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Biosci 201 > Modules 1 & 2 > Flashcards

Modules 1 & 2 Flashcards

1
Q

What did frederick griffith do

A

Catalogued bacteria

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2
Q

2 viral strains - Griffiths

A

Rough small = Avirulent
Smooth large = Virulent

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3
Q

Transforming principle

A

Observation that an element of dead bacterial cells can transform avirulent bacterial cells into virulent

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4
Q

Griffith experiment

A

Treated rough strain with heat killed smooth strain, the new strain was now virulent

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5
Q

Avery-Mccarty-Mcleod experiment

A

Proved that DNA was the transforming component in the strain through adding enzymes such as DNAse to see which survived

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6
Q

Franklin & Wilkins

A

Used X-ray diffraction to identify a double helix structure

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7
Q

Chargraff

A

determined that base pairings had equal amounts of corresponding nucleotides

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8
Q

Conservative replication

A

Replication results in a molecule containing parental dna and a new strand

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9
Q

Semi conservative replication

A

Original DNA is split into 2 where one acts as a template for a new strand

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10
Q

Dispersive replication

A

Original DNA is chopped up and dispersed in a strand

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11
Q

Components of replication fork

A
  • Helicase
  • Pol E
  • PCNA
  • Pol A
  • Pol D
  • RPA
  • RFC
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12
Q

Helicase function

A

Unwinds parental DNA using ATP

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13
Q

Pol E function

A

Replicative polymerase that extends leading strand

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14
Q

Pol D function

A

Replicative polymerase that extends the lagging strand, associates with PCNA

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15
Q

PCNA function

A

Acts as a clamp holding Pol E and D, stabilises them

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16
Q

Pol A function

A

Makes a complex with primase to synthesise primers for the lagging strand

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17
Q

RFC function

A

Clamp loader which opens the PCNA ring to enclose the DNA synthesised by Pol A

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18
Q

RPA function

A

binds to ss DNA to extend it , orientate it and protect it

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19
Q

Prokaryote replication

A

Has one point of origin, DNA unwinding site rich in AT

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20
Q

Eukaryote origin replication complex

A

Made of 6 proteins and loads CD factors, defines the orgins (pre-licensing)

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21
Q

What are replicons

A

Made of 2 replication forks which initiates synthesis

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22
Q

What is the initiation of DNA replication synchronised with

A

Cell cycle

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23
Q

What controls the cell cycle

A

Cyclins and cyclin dependant kinases

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24
Q

Cyclins and their roles

A
  • B = block DNA synthesis
  • D = activate G1/S cyclins
  • E = restriction point
  • A = Activates helicase
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25
Q

Transition to S phase

A
  • Growth factor activates Cyc D and CDK4/6 (G1 cyclin)
  • CDK phosphorylates pRB
  • E2F TF s released which activates the transcription of S genes
  • E2F upregulates G1/S cyclins
  • G1/S CDK phosphorylate SIC1
  • G1/S CDK is now active
  • Cyclin A (S phase) phosphorylate helicase and loading factors in ORC
  • ORC dissasociates
  • CDC45 bind to helicase and activates it
  • Pol A makes primers
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26
Q

mRNA processing (module 1)

A
  • 5’ capping = protects mRNA from enzymatic degradation and aids with export
  • processing of 3’ end = endonuclease creates a free 3’ - OH
  • Polyadenylation of 3’ = Adds adenylic acid using Poly A and ATP
  • Splicing = removes introns
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27
Q

Degenerative code

A

Not every codon codes for a unique amino acid

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28
Q

Translation initiation (module 1)

A
  • EIF2 with GTP binds to met- tRNA
  • 40s subunit binds to EIF1, 3 & 1A PIC forms
  • EIF complex forms recognising the poly A binding protein & 5’ cap
  • mRNA loop formed, activated
  • PIC binds to activated mRNA
  • Kozak sequence identifies the start site
  • tRNA binds to start codon = GTP hydrolysis triggered
  • 60s subunit binds
  • EIF1A binds to A site and is then released if everything is correct
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29
Q

Translation elongation

A
  • aminoacyl tRNA is delivered as a complex with EF1 A
  • complementary codon and anticodon bind at the decoding site
  • Ribosome proofs interaction
  • GTP hydrolysis occurs releasing EF1 A
  • tRNA in site A moves towards tRNA in site P
  • amino acid in A binds to met tRNA
  • EF2 binds and pushes mRNA and tRNA along using GTP
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30
Q

Translation termination

A
  • ERF1 recognises stop codons
  • ERF3 associates and hydrolyses GTP to release the polypeptide chain
  • components of the ribosome are recycled
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31
Q

Causes of mutation

A
  • UV
  • Chemical modification
  • Reactive oxygen species
  • Cosmic radiation
  • Errors in replication
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32
Q

Exouclease role

A

Proofreads in 3’ to 5’

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33
Q

Common mutations

A
  • Spontaneous deamination of cytosine
  • Benzylprene inserts itself into the double helix to disrupt it
  • Thymine dimer formation causes a bulge in DNA
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34
Q

Direct reversal of damage

A
  • Photolyase in plants uses visible light to reverse formation of thymine dimers
  • Methyl guanine methyl transferase removes methyl from guanine in O6 position and moves it to its own active site (enzyme dies after)
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35
Q

Base excision repair

A
  • DNA glycosylase removes incorrect base leaving a abasic site
  • APE1 endonuclease cleaves abasic site
  • DNA polymerase B fills gap with correct nucleotide
  • DNA ligase binds new nucleotide
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36
Q

Mismatch repair

A
  • MSH2 and MSH6 bind to mispaired segment
  • MLH1/PMS2 binds
  • DNA helicase unwinds DNA
  • DNA exonuclease removes mismatched segment
  • DNA polymerase and ligase repair section
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37
Q

Nucleotide excision repair

A
  • XPC looks for lesions
  • TF2H recruited as it has a helicase unit
  • TF2H unwinds DNA using ATP
  • RPA binds to form a protective bubble
  • XPG & XPF act as endonuclease and cut damaged DNA
  • DNA polymerase and ligase seal gap
38
Q

2 methods for double strand breaks

A
  • non homologous end joining
  • Recombinatorial repair
39
Q

Non homologous end joining

A
  • KU80/70 heterodimer and DNAPK bind the ends of DNA together
  • DNA ends are resectioned using artemis exonuclease
  • DNA ligase ligates ends together
40
Q

Recombinatorial repair

A
  • 5’ exonuclease digests broken end of template strand creating a 3’ end
  • unbroken daughter strand is ligated to the unreplicated portion of the parent chromosome
  • RecA/Rad51 bind and cause strand invasion
  • Loop of ss DNA created
  • Holliday junction forms
  • Crossover and ligation occur to generate a structure similar to replication fork
41
Q

Primary structure protein

A

Sequence of amino acids

42
Q

Secondary structure protein

A

3D shape

43
Q

Tertiary structure protein

A

How secondary elements fold together

44
Q

Quartenary structure protein

A

How proteins fit together

45
Q

Adaptation stage CRISPR cas9

A
  • bacteria identifies pathogen
  • CAS 1 + 2 assemble and cut out a short protospacer
  • Protospacer integrated into CAS 1+ 2 and becomes apart of CRISPR array
  • Array now has the pathogen as a ‘memory’
46
Q

crRNA maturation CRISPR Cas9

A
  • Cas acts as nuclease and cleaves palindromic sequence in CRISPR array
  • crRNA binds to CAS9
47
Q

Interference CRISPR Cas9

A
  • Mature crRNA acts as a template to attack pathogen
  • crRNA recognises pathogenic DNA
  • Cas9 acts as a nuclease to cut the DNA to make it unfunctional
48
Q

Targeted cleavage by Cas9

A
  • crRNA binds to tracrRNA to form a complex
  • complex recognises incoming DNA
  • PAM sequence binds to incoming DNA and aids with recognition for CAS9
  • R loop forms forming 2 different nuclease active sites
  • DNA is cut causing a double strand break
49
Q

Cas9 structure

A
  • Nuclease lobe = binds to target DNA
  • Helical recognition lobe = binds to guide RNA
50
Q

Role of RNA pol 1

A

transcribes pre r-RNA which is involved in ribosome components etc

51
Q

Role of RNA pol 2

A

transcribes mRNA etc, involved in RNA splicing and post transcription gene control

52
Q

Role of RNA pol 3

A

transcribes sort non coding RNAs such as tRNA

53
Q

RNA pol 2 structure

A
  • Unique transcription factors
  • Differs in alpha subunits from pol 1 and 3
  • Beta unit has a CTD which is the site for phosphorylation
54
Q

essential features for RNA synthesis

A
  • polymerisation is dependent on a template
  • polymerisation is 5’ to 3’
  • Watson crick base pairing
  • Transcription requires a promoter to start
55
Q

Stages in transcription

A
  • Initiation
  • Promoter clearance
  • Limited polymerisation
  • CTD phosphorylation
  • Elongation
  • Termination
56
Q

Transcription initiation

A
  • TF2D binds to TATA box in the minor groove which causes a bend
  • TF2A and TF2B bind to the TF2D complex
  • TF2B binds around the TAT box to stabilise
  • TF2A crosslinks proteins to DNA
  • TF2B recruits DNA pol 2 and TF2F
  • TF2F acts as helicase to melt
  • DNA pol 2 is stuck so TF2H has to come
  • TF2H is docked via TF2E
  • TF2H unwinds DNA infront of DNA pol 2
  • TF2H phosphorylates CTD using ATP
  • PIC open and promoter cleard
  • RNA pol 2 undergoes confrontational change and releases TF2
  • RNA pol 2 now interacts with elongation factors
57
Q

pre - rRNA processing

A
  • Nuclease cleavage via ribozyme
  • Chemical modification = pseudoridylation and methylation
58
Q

pre tRNA processing

A
  • Trimming of 5’ end via ribozyme
  • 3’ UUU replaced by CCA
    -Anticodon loop reconstructed via splicing
  • Chemical modification
59
Q

5’ capping (module 2)

A
  • Gamma phosphate is hydrolysed via phosphohydrolase
  • Guanine transferred from GTP to 5’ end via guanine transferase
  • Guanine is methlated
60
Q

Splicing (Module 2)

A

-U1 binds to 5’ splice site
- U2AF removes SF1 and allows U2 to bind to branch point
- U4-6 bind forming the spliceosome
- U6 unwinds from U4, U4 is removed
- U6 and U2 hydrolyse and have a conformational change activating the spliceosome
- 2 transesterification reactions take place

61
Q

3’ Polyadenylation (Module 2)

A
  • CPSF and CSTF bind to pre mRNA
  • CF1 & 2 recruited and bind to CSTF
  • Poly A polymerase binds to the 3 complexes
  • CF1 & 2 cleave the mRNA
  • PAP polymerises
  • PABP stabilise the PAP
62
Q

FG- Nucleoporin

A
  • Involved in the transport of mRNP
  • FGNP fill nuclear pore and interacts with mRNP allowing it to unfold
63
Q

HIV

A
  • Has a REV protein which binds to sequence elements on unspliced mRNA marking it as ‘spliced’ so the mRNP exporter transports the whole genome
64
Q

Euchromatin

A

Decondensed

65
Q

Heterochromatin

A

Condensed

66
Q

Distal promoters/enhancers

A
  • Distant from start site
  • Upstream
  • Mutations affect transcription but dont disrupt it
  • Gene specific
67
Q

Core promoter

A
  • Present in every gene
  • Vital to transcription
  • Forms PIC
68
Q

Ways to remodel chromatin

A
  • Chemical modification
  • Slide apart nucelosomes
  • Pop histones in and out
  • Modify DNA
69
Q

Acetylation

A
  • Decondenses chromatin
  • Always associated with gene activation
  • Reduces positive charge on histones to weaken interactions with DNA
70
Q

Methylation

A
  • Condenses chromatin
  • Associated with long term gene repression
71
Q

Mechanical modification of chromatin

A
  • SWI/SNF bind to condensed chromatin
  • Pushes nucleosomes apart using ATP
  • Enhancers bind and recruit TF
  • TF are enzymatic remodellers and pushes nucleosomes apart untill core promoter is exposed
  • PIC assembles
  • Mediator bridges TF with PIC
  • ## Chromatin loop forms creating a signal for gene activation
72
Q

Why was splicing maintained in evolution

A
  • Helps create multi domain proteins
  • Alterntive splicing can create many different proteins from a single gene
73
Q

Cryptic vs Non cryptic intron

A

cryptic intron has an altered base making it have a decreased affinity at the branch site for U2 and needs a splicing activator

74
Q

Sexual differentiation in flys summary

A
  • sxl protein is only produced in females via casette splicing
  • sxl repressors splicing in Tra protein in females, via alternative 3’ splice site
  • Only functional Tra protein in females
  • Tra protein binds to Rbp1 which activates splicing in dsx protein in females
  • dsx protein = alternative poly (a) splicing
  • dsx protein has a cryptic intron
75
Q

role of dsx protein

A

dsx protein repress the transription of genes required for sexual differentiation in opposite sex

76
Q

female sxl gene

A

acetylated which makes it automatically active

77
Q

male sxl gene

A

methylated condenses and a translation stop codon gene which makes it inactive

78
Q

translation repressor

A
  • binds do eif4 complex
  • displaces factors causing the mrna loop to open
  • can also affect the mrna integrity and will make it cleaved
79
Q

translation activator

A

enhance the efficiency and binding of eifs

80
Q

Exosome pathways

A
  • decapping = removes cap and eifs fall off causing loop to open
  • deadenylation = shortens poly a tail, decreases PAPB which opens loop
  • endonucleolytic = mrna is completely degraded
81
Q

active vs dormant mRNA

A
  • dormant mRNA has a short poly(a)tail which has maskin and cpeb making it stable
  • active mRNA has a long poly(a)tail with initiation factors bound
82
Q

dormant mRNA in pregnancy

A
  • eggs have all dormant mRNA needed for stages after fertilisation
  • when progesterone spikes it signals CPEB kinase
  • kinase phosphorylates CPEB and maskin is released
  • CPEB recruits PAP which extends poly(a)tail
  • mRNA is now active
83
Q

Ferritin role

A

iron quencher which decreases the availability of iron

84
Q

TFR role

A

iron transporter

85
Q

Low iron enviro

A

ferritin is down regulated and TFR is upregulated
IREBP is active and binds to IRE

86
Q

High iron enviro

A

ferritin is up regulated and TFR is downregulated
IRE-BP undergoes a conformational change and cannot bind to mRNA

87
Q

Regulator of iron

A

IRE-BP which is an allosteric protein

88
Q

IRE-BP role

A

activator of TFR and repressor of ferritin

89
Q

miRNA role

A

inhibits translation

90
Q

siRNA role

A

inhibits translation and degrades the mRNA

91
Q

RNA interference

A
  • primary miRNA transcribed by RNA polymerase 2 forming a hairpin loop
  • Drosha binds and cuts both strands at ss regions
  • precursor RNA made
  • Drosha dissociates
  • Dicer binds and cuts at the loop at the ds region
  • cuts made are uneven leaving a 2nt hangover
  • RISC with argonaut binds to miRNA that will hybridise to mRNA
  • miRNA will inhibit translation
  • siRNA will cleave the mRNA
92
Q

DSB repair mechanisms which result in the inclusion at a specific site

A
  • Nonhomologous end joining
  • Homology directed repair = uses a template with a point mutation to introduce it into the DNA which allows for targeted and specific genome edits

Biosci 201 (2 decks)

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