MGY377-2

1. 1Gram negative, unlike Gram positive, has a [blank_start]thin[blank_end] layer of peptidoglycan and has an extra [blank_start]outer[blank_end] membrane. It also has a [blank_start]high[blank_end] lipid content and contains a periplasm.

   1. Athin
   2. Bouter
   3. Chigh
2. 2Gram positive bacteria, unlike Gram negative bacteria, has [blank_start]lipoteichoic[blank_end] acid and [blank_start]teichoic[blank_end] acid in its cell structure and has [blank_start]low[blank_end] lipid content.

   1. Alipoteichoic
   2. Bteichoic
   3. Clow
3. 3In E. Coli (Gram -) the composition of the cytoplasmic membrane lipids are: 75% [blank_start]phosphatidylethanolanime[blank_end] ; 20% [blank_start]phosphatidylglycerol[blank_end] ; 5% [blank_start]cardiolipin[blank_end].

   1. Aphosphatidylethanolanime
   2. Bphosphatidylglycerol
   3. Ccardiolipin
4. 4Periplasm only exist in Gram [blank_start]negative[blank_end] bacteria and is the space between the [blank_start]outer[blank_end] and [blank_start]cytoplasmic[blank_end] membrane. It is [blank_start]iso-osmotic[blank_end] with the cytoplasm.

   1. Anegative
   2. Bouter
   3. Ccytoplasmic
   4. Diso-osmotic
5. 5LPS accounts for the [blank_start]lowered[blank_end] drug susceptibility in Gram [blank_start]negative[blank_end] bacteria. When sensed by the immune system, [blank_start]sepsis[blank_end] / septic shock may occur. It is composed of 3 parts: H2Opb [blank_start]lipid A[blank_end] region ; H2Oph [blank_start]O-antigen[blank_end] ; core oligosaccharide region connecting the above 2.

   1. Alowered
   2. Bsepsis
   3. Cnegative
   4. Dlipid A
   5. EO-antigen
6. 6[blank_start]O-antigen[blank_end] in the LPS of Gram [blank_start]negative[blank_end] bacteria contain multiple repeats (4-40) of short oligosaccharide regions and is highly variable among species.

   1. AO-antigen
   2. Bnegative
7. 7Lipid A is the membrane-anchoring region and is made of [blank_start]NAG[blank_end] dimer with 4-7 FA which are all [blank_start]saturated[blank_end]. [blank_start]KDO[blank_end] (not a part of the Lipid A) which is negatively charged help anchor Lipid A to the [blank_start]oligosaccharide[blank_end].

   1. ANAG
   2. Bsaturated
   3. CKDO
   4. Doligosaccharide
8. 8The outer membrane is asymmetric with phospholipids in the [blank_start]inner[blank_end] leaflet and LPS in the [blank_start]outer[blank_end] leaflet. This provides the antibiotic resistance of Gram [blank_start]negative[blank_end] bacteria.

   1. Ainner
   2. Bouter
   3. Cnegative
9. 9Which of the following list has the following molecules in the correct order from high to low membrane permeability?

   1. AH2O > glycerol > tryptophan > glucose
   2. Bglucose > glycerol > tryptophan > H2O
   3. CH2O > tryptophan > glycerol > glucose
   4. Dglucose > tryptophan > glycerol > H2O
10. 10[blank_start]Core oligosaccharide[blank_end] link O-antigen to lipid A and is highly conserved within members of a species. It usually contains [blank_start]heptose[blank_end] and [blank_start]KDO[blank_end].

    1. ACore oligosaccharide
    2. Bheptose
    3. CKDO

11. 11[blank_start]O-Antigen[blank_end] is the H2O ph of LPS and contains lot of variation --> contribute to wide variety of antigenic types of Gram [blank_start]negative[blank_end] species.

    1. AO-Antigen
    2. Bnegative
12. 12KDO and lipid A bind [blank_start]Mg[blank_end]2+ & [blank_start]Ca[blank_end]2+ which explains chelators make Gram [blank_start]negative[blank_end] bacteria more susceptible to antibiotics. The role of the divalent ions is to neutralize the negative charge of membrane lipids to assist tight packing.

    1. AMg
    2. BCa
    3. Cnegative
13. 13[blank_start]LPS[blank_end] is also known as endotoxin because it triggers a hyperactive immune response. The active part of endotoxin is the [blank_start]lipid A[blank_end].

    1. ALPS
    2. Blipid A
14. 14E.coli O157:H7. The O stands for the number of E. coli identified (through [blank_start]O-antigen[blank_end]) and H stands the [blank_start]flagella[blank_end] type.

    1. AO-antigen
    2. Bflagella
15. 15Peptidoglycan account for 50% - 90% of Gram [blank_start]positive[blank_end] bacteria and only about 10% of Gram [blank_start]negative[blank_end] bacteria. It determines the shape of the cell and prevent rupture in medium to low osmolarity solution.

    1. Apositive
    2. Bnegative
16. 16If the cell is popped in a [blank_start]low solute[blank_end] solution, [blank_start]H2O[blank_end] enter and lyse cell.
    If the cell is popped in an [blank_start]isotonic[blank_end] solution, the cytoplasmic membrane leave intact and can grow elsewhere as a [blank_start]protoplast[blank_end].

    1. Aprotoplast
    2. BH2O
    3. Cisotonic
    4. Dlow solute
17. 17The wall glycan of the peptidoglycan is made of [blank_start]NAM[blank_end] and [blank_start]NAG[blank_end]. [blank_start]NAM[blank_end] is only found in bacteria. The wall peptide is connected to the [blank_start]NAM[blank_end]. The wall peptide consists [blank_start]5[blank_end] amino acids.

    1. ANAM
    2. BNAG
    3. CNAM
    4. D5
    5. ENAM
18. 18Transglycosylation occur to polymerize the wall glycan via the [blank_start]transglycosylase[blank_end]. Transpeptidation occur via the transpeptidase and happen by removing one [blank_start]D-ala[blank_end] on the end and link the aa to the [blank_start]third[blank_end] aa (mDap or L-Lys) on another wall peptide.

    1. Atransglycosylase
    2. BD-ala
    3. Cthird
19. 19The wall peptide variation in Gram neg vs Gram pos.
    Second aa --> Gram neg D-iso[blank_start]Glu[blank_end] while Gram pos D-iso[blank_start]Gln[blank_end]
    Third aa --> Gram neg [blank_start]mDAP[blank_end] while Gram pos [blank_start]L-Lys[blank_end]
    The [blank_start]fourth[blank_end] aa is conserved in ALL bacteria.
    mDAP has an extra [blank_start]COO-[blank_end] group.

    1. AGlu
    2. BGln
    3. CmDAP
    4. DL-Lys
    5. Efourth
    6. FCOO-
20. 20In Gram [blank_start]positive[blank_end] bacteria, there is extra [blank_start]glycine[blank_end] amino acids in between L-Lys and D-ala.

    1. Apositive
    2. Bglycine
21. 21Cell Wall synthesis in S. Aureus:
    [blank_start]NAG[blank_end] is first made in the cytoplasm attached to UTP.
    UDP-[blank_start]NAG[blank_end] is then converted to UDP-[blank_start]NAM[blank_end].
    Another NAG is added to the NAM which is now attached to the cell membrane.
    NAM is transferred to a lipid called [blank_start]bactoprenol[blank_end].
    Then [blank_start]MurJ[blank_end] (a flipase) flip the brick to outside of cell membrane for polymerization.

    1. ANAG
    2. BNAG
    3. CNAM
    4. Dbactoprenol
    5. EMurJ
22. 22LPS is similar to peptidoglycan synthesis.
    O-antigen made in cytoplasm on [blank_start]bactoprenol[blank_end] and transferred by [blank_start]RfbX[blank_end] or [blank_start]MsbA[blank_end] 1/2 to the periplasm.
    KDO and outer core is also made in the cytoplasm and transferred to periplasm by the same enzyme.
    O-antigen polymerize in the [blank_start]periplasm[blank_end] on the LPS core.
    Then LPS is transferred to the outer membrane by a multi-protein machinery which gets its energy from [blank_start]ATP[blank_end] hydrolysis.
    
    

    1. Abactoprenol
    2. BRfbX
    3. CMsbA
    4. Dperiplasm
    5. EATP
23. 23Protein A is attached to S. auerus peptidoglycan and bind immunoglobulins. The first(very conserved) part is [blank_start]LPXTG[blank_end] and is recognized by [blank_start]sortase[blank_end]. The second part is made of ~20 [blank_start]hydrophobic[blank_end] residues. The last part consist of 5 [blank_start]positive[blank_end] aa (Lys/Arg).

    1. ALPXTG
    2. Bsortase
    3. Chydrophobic
    4. Dpositive
24. 24Sortase recognizes the LPXTG of Protein A and cleaves between [blank_start]T[blank_end] and [blank_start]G[blank_end] and attach the new [blank_start]C[blank_end] terminus to a wall peptide crossbridge.

    1. AT
    2. BG
    3. CC
25. 25[blank_start]Murein[blank_end] ([blank_start]Braun's[blank_end]) Lipoprotein is the most abundant protein in Gram [blank_start]negative[blank_end] bacteria. Its N terminus Cysteine is modified and carries a [blank_start]glycerol[blank_end] molec where 2 FAs are esterified. It acts as a seatbelt and anchors the outer membrane to the [blank_start]peptidoglycan[blank_end].

    1. AMurein
    2. BBraun's
    3. Cnegative
    4. Dglycerol
    5. Epeptidoglycan
26. 26The [blank_start]lysine[blank_end] residues of the Murein lipoprotein attach to the free COO of the [blank_start]mDAP[blank_end] residue in the peptidoglycan.

    1. Alysine
    2. BmDAP
27. 27The most abundant outer membrane protein is the [blank_start]porins[blank_end] which is divided into two major types : [blank_start]classical porins[blank_end] and [blank_start]specific channels[blank_end].

    1. Aporins
    2. Bclassical porins
    3. Cspecific channels
28. 28[blank_start]Classical porins[blank_end] are nonspecific pores/channels that allow small H2Oph molecules to pass. It forms a [blank_start]trimer[blank_end], each with [blank_start]16ß[blank_end] strands. An examples if the [blank_start]OprF[blank_end] in P. Aeruginosa which allow only small molecules to pass contributing to its hard to treat nature.

    1. AClassical porins
    2. Btrimer
    3. C16ß
    4. DOprF
29. 29[blank_start]Specific channels[blank_end] mediate downhill diffusion of specific nutrients. An example is LamB of E.coli which allow passage of [blank_start]maltose[blank_end] and [blank_start]maltodextrin[blank_end] across the outer membrane and is the receptor for phage [blank_start]lambda[blank_end].

    1. Alambda
    2. BSpecific channels
    3. Cmaltose
    4. Dmaltodextrin
30. 30OM transporters allow transfer of [blank_start]B12[blank_end] and [blank_start]iron[blank_end] siderophores which are too big and too lowly concentrated to pass through [blank_start]porins[blank_end]. These transports are [blank_start]TonB[blank_end] dependent receptors.

    1. ATonB
    2. BB12
    3. Ciron
    4. Dporins
31. 31Two examples of TonB dependent receptors are [blank_start]FhuA[blank_end] which is a ferrichrome transporter and [blank_start]FepA[blank_end] which is a ferric enterobactin receptor.

    1. AFhuA
    2. BFepA
32. 32TonB acts as a "cork" domain and [blank_start]block[blank_end] the TBDTs until the substrates interact with it. TonB with its partners [blank_start]ExbD[blank_end] & [blank_start]ExbB[blank_end] use H+ gradient in the inner membrane to facilitate the release of the substrate into the [blank_start]periplasm[blank_end]. The substrate is passed to a [blank_start]periplasm binding protein[blank_end] and shuttled into the inner membrane through the [blank_start]ABC[blank_end] using [blank_start]ATP[blank_end] as energy source.

    1. Ablock
    2. BExbD
    3. CExbB
    4. Dperiplasm
    5. Eperiplasm binding protein
    6. FABC
    7. GATP
33. 33Which of the following is the least effective antibiotics against Gram negative bacteria?

    1. Arifamycin
    2. Bpenicillin G
    3. CVancomycin
    4. Dchloramphenicol
34. 34There are four basic mechanisms for antibiotic resistance: [blank_start]hibernate[blank_end], [blank_start]destroy[blank_end] the antibiotics, [blank_start]mutate[blank_end] target of antibiotics, [blank_start]keep antibiotic away[blank_end] from target (decrease permeability and increase efflux).

    1. Ahibernate
    2. Bdestroy
    3. Cmutate
    4. Dkeep antibiotic away
35. 35ArC-AcrB-TolC Complex is a channel that span IM to OM. [blank_start]AcrB[blank_end] use energy from the proton gradient to pump antibiotics to the [blank_start]TolC[blank_end] efflux channel. This plays an important role in antibiotic resistance in bacteria and if any of the three components are missing, susceptibility highly increases.

    1. AAcrB
    2. BTolC
36. 36[blank_start]Lytic transglycosylase[blank_end] breaks wall glycan bonds and is divided into two types: [blank_start]glucosaminidases[blank_end] , which break the bond so NAG has the reducing end and [blank_start]muramidases[blank_end] which break the bond so that NAM has the reducing end.

    1. ALytic transglycosylase
    2. Bglucosaminidases
    3. Cmuramidases
37. 37[blank_start]Amidases[blank_end] break bond between wall peptide and NAM. [blank_start]Endopeptidases[blank_end] break bonds between the wall peptides.

    1. AAmidases
    2. BEndopeptidases
38. 38[blank_start]Lysozyme[blank_end] is a muramidase that is produced in human tears that destroy invading bacteria.

    1. ALysozyme
39. 39[blank_start]Lysostaphin[blank_end] is an endopeptidase produced by S. simulans and target S. aureus by cleaving the unique [blank_start]pentaglycine[blank_end] crossbridge.

    1. ALysostaphin
    2. Bpentaglycine
40. 40Round shaped bacteria elongate their walls by [blank_start]elongase[blank_end] complex. [blank_start]MraY[blank_end] and [blank_start]MurG[blank_end] help with lipid addition when NAM is attached to bactoprenol. [blank_start]Mecillinam[blank_end] is a compounds that inhibit PBP2 so bacteria cells cannot elongate further.

    1. Aelongase
    2. BMraY
    3. CMurG
    4. DMecillinam
41. 41In the elongase complex, which of the following is the transpeptidase/transglycosylase?

    1. APBP2
    2. BMraY
    3. CMurG
    4. DMreB
42. 42In the elongase complex which of the follow makes the lipid I, which makes lipid II?

    1. AMraY ; MurG
    2. BMurG ; MraY
    3. CMraY ; MreB
    4. DMurG ; MreB
43. 43In the elongase complex which of the following is proposed to make filaments inside the cell?

    1. AMraY
    2. BMurG
    3. CMreB
    4. DPBP2
44. 44Septum formation during bacteria division is mediated by the [blank_start]divisome[blank_end] which is a transmembrane protein.

    1. Adivisome
45. 45Which of the following components of the divisome is the transpeptidase/ transglycosylase?

    1. APBP3/1b
    2. BMurG
    3. CFtsZ
46. 46Which of the following components of the divisome is the enzyme for synthesizing lipid II?

    1. AMurG
    2. BPBP3/1b
    3. CFtsZ
47. 47Which of the following components of the divisome is the homolog of tubulin and proposed to make filaments inside the cell?

    1. AFtsZ
    2. BMreB
    3. CMurG
    4. DPBP3/1b
48. 48In fluorescence microscopy, energy is absorbed from UV photons and fluorescence is emitted at a [blank_start]longer[blank_end] than initial wavelength.

    1. Alonger
49. 49In immunofluorescence, [blank_start]protein[blank_end] of interest, [blank_start]antibodies against proteins[blank_end], and antibody with [blank_start]fluorescent chromophore[blank_end] against the antibodies is required. The limitation with this is antibodies cannot penetrate [blank_start]living[blank_end] cells.

    1. Aprotein
    2. Bantibodies against proteins
    3. Cfluorescent chromophore
    4. Dliving
50. 50In fluorescence microscopy with fusion, the gene of interest is inserted with GFP protein however it may or may not interfere with the original protein's functions. Two fluorescence proteins discovered is [blank_start]GFP[blank_end] from jellyfish and [blank_start]dsRed[blank_end] from coral. When light is reflected back, the [blank_start]dichoric[blank_end] mirror reflect only the emitted light wavelength to the computer. A limitation is that the [blank_start]Y-axis[blank_end] information is lost.

    1. AGFP
    2. BdsRed
    3. Cdichoric
    4. DY-axis
51. 51In [blank_start]confocal microscopy[blank_end], both the excited and emitted wavelengths of light is focused to reduce [blank_start]background scattering[blank_end].

    1. Aconfocal microscopy
    2. Bbackground scattering
52. 52In [blank_start]TIRF[blank_end] microscopy, light is lit to the inside of a prism and causes [blank_start]total internal reflection[blank_end]. An [blank_start]evanescent[blank_end] light appears right above the prism and light up only a small portion of the cell. Through this method, it was discovered that the [blank_start]elongase[blank_end] complex seems to be oscillating [blank_start]sidewise[blank_end] and not moving horizontally.

    1. Aelongase
    2. Bevanescent
    3. Ctotal internal reflection
    4. DTIRF
    5. Esidewise
53. 53During septum formation in cell vision, an [blank_start]autolysin[blank_end] called [blank_start]AmiC[blank_end] (which is an amidase) cleave the bond between [blank_start]NAM[blank_end] and peptide when a new cross-linked peptide is added by [blank_start]elongase[blank_end].

    1. AAmiC
    2. BNAM
    3. Celongase
    4. Dautolysin
54. 54A(n) [blank_start]operon[blank_end] is unit of genetic material that shares a promoter and operator. A(n) [blank_start]regulon[blank_end] are many different operons that share the same regulation.

    1. Aoperon
    2. Bregulon
55. 55E. coli promoter consists of a -10box ([blank_start]pribnow[blank_end] sequence), -35 hexamer and UP element which is [blank_start]AT[blank_end] rich. The consensus sequence for E.coli after researching 300+ strains is [blank_start]TTGACA[blank_end] -- [blank_start]161718[blank_end] --- [blank_start]TATAAT[blank_end]. [blank_start]recA[blank_end] promoter is an example of a strong promoter that differ by one bases while [blank_start]araBAD[blank_end] is an example of a weak promoter which differ by 5 bases.

    1. Apribnow
    2. BAT
    3. CTTGACA
    4. D161718
    5. ETATAAT
    6. FrecA
    7. GaraBAD
56. 56Bacterial RNAP consist of two identical alpha subnit. The [blank_start]NTD[blank_end] interact with RNAP via beta and beta', and the [blank_start]CTD[blank_end] interact with DNA.

    1. ANTD
    2. BCTD
57. 57RNAP has two [blank_start]distinct[blank_end] beta subunits which carry the catalytic reaction. The [blank_start]omega[blank_end] subunit help beta subunits assemble but little role in transcription. The [blank_start]sigma[blank_end] subunit bind the promoter and correct RNAP.

    1. Adistinct
    2. Bomega
    3. Csigma
58. 58The sigma factor unwind promoter near [blank_start]-10[blank_end] (AT rich) to expose ssDNA. When RNAP undergoes major conformation change and in elongation complex, the [blank_start]sigma[blank_end] factor is left behind with the DNA.

    1. A-10
    2. Bsigma
59. 59The following sigma factors are: [blank_start]d[blank_end] for housekeeping function, [blank_start]s[blank_end] for starvation/stationary phase, [blank_start]h[blank_end] for heat shock, [blank_start]28[blank_end] for flagellar functions, [blank_start]19[blank_end] for Fe transport, [blank_start]54[blank_end] for nitrogen-limitation.

    1. Ad
    2. Bs
    3. Ch
    4. D28
    5. E19
    6. F54
60. 60[blank_start]Class II[blank_end] activators interact with domain 4 of sigma domain. Another class of promoters [blank_start]bend[blank_end] the DNA so suboptimal spacers can still bind RNAP relatively well. [blank_start]Class I[blank_end] activators bind and interact with alpha subunits to increase affinity of RNAP with gene.

    1. AClass II
    2. BClass I
    3. Cbend
61. 61Three types of repression of bacterial gene transcription: [blank_start]simple repression[blank_end] in which there is steric hindrance, [blank_start]looping[blank_end] where the promoter is trapped so RNAP cannot bind and [blank_start]modulation[blank_end] where repressor interact with activators.

    1. Asimple repression
    2. Blooping
    3. Cmodulation
62. 62Lac Operon
    In the absence of lactose [blank_start]LacI[blank_end] bind the operator to prevent RNAP from binding the gene that code for [blank_start]LacZ[blank_end] and [blank_start]LacY[blank_end].
    In the presence of lactose, 2 molecules of lactose bind [blank_start]LacI[blank_end] so RNAP can trasncribe the genes.
    [blank_start]LacZ[blank_end] break lactose into its monosaccharide parts while [blank_start]LacY[blank_end] allow more lactose to enter.

    1. ALacI
    2. BLacZ
    3. CLacY
    4. DLacI
    5. ELacZ
    6. FLacY
63. 63Histidine kinases transfer its auto-phosphorylated P from its [blank_start]His[blank_end] to Response regulator's [blank_start]Asp[blank_end] residue. RR either bind DNA directly or transfer P to another molecule and then another in a [blank_start]phosphorelay[blank_end] system.

    1. AHis
    2. BAsp
    3. Cphosphorelay
64. 64The phosphorylated site in a two component system for eukaryotes is usually phospho[blank_start]histidine[blank_end], phospho[blank_start]aspartate[blank_end]. The prokaryote is usually phospho[blank_start]serine[blank_end], phospho[blank_start]threonine[blank_end], phospho[blank_start]tyrosine[blank_end].

    1. Ahistidine
    2. Baspartate
    3. Ctyrosine
    4. Dthreonine
    5. Eserine
65. 65ArcAB is a system that is turned [blank_start]on[blank_end] when the bacteria has low oxygen. During aerobic metabolism, [blank_start]oxidized[blank_end] Q accumulates and oxidizes the [blank_start]cysteine[blank_end] ([blank_start]twice[blank_end]) in ArcB changing its conformation [blank_start]inactivating[blank_end] it.

    1. Aoxidized
    2. Bcysteine
    3. Cinactivating
    4. Don
    5. Etwice
66. 66PhoP/PhoQ system is important strengthening the outer membrane. [blank_start]PhoQ[blank_end] is negative charged (Asp and Glu) and should be repelled by the membrane but is help close to the membrane by divalent cations such as [blank_start]Mg[blank_end]2+ and [blank_start]Ca[blank_end]2+. Low Mg2+ obviously disrupt this system. [blank_start]Antimicrobial proteins[blank_end] replace the divalent cations and disrupts this system. [blank_start]Low pH[blank_end] neutralizes the charge on the cations deeming them useless.

    1. APhoQ
    2. BMg
    3. CCa
    4. DAntimicrobial proteins
    5. ELow pH
67. 67The [blank_start]PhoP/PhoQ[blank_end] system is essential for [blank_start]Salmonella[blank_end] survival inside us because it is responsible for the adaptive responses to things such as low pH and antimicrobial proteins.

    1. APhoP/PhoQ
    2. BSalmonella
68. 68In the 2 component system, HK [blank_start]sensor[blank_end] domain is least conserved because unique for various signals. HK [blank_start]kinase[blank_end] domain is very conserved and co-evolved with its effectors having slight covariation in sequences.

    1. Asensor
    2. Bkinase
69. 69Four genes responsible for DNA alkylation repair includes: [blank_start]ada[blank_end], [blank_start]alkB[blank_end], [blank_start]alkA[blank_end] and [blank_start]aidB[blank_end].

    1. Aada
    2. BalkB
    3. CalkA
    4. DaidB
70. 70DNA alkylation gene [blank_start]ada[blank_end], the same operon as alkB, accepts the methyl group from DNA damage sites. The [blank_start]C[blank_end] domain interact with RNAP, and its [blank_start]N[blank_end] domain interact with the promoter to increase transcription of other alkylated DNA repair genes. It normally does not bind DNA because of the big [blank_start]negative[blank_end] patch in its sequence but methylation decreases the size of the negative patch.

    1. Aada
    2. BC
    3. CN
    4. Dnegative
71. 71The [blank_start]GroEL[blank_end] & [blank_start]GroES[blank_end] chaperone protein has a H2Opb stripe where the folding intermediate enters. Using [blank_start]7[blank_end] ATP, the protein is allowed to fold into its natural folding state.

    1. AGroEL
    2. BGroES
    3. C7
72. 72Normally sigma H factor is degraded by [blank_start]FtsH[blank_end] along with chaperones' [blank_start]positive[blank_end] regulation. During heat shock, chaperone concentration decreases because surround proteins and therefore sigma H is active for a longer period of time.

    1. AFtsH
    2. Bpositive
73. 73Sigma H coding gene is normally inaccessible to RNAP because it has [blank_start]complementary[blank_end] sequences and fold into a special structure. Heat cause those [blank_start]H-bonds[blank_end] to break and expose [blank_start]AUG[blank_end].

    1. Acomplementary
    2. BAUG
    3. CH-bonds
74. 74[blank_start]Koch[blank_end] discovered Anthrax was spores when his wife gave his a microscope. [blank_start]Pasteur[blank_end] developed the vaccine against Anthrax.

    1. AKoch
    2. BPasteur
75. 75Spore formation is a stress response primarily in Gram [blank_start]positive[blank_end] bacteria during starvation of various nutrients. Spores have high [blank_start]refractivity[blank_end] because of highly concentrated protein levels. [blank_start]Teichoic[blank_end] acid is not present in spores.

    1. ATeichoic
    2. Bpositive
    3. Crefractivity
76. 76The [blank_start]spore coat[blank_end] is the outermost layer in the spore. The [blank_start]spore cortex[blank_end] surround the core and is mostly made of peptidoglycan but there is very little cross-linking; it is also important for the [blank_start]wet-heat[blank_end] stress. The [blank_start]core wall[blank_end] is below the cortex, and its peptidoglycan is very similar to vegetative cell wall. The core has a pH [blank_start]one[blank_end] unit lower than normal cells with the nucleoid bound by [blank_start]SASPs[blank_end]; there is also a high concentration of [blank_start]dipicolinic acid[blank_end] which responds to heat stress.

    1. Aspore coat
    2. Bspore cortex
    3. Cwet-heat
    4. Dcore wall
    5. Eone
    6. FSASPs
    7. Gdipicolinic acid
77. 77[blank_start]SpoOA[blank_end] is responsible for sporulation and is regulated by a two component system. It is activated when multiple signals of starvation is sensed.

    1. ASpoOA
78. 78The steps of spore formation is outlined. First there is [blank_start]polar division[blank_end] then [blank_start]asymmetric[blank_end] cell division. Third is [blank_start]engulfment[blank_end]. Fourth is [blank_start]cortex[blank_end] formation. Fifth is the formation of a [blank_start]spore coat[blank_end]. Then finally the [blank_start]mother cell lysis[blank_end].

    1. Apolar division
    2. Basymmetric
    3. Cengulfment
    4. Dcortex
    5. Espore coat
    6. Fmother cell lysis
79. 79The first step of germination involve [blank_start]water[blank_end] entry into the cell and [blank_start]DPA[blank_end] release. In the second step, [blank_start]cortex[blank_end] hydrolyze and dormancy lost. In the third step, [blank_start]SASPs[blank_end] degrade and cell leave [blank_start]spore coat[blank_end].

    1. Awater
    2. BDPA
    3. Ccortex
    4. DSASPs
    5. Espore coat
80. 80In a flagella, [blank_start]ROTOR[blank_end] is the part of the basal body that rotates while [blank_start]STATOR[blank_end] is the part that remains stationary. [blank_start]Mot[blank_end] of the basal body allow flow of H+ gradient. [blank_start]Fli[blank_end] is the motor switch. [blank_start]Cap[blank_end] aid in flagella assembly.

    1. AROTOR
    2. BSTATOR
    3. CMot
    4. DCap
    5. EFli
81. 81In flagella movement when it is single flagella, it movie [blank_start]counterclockwise[blank_end] for forward movement or [blank_start]clockwise[blank_end] for backward movement. In bundled flagella, counterclockwise movement propel it forward while clockwise movement let it [blank_start]tumble[blank_end] to change directions.

    1. Acounterclockwise
    2. Bclockwise
    3. Ctumble
82. 82[blank_start]Swarming[blank_end] is moving on solid surfaces with some fluid/moisture on it. [blank_start]Gliding[blank_end] is movement without flagella or pili. [blank_start]Twitching[blank_end] is movement on solid surface and facilitated by pili (Type 4).

    1. ASwarming
    2. BGliding
    3. CTwitching
83. 83In Chemotaxis, the Che system plays an important role. In the presence of an attractant, the receptor is unmethylated ([blank_start]CheB[blank_end]) and therefore [blank_start]CheA[blank_end] +P levels are low. In the presence of a repellant, [blank_start]CheR[blank_end] methylate receptor attached to [blank_start]CheW[blank_end] and [blank_start]CheA[blank_end]. CheA is a histidine kinase and +P [blank_start]CheB[blank_end] and CheY. [blank_start]CheY[blank_end] causes tumbling of flagella to move away from repellant.

    1. ACheB
    2. BCheA
    3. CCheR
    4. DCheA
    5. ECheW
    6. FCheB
    7. GCheY
84. 84In the Che system for chemotaxis, [blank_start]methylated[blank_end] receptor respond best to repellants because CheB activity in presence of attractant. [blank_start]Unmethylated[blank_end] receptor respond best to attractants.

    1. Amethylated
    2. BUnmethylated
85. 85Aerotaxis has [blank_start]Aer[blank_end] and [blank_start]Tsr[blank_end] receptors which sense [blank_start]redox[blank_end] changes. It also activate [blank_start]CheY[blank_end] to control the flagella.

    1. AAer
    2. BTsr
    3. Credox
    4. DCheY
86. 86An example of a good biofilm is [blank_start]rhizosphere[blank_end] bacteria that lives on red clover root hair.

    1. Arhizosphere
87. 87Ways that good biofilm help prevent infection is by: [blank_start]blocking binding site[blank_end] for pathogens, [blank_start]competing[blank_end] with pathogens for nutrients, producing [blank_start]anti-microbial[blank_end] compounds and [blank_start]priming[blank_end] our immune responses.

    1. Ablocking binding site
    2. Bcompeting
    3. Canti-microbial
    4. Dpriming
88. 88Advantages to surface sticking include: [blank_start]safety[blank_end] in numbers where predator gets your neighbour before you, [blank_start]buffet[blank_end] benefits where food comes to you and [blank_start]commerce[blank_end] where DNA fragments are swapped.
    Disadvantages include: [blank_start]small town[blank_end] syndrome (stuck where you are), [blank_start]famine[blank_end], [blank_start]bad neighbourhood[blank_end] (neighbours may attract unwanted things).

    1. Asafety
    2. Bbuffet
    3. Ccommerce
    4. Dfamine
    5. Esmall town
    6. Fbad neighbourhood
89. 89The following methods are used to study biofilms.
    [blank_start]Chemostat[blank_end] works by putting something in it and flow through with bacteria.
    [blank_start]Robbins device[blank_end] work by growing microbial culture in pegs and removable studs allow easier research.
    [blank_start]Static system[blank_end] works by growing the cultures in microtitre disks.
    [blank_start]Flow cell[blank_end] works by frowing them on a microscope slide.

    1. AChemostat
    2. BRobbins device
    3. CStatic system
    4. DFlow cell
90. 90In a static biofilm, the free cells are washed off with a strip of biofilm cells growing. [blank_start]Crystal violet[blank_end] is added to dye the bacteria. Alcohol is then used to solubilize the dye to measure the [blank_start]optical density[blank_end].

    1. ACrystal violet
    2. Boptical density
91. 91In [blank_start]pilB[blank_end] mutants, cells sticks to surface but no pods are formed. In [blank_start]flgK[blank_end] mutants, cells do not stick to surface at all.
    Flagella is essential for biofilm formation. [blank_start]motB[blank_end] mutants are unable to make biofilm.
    

    1. AmotB
    2. BflgK
    3. CpilB
92. 92Steps of biofilm formation:
    [blank_start]FlhDC[blank_end] is expressed to control flagella expression.
    [blank_start]OmpR/EnvZ[blank_end] is expressed to control adhesion expression.
    [blank_start]RcsCDB[blank_end] is expressed to control capsule production.
    [blank_start]Exopolysaccharide[blank_end] is made in copious amount in biofilm to cement the bacteria to their surface and can be broken down as food source in times of need.

    1. AFlhDC
    2. BOmpR/EnvZ
    3. CRcsCDB
    4. DExopolysaccharide
93. 93Protein expression during biolfilm formation:
    [blank_start]RbmA[blank_end] is first produced when the bacteria attaches and divide on surface.
    [blank_start]Bap1[blank_end] is then produced in between the bacteria and the surface.
    An envelope is later formed composed of [blank_start]RbmC[blank_end], [blank_start]VPS[blank_end] and Bap1.

    1. ARbmA
    2. BBap1
    3. CRbmC
    4. DVPS
94. 94[blank_start]Antibiotic resistance[blank_end] is genetically encoded while [blank_start]tolerance[blank_end] is resistance present only in biofilms.

    1. AAntibiotic resistance
    2. Btolerance
95. 95In the theory of [blank_start]lack of penetration/diffusion[blank_end], an experiment was done to measure the antibiotic penetrability with different bacterial strain biofilms. The limitation is it applies to some but not all. It may be enhanced by [blank_start]beta-lactamase[blank_end] which breakdown the antibiotics as they diffuse.

    1. Abeta-lactamase
    2. Black of penetration/diffusion
96. 96In the slow growth effect, [blank_start]beta-lactams[blank_end] that target [blank_start]cell wall[blank_end] synthesis is dependent on growth but other drugs such as [blank_start]fluoroquinone[blank_end] which target other growth factors do not apply to this theory.

    1. Abeta-lactams
    2. Bcell wall
    3. Cfluoroquinone
97. 97In the theory of phenotypic tolerance, P. [blank_start]aeuroginosa[blank_end] genome was bashed with many transposon to see which clones would be susceptible to antibiotic. It was found that [blank_start]NdvB[blank_end] plays a role in the resistance. It encodes a glucosyltransferase and make a [blank_start]cyclic-beta-(1,3)-glucan[blank_end] which traps antibiotics. Glucan's function was confirmed using column chromatography. However NdvB seem to be important in only a few strains of Gram [blank_start]negative[blank_end] bacteria.

    1. Aaeuroginosa
    2. BNdvB
    3. Ccyclic-beta-(1,3)-glucan
    4. Dnegative
98. 98The [blank_start]persister[blank_end] theory seems to be more responsible for biofilm resistance because biofilms tend to accumulate more [blank_start]persisters[blank_end].

    1. Apersister
    2. Bpersisters
99. 99Black death was caused by [blank_start]Yersinia pestis[blank_end] ( a Gram negative bacteria). It was spread by fleas. It forms a biofilm in between the [blank_start]esophagus[blank_end] and [blank_start]gut[blank_end] area of the fleas preventing blood from passing. The fleas feed on more blood by biting more into the host and hence enhance transmission.

    1. AYersinia pestis
    2. Besophagus
    3. Cgut
100. 100Y. pestis differ from its close soil harmless relative in that it has two extra plasmids: [blank_start]PMT1[blank_end] & [blank_start]pPCP1[blank_end]. [blank_start]PMT1[blank_end] is responsible for living in the fleas and [blank_start]pPCP1[blank_end] encode proteases. The [blank_start]target capture[blank_end] method to compare ancient and current Y. pestis gene is limited in that you can only get what you're looking for therefore possible ancient genome has an extra pathogenicity island.

     1. APMT1
     2. BpPCP1
     3. CPMT1
     4. DpPCP1
     5. Etarget capture
101. 101Quorum sensing was discovered and studied in bobtail squid. They are colonized by [blank_start]Vibrio fisherii[blank_end] in their light organ. During the day, the [blank_start]concentration of bacteria[blank_end] is low therefore no light is made. The bacteria accumulate and eventually reach high enough concentration at night and produce light. This help get rid of their shadows casted by the [blank_start]stars[blank_end] to avoid [blank_start]predators[blank_end]. The next morning, a large portion of the bacteria is [blank_start]ejected[blank_end] and the cycle starts over.

     1. AVibrio fisherii
     2. Bstars
     3. Cpredators
     4. Dejected
     5. Econcentration of bacteria
102. 102Gram negative autoinducers-1 is derived from [blank_start]acyl-homoserine lactones[blank_end]. Autoinducers-2 is derived from [blank_start]DPD[blank_end].
     Gram positive autoinducers are derived from [blank_start]peptides[blank_end] and modified to be cyclic.

     1. Aacyl-homoserine lactones
     2. BDPD
     3. Cpeptides
103. 103Bacteria that light up marine animals uses [blank_start]luciferase[blank_end] to catalyze the bacteria luminescence reaction. Aldehyde and reduced flavin mononucleotide is [blank_start]oxidized[blank_end].
     [blank_start]FMNH2[blank_end] + [blank_start]RCHO[blank_end] + O2 ---> FMN + RCOOH + H2O + light

     1. Aluciferase
     2. Boxidized
     3. CFMNH2
     4. DRCHO
104. 104In a simply system, AI-1 is made by [blank_start]LuxI[blank_end] and diffused out of cell. AI-1 diffuse into the cell and bind [blank_start]LuxR[blank_end] to turn on/off genes.
     In a 2 component system ([blank_start]V. harveyi[blank_end]), different LuxI like enzymes make different autoinducers. They all bind different receptors but all feed to the same system ([blank_start]LuxU[blank_end]--> LuxO). LuxO make small RNAs which inhibit LuxR making it turn [blank_start]on[blank_end] light genes and [blank_start]off[blank_end] type III secretions.

     1. ALuxI
     2. BLuxR
     3. CLuxU
     4. DV. harveyi
     5. Eon
     6. Foff
105. 105AI-1 and AI-2 are both made from [blank_start]SAM[blank_end]. [blank_start]lasI[blank_end] mutants are unable to form biofilms but restored when add AI-1 to bacteria. Unlike V. harveyi, quorum sensing turn on type III secretions (toxins) for [blank_start]E.coli[blank_end] .

     1. AE.coli
     2. BSAM
     3. ClasI
106. 106Salmonella lack [blank_start]LuxI[blank_end] and therefore does not make AHL but can detect other's autoinducers to turn on its own virulence. It also makes a modified [blank_start]AI-2[blank_end] which others cannot recognize. The AI-2 lacks the [blank_start]boron[blank_end] ring.

     1. Aboron
     2. BLuxI
     3. CAI-2
107. 107In Gram [blank_start]positive[blank_end] bacteria, autoinducers are made and actively exported out of the cell. It binds to membrane receptors and cause a cascade to turn on genes.

     1. Apositive
108. 108Bacteria anti-QS strategies include [blank_start]metabolizing[blank_end] other autoinducers, [blank_start]degrading[blank_end] others' autoinducers ([blank_start]B. subtilis[blank_end]) and using own autoinducers to turn [blank_start]off[blank_end] others' virulence genes.

     1. Ametabolizing
     2. Bdegrading
     3. CB. subtilis
     4. Doff
109. 109In the experiment using [blank_start]P. aeruginosa[blank_end] autoinducers it was discovered that human epithelial cells are highly impermeable for [blank_start]3OC12-HSL[blank_end] and [blank_start]C6-HSL[blank_end]. The degradation is also [blank_start]heat-sensitive[blank_end].

     1. AP. aeruginosa
     2. B3OC12-HSL
     3. CC6-HSL
     4. Dheat-sensitive

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Bachelors MGY377 Quiz on MGY377-2, created by try2bangel on 01/11/2015.

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