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Final Flashcards

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Biology 101 flashcards
1
Q

What is the genome of influenza?

A

8 pieces of negative ssRNA

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2
Q

Describe the process of transcription of the influenza genome

A

Genome comes with viral replicase and is a template to make + mRNA which is then translated into 10 proteins

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3
Q

What segments of the influenza genome are alternatively spliced and what do those proteins do

A

segement 7 can make the M1 matrix or M2 protein while segment 8 can make the NS 1 or 2 protein

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4
Q

What is the life cycle of the influenza virus

A

cell takes up virus by fusing membranes together, RNA and RNAP are released into the cytoplasm, they enter the nucleus, transcription is primed via decapitated host cap, then paths diverge

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5
Q

After divergence of paths, what happen in the nucleus for influenza

A

+mRNA is made in the nucleus, mRNA is brough to the cytoplams for translation where is encodes membrane glycoproteins that go to the ER and makes envelope proteins that embed themselves on the surface of the cell to wait for the virus

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6
Q

After divergence of paths, what happens in the cytoplasm for influenza

A

mRNA goes to cytoplasm then nucleus and waits for high concentration where it will switch to replication.
-mRNA is transcribed into +mRNA without 5’ caps allowing full lenght copies of mRNA to be made. This becomes template for multiple copies of -mRNA that are packed by NP protein and transported to envelope proteins.

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7
Q

Once viruses are packaged, how do they leave the cell for influenza

A

Virus buds off cell and neuraminidase cleaves sialic acids that tangle virus only viruses are not infectious yet. Hemagglutinin protein needs to be cleaved into HA1 and 2 via host protease

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8
Q

How does influenza make it into a cell

A

Hemagglutinin binds to sialic acid of cell, cell then takes in virus via endocytosis. Once in endosome of cell, acidification happens to try and destroy virus but this helps virus by altering structure resulting in hemagglutinin conformation change such that membranes fuse together.

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9
Q

How does influenza acquire 5’ caps

A

5’ caps are taken from host mRNA allowing primer for virus to make +ssRNA and stops protein synthesis for host

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10
Q

Why is there no spread of avian influenza from person to person

A

The avain hemagglutinin is likely not able to be process by human proteases into HA1 and 2 so it does not become infectious or the HA might find more receptors in the lower respiratory tract rather than upper tract so not spread as mcuh

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11
Q

What is the use of influenza A having 11 pieces of RNA

A

In the event that disadvantagous mutations occur there will be some outcomes in which the correct 8 segments come together

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12
Q

What is antigenic shift

A

Rapid alteration in genotype and phenotyp of virus due to different RNA segments

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13
Q

What is Antigentic drift

A

random genetic mutation of an infectious agent resulting in changes in proteins

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14
Q

How does antigenic drift happen in influenza

A

viral replicase is not checked resulting in a high mutation rate and a lot of viral deaths

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15
Q

What is the genome of retroviruses

A

two identical +ssRNA strands

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16
Q

What enzymes does retrovirus bring into the cell

A

Reverse transcriptase to make a DNA copy of RNA, integrase to recombine DNA and protease which processes proteins when they leave cell

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17
Q

What are the three genes of a typical retrovirus

A

GAG group antigens that are capsid proteins, POL polymerase and integrase, and ENV envelope glycoproteins

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18
Q

What are the receptors the HIV binds to and how

A

CD4 and either CCR5 that is used for initial infections and CXCR4 used later in infection to attack immune system. Bound to via gp 160 that cleaves into gp 120 and 41 which causes membrane fusion

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19
Q

What is the processes of CD4 infection

A

Once genome is in cell, GAG genes encode capsid protein that goes to nucleus along with other genes for replication. Reverse transcriptase makes a dsDNA copy of genome resulting in LTRs on genome instead of repeats. Integrase uses LTRs to place genome into host genome so that mRNA is made exactly like the one that entered cell

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20
Q

What are the two forms of retroviral mRNAs

A

Spliced which has ENV genes and unspliced which has GAG and POL genes

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21
Q

How does the unspliced from of retroviral mRNA get translated

A

Ribosomes bind to mRNA and translate to stop codon making giant GAG protein that goes through autoproteolysis. 10% of the time stop codon is ignored resulting in GAG and POL protein that is cleaved resulting in reverse transcriptase and integrase. Stop codon is a programmed frameshift due to pseudoknot that confuses ribsome before is continues on with an extra codon

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22
Q

What are the regulatory proteins in HIV 1, what do they do, and when are they expressed

A

nef, negative factor that downregulates CD4 expresssion to prevent superinfection and is expressed early, rev, allows unspliced forms of mRNA into the cytoplasm and is expressed early, and vpu, viral protein U allows viruses to not get stuck to cell once released from cell

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23
Q

What is the genome of coronavirus and what does it enter the cell with

A

+ ssRNA and is a really really big genome and enters cell with exonuclease that proofreads RNAP products

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24
Q

Why are bats great reservoirs of diseases

A

They are the only mammals to fly and have tremendous metabolic demand which might have caused damage to cells releasing a lot of DNA. This likely resulted in bats’ mutation of STING causing a reduced inflammatory response to viurses thus they built tolerance to viral infections

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25
Q

How does coronavirus enter a cell

A

Spike proteins bind to ACE2 and protease which cleaves spike protein into S1 and 2 causing membranes to fuse together and genome to be released

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26
Q

Once coronavirus genome is in cell what happens

A

+ssmRNA is translated and ribosomes make PP1A or PP1AB. Poly proteins are cleaved and begin to assmble replication transcription complex inside the ER. RDRP takes genome and either replicates or transcribes it.

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27
Q

What is the process of RDRP transcription coronavirus

A

-sense genomes are made so that different lenght + sense RNAs can be made. M, E, and S proteins are translated in the ER then go to the Er golgi intermediate complex where the viruses are assembled. N proteins bind to nucleic acids and bring genome to golgi apparatus to leave cell

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28
Q

What are the four structural proteins of coronavirus

A

Spike protein, E (envelop) protein, M (membrane) protein, and N (nucleic acid) protein

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29
Q

What is the difference between PP1A and PP1AB

A

PP1A makes the first 11 non structural proteins while PP1AB makes the first 10 NSPs and NSPs 11-18

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30
Q

What does NSP1 of coronavirus do

A

Stop cell cycle expression of the host by blocking teh 43S complex assembly

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31
Q

How do mRNA vaccines work

A

Cells naturally respond to foreigner mRNA and illicit the immune response but if the uracils are substituted with pseudouridine the body doesn’t fight it off.

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32
Q

What makes C. difficile infectious

A

When antibiotics are used, other bacteria are killed off allowing C. diff to grow in size and generate more toxins making the colon more permeable so inflammatory cells leak into tissue causing over repsonse thus, pseudomembranes

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33
Q

Why was there an increase in gonorrhea with the use of birth control yet decrease in syphilis

A

Glycogen is used by microbiota for E and vagina is usually dominated by Lactobacillus and other species however the use of birth control causes a hormonal change decreasing glycogen thus lactobacilli which inhibits pathogens like gonorrhea and yeast infections

34
Q

What are the three types of exotoxins

A

Those that damage cellular membranes, those that inhibit protein synthesis, and those that activate second messenger pathways

35
Q

How does diptheria cause infection

A

disease is only caused by toxin when a temperature bacteriophage is present and toxin is only released when the bacterium is stressed for iron which the body usually causes

36
Q

What is the process of diptheria infection

A

AB toxin binds to receptor, clathrin-coated pits take up toxin, endosome becomes acidified causing A portion to escape into cytoplasm where is breaks down NAD+ into ADP ribose and nicotinaminde. ADP ribose is linked to EF 2 casuing the inhibition of protein synthesis thus, cell death

37
Q

How does E. coli cause infection

A

Enterotoxigenic E. coli binds to colonization factor allowing intoxication. B subunit of toxin binds to receptor causing endocytosis. Acidification releases A subunit into cytoplams and finds NAD+ and links ADP ribose to adenylyl cylase. Causes adenylyl to be unregulated causing phosphorylation of CFTR pumping Cl- out of cell blocking enterance of NaCl resulting in osmotic imbalance

38
Q

How does E. coli cause infection via secondary messenger pathway

A

E. coli mimics hormone and binds to receptor causing cGMP to be produced which binds to G kinase that phosphorylates CFTR pumping Cl- out of the cell and sodium to be kept out of the cell cuasing osmotic balance

39
Q

Explain the process of how salmonella infect cells via the type 3 system

A

salmonella attaches to M cells and via type 3 system injects SPI1 (pathogenicity island 1). This allows secretion of up to 15 effecotr proteins that help salmonella get in the cell by changing the cytoskeleton of the cell so it takes up the virus. Effector proteins change gene expression in the cell so that cytokines are released that bring in neutrophils that kill salmonella’s competitors via ROSs that creates H2S that salmonella uses for respiration

40
Q

What does salmonella do once in the cell

A

Releases SPI2 effectors in vacuole so that it is invisible to lysosomes. this allows salmonella to replicate in the vacuole while it travels along microtubles to nucleus where it fuses with membranes so salmonella enters the bloodstream

41
Q

What are antibotics

A

substance produced by microorganisms to kill or reduce other microorganisms

42
Q

What are antimicrobials

A

Substance natural or synthetic that kills/inhibits growth of organisms

43
Q

What are sulfa drugs

A

drugs that inhibit metabolite synthesis so bacteria can’t multiply

44
Q

What is the therapeuitc index

A

ratio of toxic dose of antibiotics that are toxic to patient compared to dose that will eliminate infection

45
Q

What are the two types of therapeutic indeces and how do they work for patients

A

Wide therapeutic index allows the patient to take drugs at home while narrow index means the patient should be watched since it doesn’t take to much to cause a toxic reaction

46
Q

What is the difference between bacteriostatic and bactericidal antibiotics

A

antibiotics that keep bacteria from growing while bactericidal kill them

47
Q

How does streptomycin work and how do bacteria overcome it

A

binds to the 30s subunit of bacterial ribosome so that it makes the wrong amino acids. Can be overcome by as few as 2 amino acid changes so that it cannot bind to ribosome

48
Q

What are gram negative bacteria made up of

A

some peptidoglycan, periplasmic space, and an outer membrane

49
Q

What are gram positive bacteria made of

A

lot of peptidoglycan in the cell wall

50
Q

What is peptidoglycan made of

A

Glycan portion that alternates between NAM and NAG linked by beta 1-4 linkages and peptide portion made of four amino acids: L alanine, D glutamic acid, D-alanine and DAP that can form another peptide bond to increase structural integrity

51
Q

How does cross linking occur in gram negative bacteria

A

by connecting adjacent strands of peptidoglycan

52
Q

How does cross linking occur in gram positive bacteria

A

interbridge is used that is made of 5 glycines

53
Q

What is the process of chemotaxis

A

MCPs are exposed to the cytoplasm. Attractant binds to it for a couple seconds then jumps out. The more the MCP is engaged the more Che A is left unphosphorylated. This causes CheA to autophosphorylate itself then the phosphate is transfered to CheB and Y which then goes to basal body of flagellum telling the bacteria to tumble. CheZ takes phosphate off of CheY to stop tumbling

54
Q

How do chemotaxis proteins work

A

CheW connects the MCPs to allow them to communicate. If a MCP senses an attractant while another senses a repellant so CheW will allow the activation of CheA to cause tumbling

55
Q

What is the two component signal transduction system

A

sensory arm that is made of a transmembrane protein and histidine kinase. Once a ligand binds to sensory arm a phosphate is given to response regulator causing change in gene expression

56
Q

What are the porin proteins of E. coli for adaptation

A

OmpF and OmpC. F is for aqueous environments and is larger for more ion intake while C is for the colon and is smaller for lower ion intake

57
Q

How does E. coli use a two component system to maintain osmotic regularity

A

Sudden change in osmotic pressure causes pressure on membrane thus protein changes and phosphorylation of OmpR which will bind to a high affinity and promote transcription of OmpF when in low concentrations. When in high concentrations OmpR binds to high and low affinity sites causing activation of OmpC and repression of OmpF

58
Q

What are plasmids

A

extra chromosomal elements of DNA that use bacterial resources to go through replication

59
Q

What are the two means of plasmid replication

A

Theta and rolling circle

60
Q

How does theta replication work

A

two replication forks so that DNA is replicated in both directions

61
Q

How does rolling circle replication work

A

Nuclease makes a nick in the plasmid of one strand, polymerase binds to 3’ side to add nucleotides making a single strand while the other strand just makes copies of itself

62
Q

What are the two ways that plasmids ensure they live on in daughter cells

A

pR1 system and post translational killing

63
Q

How does the pR1 system work

A

ParC on plasmid binds to ParR polymer, ParM binds to form polymers that bind to ParR, polymer grows to push plasmids to the sides of the cell then degrades

64
Q

how does post translation killing happen

A

Ensures that if a cell does not have a plasmid it is killed. Done via a 2 gene molecule CcdA is antidote while CcdB is toxin that can only be broken down by CcdA. Antidote needs to continuously be produced for cell survival

65
Q

How does symbiotic N fixation work between bacteria and plants

A

bacteria are attracted to plants via flavanoids. As bacteria move towards the plant, Nod factors are released which change gene expression in the plant as well as rhicadhesion which allow the bacteria to adhere to the root hair. Once bacteria infect the plant they proliferate to make a nodule. In the nodule nitrogenase enzymes are made that fix N. Nitrogenase breaks triple bonds in N to produce ammonia which is made into amino acids for bacteria

66
Q

How do cyanobacteria fix N

A

They have specialized cells, heterocysts, that can fix nitrogen. They have specialized membranes that exclude oxygen from entering them so that they can fix N while the other cells can go through photosynthesis

67
Q

Where does does nitrogenase get the E to convert N to ammonia

A

Bacteroids convert sugar in organic acids which is put into the CAC then the ETC to make a PMF for ATP synthesis

68
Q

What happens to bacteria once they make it into the plant for N fixation

A

A shepherd’s hook forms that wraps around the bacteria to hold it, a symbiosome is formed, keeping the bacteria in one place. The bacteria then become bacteroids that contribute to ATP synthesis

69
Q

What do bacteria do in nitrosification, whay do they use for it, and what else is needed for it

A

Converting NH4 to NO2 via ammonia monooxygenase (AMMO). Requires a lot of thylakoid membranes to increase SA for more AMO

70
Q

what is quorum sensing?

A

when bacteria are able to detect population density and alter gene expression

71
Q

How does quoroum sensing work in gram negative bacteria

A

AHLs are specific for each species and diffuse throughout the cell. AHLS bind to LuxR proteins in the cell causing them to from a dimer. LuxR binds to genome causing synthesization of molecules and decrease in synthesization of others.

72
Q

How does quorum sensing work in gram positive bacteria

A

Peptides are sensing molecules that never come back into the cell but attach to a kinase that can phosphorylate response regulators to affect gene expression

73
Q

What are catabolites

A

molecules that are broken down for E

74
Q

How does enzyme induction occur in the lac operon?`

A

Repressor allow a minor amount of transcription which is needed to allow some lactose into the cell. When beta galactosidase is low lactose is isomerized to form allolactose. This binds to the repressor to act as an inducer. The inducer causes a conformational change in the repressor which then cannot bind to the operon

75
Q

How does the CAP protein work in the lac operon

A

When bound by cAMP, CAP site promotes transcription by making the RNAP more stable. But when there is a lot of glucose, cAMP is not being produced so there is a lack of transcription and lactose is not being brought into the cell though some is being transcribed

76
Q

How does the phospho-transferase system work in the lac operon

A

If there is no glucose then enzmyes 2B and 2A become phosphorylated. 2A binds to adenyl cyclase causing cAMP production and affecting the production of glycerol and other carbs. When glucose is present the phosphate goes from 2B to 2A to glucose causing no production of cAMP and 2A to block lactose permease and glycerol transport (inducer exlusion)

77
Q

Explain how the lexA operon works

A

Is a regulon that controls gene repair. When a mutation occurs making ssDNA recA attaches to it and lexA (repressor) so that lexA then degrades itself so that the regulon is then on causing transcription and DNA repair

78
Q

What is a regulon

A

group of genes that are under control of one regulatory molecule

79
Q

Explain tranlesion systhesis

A

The umuDC operon repairs DNA damaged by UV lights. recA stimulates lexA cleavage causing umuDC proteins to be made which allow DNAP to occur across from the damaged DNA dimer. The nucleotides put in are random so mutations are very common

80
Q

How does attenuation works in the trp operon

A

It gets rid of leaking by stopping transcripts from going to completion. A leader peptide is formed by using tandem trps. When there are low levels of trp the ribosome has to wait for the two trps to come indicating that there is a lack of them. When this happens the ribosome covers region one creating a stem loop in regions 2 and 3 which becomes an antiterminator to prevent termination and keep transcription going. When there is a lot of trp, the peptide is easily made thus the ribosome covers region 2 making a stem loop in regions 3 and 4 which becomes a terminator.

Microbiology (5 decks)

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