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CEDB30002 Cell Biology > Core Cellular Functions - Transcription and Translation > Flashcards

Core Cellular Functions - Transcription and Translation Flashcards

1
Q

What did Avery and Macleod show?

A

DNA is the heritable material.
• Smooth bacteria (S) = pathogenic
• Random mutation, rough (R) = not pathogenic
• Live R strains transformed by dead S trains and progeny are S/pathogenic
• Therefore the molecules with heritable information were in S cells
• Fraction up S cells to molecules (RNA, protein, DNA, lipid, carbs)
o See in R cells transformed
o R cells only transformed with DNA addition

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2
Q

What controls transcription?

A

Proteins binding to regulatory DNA sequences.
General transcription factors (eukaryotes).
Interactions between RNA polymerase II, promoters and activator proteins.

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3
Q

What allows transcription to occur in a specific manner?

A 
Tissue specific activator proteins
o	Regulatory or transcription factors 
o	Bind gene promoters
o	Interact with RNA polymerase 
o	Control expression via presence/absence, ability/inability to enter nucleus
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4
Q

What are characteristics of gene activator proteins? What are some examples to show this?

A

Modular structure
 E.g. Gal4 protein has Gal4 DNA binding domain and Gal4 activation domain (gene for galactokinase on)
 Swap for LexA DNA binding domain (still have Gal4 activation domain)
 Recognise LexA sequence, interact with TATA, lacZ on

Work synergistically
 E.g. more product if more gene activator proteins

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5
Q

What usually makes up the gene control region?

A

regulatory sequences, regulatory proteins, TATA box in promoter, GTFs, RNA pol II, the gene

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6
Q

How can gene activator proteins alter chromatin structure? What does this allow?

A
  • Altered to allow transcription to occur
  • Loosen up nucleosome, easier to access DNA
  • Chromatin remodelling complex – remodel nucleosomes
  • Histone chaperon – remove or replace histones
  • Histone modifying enzyme – specific histone modification (e.g. acetylation)
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7
Q

How can repressor proteins inhibit expression?

A
  • Antagonise activator proteins
  • Competitive DNA binding
  • Masking activation surface
  • Direct interactions with GTFs
  • Recruitment of chromatin remodelling complexes
  • Recruitment of histone deacytelases
  • Recruitment of histone methy transferase (methylation)
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8
Q

Do activator and repressor proteins usually act as a single protein?

A

No

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9
Q

What can impact whether co-operative binding occurs prior to transcription?

A

Motif orientation, motif relative position, motif distance

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10
Q

How is combinatorial control of transcription showed by Eve stripe 2?

A
  • Competition between regulatory proteins
  • Region where it is turned on has high levels of hunchback and bicoid activators and low levels of giant and kruppel repressors
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11
Q

What does glucocorticoid hormone show about combinatorial control?

A
  • Genes expressed to low level when glucocorticoid receptor absent of glucocorticoid
  • Glucocorticoid binds to receptor, expression of the genes increases
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12
Q

In what ways can the activity of gene regulatory proteins be regulated?

A
  • Protein synthesis
  • Ligand binding
  • Covalent modification (phosphorylation)
  • Addition of second subunit
  • Unmasking
  • Nuclear entry stimulation
  • Membrane release
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13
Q

What does eyeless demonstrate about cell fate ad regulatory proteins?

A

• Entire organ formed by expression of single gene regulatory protein
• Master regulator
• Can grow eyes on legs
Cell Fate can be determined by accumulation of different gene regulatory proteins (different regulatory proteins = different cell fate)

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14
Q

How can ligands turn genes on or off?

A

Bind and remove regulator from DNA.

Bind and allow regulatory protein to bind DNA.

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15
Q

How can the lac operon act as a genetic switch?

A
  • Activator (CAP)
  • Repressor (Lac repressor)
  • LacZ broken down to galactose and glucose
  • High lactose and low glucose = need lacZ
  • High lactose: bind lac repressor, remove from DNA
  • High glucose: less cAMP, CAP dissociates from DNA
  • Activation when repressor not bound and CAP is bound
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16
Q

What is special about the transcription of globin genes?

A
  • Transcribed in erythroid cells at different stages of development
  • Each has a set of regulatory proteins for turning on when right time
  • Share common regulatory region upstream (locus control region LCR) which amplifies transcription (lots of globin made)
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17
Q

What is the role of insulator elements?

A

Between genes prevent enhancers activating wrong gene

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18
Q

How can boundaries of a gene be defined?

A

Transgenic rescue of mutant phenotype

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19
Q

What makes up DNA? What happens for it to become final mRNA?

A 
DNA
•	Promoter
•	TATA box
•	5’ UTR
•	Exons (coding region) 
•	Introns (coding region)
•	3’ UTR
 Spliced into exons
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20
Q

What makes up the splicesome?

A

SnRNAs and protein

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21
Q

What sequences are involved in intron removal sites?

A
  • 5’ AG – A – G 3’

* Consensus sequences at end of intron and in middle

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22
Q

What is the process of intron removal?

A
  1. Initiated by A residue in intron attacking 5’ splice site (form looped intermediate)
  2. 3’ OH group release, attaches to start of next expn, two exons joined, intron released as lariat
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23
Q

Which splice site (3’ or 5’) acts as the donor and which acts as the acceptor?

A
  • 5’ splice site is donor

* 3’ splice site is acceptor

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24
Q

What is special about the drosophila Dscam gene?

A
  • 4 blocks of exon, but only one exon taken from each block for each final mRNA
  • 38,000 possible mRNAs
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25
How can B cells produce secreted antibodies that have the same specificity as membrane bound antibodies?
• Antibody mRNAs have two different lengths to allow this • Long RNA transcript o Intron sequence removed o Terminal hydrophobic peptide o Hydrophobic = want to be membrane bound • Short RNA transcript o Intron sequence not removed, acceptor splice junction missing o Terminal hydrophilic peptide o Hydrophilic = happy to be secreted
26
How can activators and repressor proteins regulate splicing?
• Negative Control o Repressor present, lessens signal, prevents splicing • Positive Control o Activator present, amplify signal, promote splicing
27
What happens during sex determination in drosophila?
o X chromosome/Autosome ratio o Males X:A 0.5 o Females X:A 1 o Sxl gene product (sex lethal gene. Activates pathway for female) o Tra gene product (transformer = RNA binding protein) o Dsx gene product (doublesex = transcription regulator) o Female: splice site blocked, all proteins functional and repress male differentiation genes o Male specific exons contain stop codons
28
What are cis and trans splicing and how are they different?
Cis splicing: same gene | Trans splicing: between 2 genes
29
What is drosophila mdg4 gene an example of?
Trans splicing
30
What is a SL sequence?
worms, independently transcribed and spliced onto most mature RNAs in cell, giving common 5’ end
31
What is RNA editing?
• Nucleotide insertion/deletion • Editing (deamination) o C to U o A to I
32
How do octopi show an example of RNA editing?
in colder environments, lots more A to I editing than warmer climates
33
How can processing of apolipoprotein-B mRNA impact it’s function as a protein?
 Not edited in liver = apo-B100 protein: cholesterol transport in blood  Edited in intestine = apo-B48 protein: lipid absorption
34
How is circular RNA viewed these days? Why?
* Abundant, stable, conserved, non-random, potentially functional * Exon skipping means lariat might have exons that can be further spliced
35
What are Small RNAs?
Small RNAs • 21-24 nt • Gene silencing (post transcription) via affecting mRNA translation or stability • Transcriptional gene silencing via epigenetic modifications to chromatin
36
What are miRNAs?
MiRNAs • microRNAs • Regulate gene expression by blocking translation of selective mRNAs • mRNA slicing and translational repression • Originate from cell genome • Trans acting regulatory factors encoded for by MIR genes
37
What are siRNAs?
* Small interfering RNAs * Turn off gene expression by directing degradation of selective mRNAs and establishment of compact chromatin structure * Post transcriptional and transcriptional gene splicing * Originate from exogenous dsRNA * Cell defence mechanism against exogenous dsRNA
38
How can small RNAs silence genes?
Post transcriptional or transcriptional (siRNA) mRNA slicing or translational repression (miRNA)
39
What is the action of Dicer and Argonaut?
• dsRNA processed by Dicer (DCL, dicer like) and its homologues into short RNA duplexes o cleave dsRNA into uniformed pieces • small RNAs associate with members of Argonaut family and silenced o bind small RNAs and targets o catalytic parts of RNA-induced silencing complex (RISC) o Cleave one strand, expose other strand, match up to complimentary mRNA
40
What is RISC? What is it made of?
RNA-induced silencing complex | Made up of Argonaut
41
How do miRNAs and siRNAs differ?
Post transcriptional or transcriptional (siRNA) mRNA slicing or translational repression (miRNA) siRNA = Originate from exogenous dsRNA and Cell defence mechanism against exogenous dsRNA miRNA = originate from genome
42
Where are miRNAs and AGO proteins located?
In P bodies
43
How can siRNAs protect cells?
``` defenders o suppress invading virus (interfere with replication( o silence aberrant RNA o silence transposons o Maintain genes in silent state ```
44
What makes up TMV (Tobacco mosaic Virus) ? How can it be silenced?
o Coat protein subunits, ssRNA genome which encodes CP and RdRp o During replication, ds intermediate formed o Cleaved by DCL, produce siRNA, associates with AGO, silence virus replication and expression
45
How can viruses avoid RNA silencing?
Suppressor Proteins
46
Using an example show how siRNAs aid host plant recovery and resistance to viruses
o Younger leaves virus free (resistant) because RNA silencing has been induced from previous infection o Small RNA homologous to viral RNA present in leaves previously infected by virus o Virus infection = systemic siRNA accumulation
47
What is the action of miRNAs?
• Silence mRNAs (plants, good fidelity) or interfere with translation (animals, poor fidelity)
48
How are MIR genes transcribed?
o Encode miRNAs o Primary miRNA folds back into ds structure and then processed by dicer to shorten o The other strand is degraded and the target strand can bind target mRNA
49
How can miRNAs impact vegetative phase change?
o Juvenile to adult growth leaf changes o miR156 overexpression = longer juvenile phase o Targets SPL (promoter for phase change) o WT = miR156 expression decreases with age to encourage phase change as SPL accumulates o MiR156 resistant SPL have early phase change (SPL not inhibited)
50
How do miRNAs differ between plants and animals?
* Animals: block protein translation (low fidelity) | * Plants: slice target mRNAs (high fidelity)
51
How does DEK1 show the benefits of using DEK1 in research?
Knock out DEK1 = lethal | Knock down with miRNA = viable but no epidermis
52
How do bacteria protect themselves from viruses? What system do they use?
CRISPR System • Use small noncoding RNAs • Bacterial genome has CRISPR locus • Short viral DNA sequence integrated into CRISPR locus • RNA transcribed from locus, processed, bound to Cas protein • Small crRNA in complex with Cas seeks out and destroys viral sequences
53
When does protein folding usually begin?
Translation
54
When are proteins in molten globule states? What does this mean?
``` • Initial structure = molten globule o Not final o Need energy input o Final state = favourable in terms on energy o Chaperones help ```
55
What is required for proteins to leave the molten globule stage?
Energy/ATP
56
Why are many chaperones HSPs?
Because heat denatures proteins
57
What are HSP60 and HSP70?
* Large protein families, different members function in different organelles * Both pathways require energy (ATP hydrolysis)
58
How do HSP60 and HSP70 differ?
HSP70 functions early (translation) whilst HSP60 functions later
59
What is the action of HSP70?
* Functions early (translation) * Prevent hydrophobic patches of AA aggregating and trapping protein in wrong conformation/aggregating * Stretches of AAs bind to peptide binding grove on HSP70 and ATP hydrolysed to ADP (prevent aggregation) * Occurs as polypeptide emerges from ribosome * Multiple cycles
60
What is the action of HSP60?
* Functions later * Form barrel structures * Mis-folded protein captured when hydrophobically interacts with barrel rim * ATP binding and GroES cap widen barrel, stretch protein * Protein in enclosed space, refolding occurs and ATP hydrolysis weakens complex * Protein released after more ATP binding * Cycle can repeat
61
What is the 26S proteasome? What components does it have?
* ATP dependent protease that degrades aberrant proteins * 20s core particle = gate * 19s regulatory particle
62
What is the action of the 26S proteasome?
* 20s core particle = gate * 19s regulatory particle = receptor for proteins that need degrading, transfers to catalytic core * Degrades polyubiquitinated proteins
63
What does ubiquitin ligase do? Is it a random process?
* Selectively ubiquitinate target proteins | * Not a random process
64
What is the role of the F-box/E3?
receptor that binds specific site on target protein
65
What is the role of E2?
* Ubiquitin polypeptides added to lysines on target protein | * Protein marked for degradation
66
What is the process of ubuitinylation?
* F-box (E3) = receptor that binds specific site on target protein * Ubiquitin polypeptides added to lysines on target protein * Protein marked for degradation (E2 conjugating enzyme attaches ub)
67
How are ARF and Aux/IAA different?
* ARF = activator of auxin responsive genes, forms auxRE dimer when active * Aux/IAA = repressor of auxin responsive genes (short lived, nuclear proteins prevents activator binding)
68
What is the receptor of auxin?
Tir1 (F box)
69
What is the process that occurs leading to the activation of auxin responsive genes?
1. Tir1 recognises auxin (auxin like glue and holds TIR1 and target together) 2. Target is Aux/IAA (this is signalled for degradation due to ub) 3. Auxin induced genes can be transcribed

CEDB30002 Cell Biology (10 decks)

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