Q

inducers and corepressors

A

both direct signals
- inducers bind to a TF (repressor or activator) to INDUCE transcription
- corepressors bind allosterically to repressor to HELP it repress transcription

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25
Q

describe the 2 component system:

A
  1. sensor kinase
    - transmembrane his kinase
    - autophosph = activates
    - passes the P to response regulator
  2. response regulator
    - active when phosphorylated by 1
    - binds at operator and acts as a TF

*phosphatase then removes (inactivates) 2

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26
Q

what is quorum sensing

A

a density-dependent mechanism for cellular communication will induce a population or whole community response

regulates: biofilm formation, sporulation, competence, bioluminescence, production of virulence factors

kinda like a threshold activation depending on the conc of a molecule it will activate a response (reached quorum), positive feedback in which it will upregulate the signal molecule

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27
Q

g (-) autoinducers

A

g - bacteria regulate gene expression by making AHL which are autoinducers

  • AHLs DIFFUSE out of cell, increase in conc inside and outside of cells
  • AHLs bind TFs and activate transcription
  • coordinated upregulation of quorum related proteins
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28
Q

g (+) autoinducers

A
  • make oligopeptide AI (AIP)
  • AIPs TRANSPORTED outside of cell
  • activated OUTSIDE of cell
  • AIPs bind sensor kinases, can result in up or down-regulation
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29
Q

how does Aliivibrio fischeri protect the bobtail squid?

A

it provides counter-illumination at night to protect squid while it hunts

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30
Q

pyrogenic infections

A

fever

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31
Q

acne, necrotizing pneumonia, food poisoning, and meningitis are examples of infections caused by?

A

Staphylococcus

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32
Q

disease vs infection:

A

infection: growth of the microorganism in/on a host

disease: injury to the host due to the infection

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33
Q

what is the LD50 or V. cholera and S. dysenteriae?

A

V. cholera: 10^4

S. dysenteriae: 10

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34
Q

defensins

A

punch holes in bacterial membranes, leads to cell lysis of pathogen trying to infect a host

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35
Q

sIgA

A

S. immunoglobulin, an antibody in mucous layer

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36
Q

mucin

A

made of glycoproteins and polysaccharides
contains sIgA and defensins

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37
Q

septicemia

A

growth of bacteria in blood

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38
Q

bacteremia

A

presence of bacteria in blood

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39
Q

what do invasins do in the process of a bacterial infection

A

invasins activate the host cell signaling pathways to reorganize the cytoskeletal actin in order to engulf the bacterium

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40
Q

whats a major virulence factor of intestinal pathogens?

A

IgA protease

destroys Ig proteins to avoid getting coasted in antibodies

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41
Q

what are some ways viruses get nutrients in their host

A
  • can lyse cells to release their nutrients
  • can steal their iron
  • elicit minor immune responses to cause cells to leak nutrients or lyse
42
Q

what are pathogenicity islands?

A

clusters of genes coding for virulence factors in the pathogen’s plasmid genome

facilitate the spread of VFs to other organisms by HGT

43
Q

phage vs prophage

A

phage = bacteriophage is the actual virus that infects the bacteria

prophage = is the genetic information of the virus after it has been inserted and incorporated into the bacterial DNA

44
Q

enterotoxins

A
  • toxins produced by pathogen
  • active in GI tract
45
Q

endotoxin

A

part of cell wall structure of pathogen
lipid A part of LPS in g -
lipoteichoic acids in g +

46
Q

what does HA do?

A

its a polysaccharide that maintains organization of cells in tissues

47
Q

hyaluronidase

A

an enzyme that breaks down HA in ECM to help pathogen invasion of epithelium

48
Q

what bacterial toxin can actually be beneficial for diseases such as cerebral palsy?

A

botulism toxin (BoNT)

49
Q

which bacterial toxin creates flaccid paralysis

A

botulism toxin

50
Q

botulism vs tetanus affects on muscle control

A

*both target SNARE proteins and mess up vesicle fusion with cell membrane tho

bot: this toxin blocks vesicles from fusing w cell membrane, no release of acetylcholine = no muscle contraction (flaccid paralysis)

tet: blocks inhibitory neurons, these then cant release glycine which inhibits the motor neurons from stimulating muscle contraction, leads to not being able to stop contraction (spastic paralysis)

51
Q

what 2 toxins ADP-ribosylate target molecules??

A

Diptheria toxin
cholera toxin

52
Q

cholera toxin does what?

A

elevated cAMP in intestinal cells:

causes NET ANION (-) MOVEMENT INTO LUMEN (out of cells), this causes imbalance of water activity since now there’s way less solutes inside of cells and way more outside of cells, water rushes out of cells

53
Q

what led to the discovery of superantigens?

A

TSS outbreak due to staph aureus infections from giant tampons in 1978

54
Q

are endo or exotoxins usually more potent?

A

exotoxins are usually more harmful
botulism toxin is the worst and is exo

55
Q

basics of innate immune system

A
  • 1st line of defense
  • Automatically recognizes and destroys pathogens and products
  • Innate immune system is ALWAYS ON
  • Fast (within hours or instant results)
  • General (non-specific) response
  • No previous exposure required
56
Q

where do lymphocytes develop?

A

primary lymphoid organs like thymus or bone marrow

57
Q

what can lymphoid precursor cells make?

A

B cells (to plasma)
T cells
NKC

58
Q

myeloid precursor cells make:

A

all the innate immunity cells
dendritic, macrophage, neutrophil, eosinophile, basophil, mast cell

59
Q

most abundant WBC

A

neutrophil

60
Q

granulocytes

A

neutrophils
eosinophils
inflammatory grans

61
Q

describe the inflammation process after tissue damage

A
  • damaged tissue releases chemokines and cytokines, and histamine
  • cytokines activate neutrophils
  • active neutrophils follow chemical gradient of the chemokine attractant
  • neutrophils arrive at damaged tissues with blood, inflammation occurs
62
Q

hematopoiesis

A

blood stem cell division and maturation

63
Q

how do phagocytes recognize pathogens?

A

microbes have unique surface structures (MAMPS), pathogens have PAMPS
phagocytes have PRRs
the PAMP-PRR binding wakes up neutrophils, induces phagocytosis, cytokine production, release of antimicrobials

64
Q

what situation results in a cytokine storm?

A

toxic/septic shock
mass release of histamine, cytokines, etc
causes systemic inflammation
very serious infection

65
Q

MAC attack is?????????

A

the classic activation pathway
C1 –> activates C2 and C4
C4 and C4 split into a + b
C2a and C4b recruit and activate C3 and C5
C3b and C5b recruits C 6, 7, 8, 9 –> these all form the Membrane Attack Complex (MAC)
pathogen cell membrane is lysed

b = bind
a = away

66
Q

which components make up MAC?

A

C5b, C6, C7, C8, C9

67
Q

OPSONIZATION IS

A

Antibody opsonization is a process by which a pathogen is marked for phagocytosis.

68
Q

on phagocytes, what recognizes and binds to antibodies?

A

FcR
(a receptor)

69
Q

which cells release histamine? (update as u go)

A

damaged tissues
mast cells once C3a and C5a have bound to it

70
Q

whats an interferon?

A

a type of cytokine, they are released by infected cells and migrate to surround cells to activate expression of antiviral genes (this will slow and limit the spread of the virus)

interferes w viral infection

71
Q

Virulence factors that assist pathogen avoidance of the immune system include:

A

Immunoglobulin proteases

72
Q

An enzyme that helps pathogens invade deeper into host tissues by dissolving clots:

A

streptokinase

73
Q

Diphtheria and cholera toxin share what in common?

A

Both ADP-ribosylate target molecules

74
Q

what 2 toxins target SNARE protein?

A

tetanus and botulism

75
Q

Hematopoiesis results in:

A

lymphoid and myeloid cells

76
Q

Myeloid antigen-presenting cells (APCs) include:

A

macrophages and dendritic cells

77
Q

T or F: cytokines can induce hematopoiesis

A

TRUE U DUMBASS

78
Q

MAC attack: Which complement proteins do NOT bind to pathogens?

A

C3a and C4a

79
Q

epitopes

A

part of the antigen that interacts w the immune system - this part is what binds w a T cell, antigens can have multiple

80
Q

where do t and b cells mature?

A

b = in bone marrow
t = in thymus

81
Q

where do the macrophages and dendritic cells go after they phagocytosed a pathogen?

A

dendritic will enter lymphatic system
macrophages will stay in the area to continue eating up pathogen

82
Q

where are MHC2s found ?????????????????????

A

only on APCs: dendritic, macrophages, B cells

83
Q

difference btw B and T cells

A

both B and T cells are important components of the immune system, B cells produce antibodies that recognize and mark antigens for destruction, while T cells directly kill infected cells and help to control the immune response.

  • b cells are an APC
  • t cells help kill the virus, also they don’t present an antigen, they bind w an epitope
84
Q

what type of cell will kill our own defective cells (infected or tumors, etc)?

A

NKC

85
Q

Natural killer cells, which are part of the innate immune system, use granzymes to kill their targets. Which other cells of the immune system use granzymes?

A

idk

86
Q

Which of the following viruses does not encode an RNA-dependent RNA polymerase in its genome?

A) Rous Sarcoma virus

B) Measles virus (Morbillivirus)

C) E. coli phage MS2

D) Rabies virus (Lyssavirus)

E) Poliovirus (Enterovirus)

A

A) Rous Sarcoma virus

87
Q

Which protein plays an essential role in both recombination and DNA repair in bacteria ?

A

RecA

88
Q

what do all these do in the lux operon:
LuxB
LuxR
LuxI
LuxA

A

LuxB: Part of the luciferase heterodimer
LuxR: response regulator, transcriptional activator
LuxI: The AHL synthase
LuxA: Part of the luciferase heterodimer

89
Q

Major Histocompatibility Complex (MHC) proteins are expressed on which cells?

A

all healthy cells

90
Q

A bacterial operon that produces a polycistronic mRNA that translates into 5 proteins must always have 5 ribosome binding sites.

A

FALSE

91
Q

Which of the following beneficial functions do GI microbiota perform?

Select 3 correct answer(s)
Question 5 options:

Amino acid biosynthesis

Production of bacteriocins

Production of bile acids

Digestion of complex carbohydrates

A

Amino acid biosynthesis

Production of bacteriocins

Digestion of complex carbohydrates

92
Q

Bacteria present in the blood is called _____. Bacteria growing in the blood is called _____.

A

bacteremia
septecemia

93
Q

what is IgM?

A

IgM is a type of antibody that is particularly effective at activating the complement system, which is an important part of the immune response that helps to eliminate pathogens and damaged cells. IgM has multiple antigen-binding sites and forms pentamers, which allow it to bind to and cross-link antigens more efficiently than other antibody types. This results in the activation of the complement system through the classical pathway, leading to the formation of the membrane attack complex (MAC) and ultimately the destruction of the target cell.

94
Q

The microbiota of most microhabitats are dominated by Gram-positive organisms

A

True

95
Q

Which of the following complement proteins bind to the target cell? Select all that apply.

C8

C1

C3b

C5a

C3a

C2b

A

C3B
C1
C8

96
Q

How do cytotoxic T cells kill pathogens?

A

They induce apoptosis

  1. Recognition: Tc cells recognize and bind to the surface of infected cells, specifically recognizing and binding to peptides presented on the surface of the infected cell by major histocompatibility complex (MHC) class I molecules.
  2. Activation: Once bound to the infected cell, the Tc cell becomes activated and begins to proliferate and differentiate into effector cells.
  3. Perforin and granzyme release: The effector Tc cells release perforin and granzyme molecules, which are cytotoxic molecules that create pores in the membrane of the infected cell.
  4. Apoptosis induction: The perforin and granzyme molecules enter the infected cell through the pores and trigger a process of programmed cell death, or apoptosis, within the infected cell.
  5. Clearance: The infected cell is then cleared by other immune cells, such as macrophages, which engulf and digest the remains of the apoptotic cell.
97
Q

what immunoglobulin makes up the majority of serum antibodies?

A

IgG monomer

98
Q

which Ig will trigger the release of histamine and cytokines?

A

IgE

99
Q

what are intracellular pathogen / virus antigens presented on?

A

MHC1

100
Q

which t cells bind to MHC1? wb MHC2?
what do they release?
what do they cause?

A

Th cells (helper) bind w MHC2 complex, releases cytokines –>inflammation

Tc cells (cytotoxic) bind w MHC1 complex, releases granzyme + perforin –> target cell lysis

101
Q

what will happen if an NK cell sees a cell w out an MHC1?

A
  • Lots of infected cells or cancer cells wont display MHC1  no response from Tc cells to help fight infection and kill the bad cell
  • This is a warning sign for NK cells tho if the cell doesn’t have MHC1  they get suspicious
  • If these bad cells are displaying stress proteins then the NK cells activate and then they release perforin and granzyme  apoptosis
102
Q

what types of genes have not yet been found encoded on any viral genome?

A

Genes for ribosomal proteins and ribosomal RNA

CMMB 343 (3 decks)

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