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Alevel Biology > Prokaryotic & Eukaryotic Genome > Flashcards

Prokaryotic & Eukaryotic Genome Flashcards

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1
Q

Compare eukaryotic and prokaryotic cells

A 
Size
Nucleus
Organelles
Ribosomes
Cell wall
Plasma membrane (S)
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2
Q

Compare the prokaryotic and eukaryotic genomes (exclude organisation)

A 
Size & no. of genes
Appearance
Molecule
Association w proteins
Location
Extrachromosomal DNA
Level of DNA packing/coiling
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3
Q

Why is the packing of DNA important?

A
  • compact–> fit in nucleus (eu)
  • regulate gene expression (eu)
  • prevent DNA entanglement and breakage
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4
Q

Describe how DNA is packed in eukaryotes

A
  • -vely charged DNA double helix winds arnd octamers of 8 +vely charged histone proteins via electrostatic interactions. → nucleosome (10nm fibre). Linker DNA joins adjacent nucleosomes.
  • 10nm fibre coils around itself→ 30nm chromatin fiber/solenoid (interphase DNA)
  • 30nm fibre form looped domains when associated w scaffold proteins→ 300nm fibre
  • Supercoiling→ metaphase chromosome
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5
Q

Describe how DNA is packed in prokaryotes

A

DNA double helix folds into looped domains by protein-DNA associations→ supercoiling w the help of DNA gyrase & topoisomerase

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6
Q

Compare the organisation of eukaryotic and prokaryotic genome

A 
Non-coding regions
- introns
- promoters (s)
- enhancers/silencers
- repeated seq
Operon
Ori
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7
Q

Explain why the end replication problem occurs

A

DNA polymerase needs free 3’ OH grp to add free nt to growing DNA strand→ RNA primer synthesised to provide the free 3’ OH end for the addition of nt

⇒ 5’ end of newly synthesised strand will have RNA primer removed wout replacement of DNA due to no 3’ end available for DNA polymerase→ 3’ overhang → chromosomes shorten every replication ⇒ shortening of telomeres

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8
Q

Describe the role of telomeres

A

Definition: non-coding DNA made up of a series of tandem repeat seq, found at both ends of eu chromosomes

  1. Non-coding telomeres ensure vital genetic information are not lost due to end replication problem, where daughter chromosomes shorten at the telomeres w each round of DNA replication, as DNA polymerase can’t replace RNA primers w DNA
  2. Telomeres protect and stabilise terminal ends of chromosomes, by forming a loop w 3’ overhang, preventing ends of chromosome from fusing w those of other chromosomes→ prevent DNA repair machinery from recognising ends of chromosomes as DNA damage, protecting the chromosome, prevent apoptosis
  3. Telomeres allow for own extension, as 3’ overhang providing an attachment point for the correct positioning of telomerase enzyme
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9
Q

Describe the function of telomerase

A
  • AS complementary in conformation and charge to a specific telomeric DNA sequence
  • Catalyses the formation of phosphodiester bonds
    translocate in 5’ to 3’ direction→ series of tandem repeats of GGTTAG→ elongate telomere
  • Telomerase RNA
    > Anneal via cbp w ss 3’ overhang of telomere→ align telomerase in correct orientation wrt DNA
    > Template for elongation of 3’ overhang, synthesise complementary DNA seq via cbp, where A pairs w U, T w A, C w G→ tandem repeat seq
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10
Q

Describe the role of centromeres

A

Structure: seq of non-coding DNA region of chromosome made up of tandem repeats
- Allowing sister chromatids to adhere to each other
- Allow kinetochore proteins & subsequently kinetochore microtubules to attach→ bivalents can be aligned along metaphase plate during MI of meiosis + chromosomes aligned singly along metaphase plate during M/MII of meiosis→ kinetochore microtubules shorten and separate them to opposite poles during A/AI/AII
⇒ allows proper alignment and segregation of chromosomes

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11
Q

Describe splicing

A

introns excised, exons joined tgt by spliceosome, a snRNA (small nuclear RNA)-protein complex, which recognises seq at intron-exon boundary→ produce functional proteins

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12
Q

Describe alternative RNA splicing

A

different exons of a single pre-mRNA joined to produce different mature mRNAs → one gene can code for >1 polypeptides; diff proteins can be produced

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13
Q

What is the function of promoters?

A

Recognition & binding site for GTFs, which recruits RNA polymerase→ transcription initiation complex→ initiate transcription
- Critical elements: TATA box determines precise location of transcription start site

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14
Q

What is the function of enhancers ?

A
  • positive regulatory elements
  • Recognition & binding site for specific transcription factors called activators→ promote assembly of transcription initiation complex by…
    → bending spacer DNA allows activators to bind & stabilise transcription initiation complex at promoter
    → recruit histone acetyl transferase & crc to decondense chromatin, ↑ accessibility of RNA pol & GTFs to promoter
    ⇒ upregulate/↑ freq of transcription; gene activation
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15
Q

What is the function of silencers?

A
  • Negative regulatory elements
  • Recognition & binding site for specific transcription factors called repressors→ prevent assembly of transcription initiation complex by…
    → interfere w action of activator by: competitive DNA binding, masking activation surface & bending spacer DNA for repressor to directly interact/bind to GTFs
    → recruit histone deacetylase & repressible crc to condense chromatin, ↓ accessibility of RNA pol & GTFs to promoter
    ⇒ downregulation/ ↓ freq of transcription; gene silencing/repression
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16
Q

Explain the importance of gene regulation

A
  • Cellular differentiation: Regulation of gene expression→ each specialised cell hv different genes expressed→ different, tissue-specific proteins synthesised→ diff function
  • Adapt to changes: proteins produced depends on circumstances & demand
  • Conserve resources: transcriptional lvl, the most efficient mechanism w minimal wastage
  • More varied proteome despite limited genome size: by alternative splicing
17
Q

How does histone acetylation regulate gene expression?

A

Histone acetylation, catalysed by histone acetyltransferase: add acetyl grps to (lysine residues) histones→ removes +ve charge on histones, ↓ electrostatic interactions between -vely charged DNA and histones→ chromatin decondense

RNA pol & GTFs can access and bind to promoter, assembles transcription initiation complex→ increase/initiate transcription

18
Q

How does histone deacetylation regulate gene expression?

A

Histone deacetylation, catalysed by histone deacetylase: remove acetyl grps→ restoring +ve charges on histones, restores tighter interaction/↑ electrostatic interactions→ chromatin condenses

RNA pol & GTFs cannot access and bind to promoter (blocked) → prevent formation of transcription initiation complex→ prevent transcription

19
Q

How does DNA methylation regulate gene expression?

A

DNA methylases add methyl grps to selected cytosine nt in specific CG seq
→ recruit DNA-binding proteins aka transcriptional repressors, histone deacetylase, repressive chromatin remodelling complexes to condense chromatin
→ block binding of GTFs, prevent assembly of …

RNA pol & GTFs cannot access and bind to promoter (blocked) → prevent formation of transcription initiation complex→ prevent transcription

20
Q

How does CRC regulate gene expression?

A

CRC alters struc of nucleosomes temporarily: DNA less tightly coiled to histones → chromatin decondense

RNA pol & GTFs can access and bind to promoter, assembles transcription initiation complex→ increase/initiate transcription

21
Q

How does repressible CRC regulate gene expression?

A

alters struc of nucleosomes temporarily: DNA more tightly coiled arnd histones→ chromatin condenses

RNA pol & GTFs cannot access and bind to promoter (blocked) → prevent formation of transcription initiation complex→ prevent transcription

22
Q

How does adding 5’ cap regulate gene expression?

A

Adding 7-methylguanosine nt to 5’ end of pre-mRNA shortly after transcription begins

  • Helps the cell recognise mRNA, so subsequent steps like splicing & polyadenylation can occur
  • Acts as a signal to export mRNA out of nucleus
  • Stabilises and protects growing pre-mRNA from degradation by ribonucleases
  • Recognised by Eu initiation factors, which bind to it→ help recruit mRNA to small ribosomal subunit→ promotes translation initiation
23
Q

How does polyadenylation regulate gene expression?

A

3’ end of pre-mRNA cleaved downstream of polyadenylation signal (AAUAAA) → poly-A polymerase adds a long seq of adenine nt to 3’ end of pre-mRNA (poly-A tail)

  1. Acts as a signal to export mRNA out of nucleus
  2. Stabilises and protects growing pre-mRNA from degradation by ribonucleases→ more proteins made
  3. Interacts w Eu initiation factors and 5’ cap for initiation of translation
24
Q

Describe the formation of translation initiation complex

A

When small ribosomal subunit, eukaryotic initiation factors & initiator tRNA form a complex, which binds to 5’ cap & poly-A tail→ mRNA circularises→ complex moves in 5’ to 3’ direction to locate start codon, AUG → binding of large ribosomal subunit completes translation initiation complex

25
Q

Explain how the length of 3’ polyA tail affects the half-life of mRNA and how it affects gene expression?

A

mRNA stability/half-life determined by length of poly-A tail. Longer = longer time mRNA can be used as template to make proteins

26
Q

How is mRNA degraded?

A

poly-A tail removed by ribonucleases in 3’ to 5’ direction until a critical length is reached→ trigger removal of 5’ cap & degradation from 5’ end too

27
Q

How is the formation of translation initiation complex regulated?

A
  • translational repressors bind to 5’ cap & UTR, 3’ UTR→ interferes w interaction between poly-A tail, 5’ cap, initiation factors & small ribosomal subunit
  • activation/inactivation by phosphorylation/ dephosphorylation of eIFs→ affect availability of activated eIFs
  • Anti-sense RNA, complementary to part of mRNA to be degraded, is synthesised & binds to mRNA, forming a dsRNA→ block translation of mRNA + dsRNA targeted for degradation by nucleases
28
Q

Describe the gene regulation at the post-translational level

A
  • Covalent modification/cleavage (eg glycosylation) of polypeptides→ functional proteins
  • Phosphorylation/dephosphorylation of translation IFs (eIFS) activates/deactivate protein→ up/down regulate activity
  • Proteins targeted for degradation tagged with ubiquitin (by enzyme ubiquitin ligase), recognised & degraded by proteasomes into small peptides
29
Q

What factors increase the chance of cancer?

A
  • Environmental factors: exposure to carcinogens (eg tar) and ionizing radiation (eg UV radiation) → mutations
  • Loss of immunity due to infection with certain viruses: HIV weakens immune system, reduces body’s ability to fight infections by other viruses that can cause cancer
  • Genetic predispositions: gene mutations inherited
  • Age: increase age, increase chance of cancer due to accumulation of mutations in cell over a lifetime
30
Q

Define proto-oncogene

A

normal gene coding for proteins (growth factors/activators/growth signal transduction factors) that stimulate normal cell division/proliferation

31
Q

Explain what is meant by a oncogene

A

Gain-in-function mutations in proto-oncogene (only 1 copy)→ oncogenes
- excessive production of gene product that stimulates cell cycle
- ↑ intrinsic activity of gene product: hyperactive or more resistant to degradation
==> uncontrolled cell division

32
Q

Define tumour supressor gene

A

normal gene coding for protein products that inhibit cell divisions / activate cell cycle arrest, DNA repair, apoptosis→ preventing uncontrolled cell division

33
Q

Explain the role of p53 gene in preventing uncontrolled cell division

A

p53 gene codes for specific transcription factor (p53 protein), an activator, that activate/upregulate expression of genes involved in:

  • Cell cycle arrest: time to repair damaged DNA & prevent formation of mutant daughter cells
  • DNA repair: prevent mutations that forms of oncogenes/inactivated tumour suppressor genes
  • Initiating apoptosis when DNA is beyond repair: removes cells w damaged DNA & potential for cancer
34
Q

How does loss-in-function mutation lead to uncontrolled cell division?

A

Loss-of-function mutation by point mutation/chromosomal translocation/retroviral integration (both copies)→ inactivate gene→ cell cycle continues wout repairing DNA/apoptosis/inhibition of cell division

35
Q

Compare gain-in-function mutation and loss-in-function mutation

A

Definition
Gene that mutation affect
Type of mutation and no. of allele to be mutated to be cancerous
Effect on cell cycle in cancer cells

36
Q

What makes a tumour malignant?

A

Invasive, can metastasise

37
Q

How does a primary tumour form a secondary tumour?

A

primary tumour breaks through basal lamina, invades capillary→ cancer cell adhere to blood vessel walls, escape from blood vessel→ proliferate to form secondary tumour

38
Q

Compare normal cells and cancer cells

A 
Genes
Cell division
Nuclei
Apoptosis
Cells
Contact inhibition
Differentiation
Cell adhesion / metastasis
Angiogenesis
39
Q

Why is cancer a multi-step process?

A
  1. Accumulation of mutations in genes which control regulatory checkpoints of cell cycle, in a single cell→ disrupts normal cell cycle→ cell has excessive cell growth and proliferation→ uncontrolled cell division
  2. (criteria 1) Gain-in-function mutation is a dominant mutation where mutation in just one copy of a proto-oncogene→ overexpression→ production of excessive amounts of growth factors; production of hyperactive/degradation resistant growth factors
  3. (criteria 2) Loss-in-function mutation is a recessive mutation, mutation in both copies of a tumour suppressor gene will disrupt their ability to inhibit cell cycle, enable DNA repair and promote apoptosis.
  4. (criteria 3) Activation of genes coding for telomerase→ telomeres lengthened, cell can divide infinitely
  5. Loss of contact inhibition→ cells grow into benign tumour
  6. Angiogenesis within the tumour→ blood vessels formed can transport oxygen and nutrients to it for its growth & remove metabolic waste products and CO2 → form malignant tumours that metastasise via bloodstream & form secondary tumours there.

Alevel Biology (16 decks)

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