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H2 Biology > Pro n Eu > Flashcards

Pro n Eu Flashcards

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1
Q

What are tell-tale signs of a Prokaryote? [4]

A
  1. No membrane-bound organelles
  2. Has nucleoid instead of a nucleus
  3. Has circular DNA a./w small amt of histone-LIKE proteins
  4. Has 70S ribosomes (vs 80s)
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2
Q

Why must the genome in eukaryote be so compact? [3]

A
  1. Make long molecule of DNA more compact to fit in nucleus
  2. To prevent entanglement → prevent DNA breakage or damage → prevent cancer
  3. Regulation of gene expression → DNA wound around histones prevents GTFs and RNA pol access
    to genes that are not needed to be expressed
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3
Q

What are some genomic regulation in Eu [4]

A
  1. Chromatin Remodelling Complexes
  2. DNA Methylation
  3. Histone (De)acetylation
  4. Gene amplification
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4
Q

What are the MAIN role of telomeres? [4]

A

Counteracts end-replication problem, NOT solve it
1. [Define] Telomeres are non-coding tandem repeats sequence found at both ends of linear chromosomes
2. [Describe End-Replication Problem] Each round of DNA replication results in shortening of daughter
DNA molecules at telomeres
3. Because DNA polymerase unable to replace RNA primers with DNA, this is end-replication problem
4. Since telomeres are non-coding, this ensures vital genetic information is not eroded with replication

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5
Q

What are the other roles of Telomeres (3)

A

Other functions: Protect & Stabilise terminal ends of chr, prevent Apoptosis, Attachment pt for Telomerase
* By forming a loop with 3’ overhang, they protect & stabilise chromosomal ends, preventing fusion of
the ends with those of other chr
* Prevent DNA repair machinery from recognising ends of chr as DNA damage, preventing apoptosis
* 3’ Overhang of telomeres provides attachment point for correct positioning of Telomerase → allow for
elongation of telomeres → (prevent telomeres from reaching critical length

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6
Q

In Cancer, other than proto-oncogenes and Tumour Suppressor Gene mutations, what is another reason that cancer are “immortal”?

A

Due to the activation of telomerase which extends the length of telomeres, preventing the critical length of telomeres to be reached, hence the cell will NOT undergo normal apoptosis.

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7
Q

How does telomerase work? (4)

A

Function: Elongate Telomeres → maintain Telomere length & prevent loss of genetic info
* Nucleotides of the telomerase RNA anneals and forms complementary base pairs with single-stranded
overhang at 3’ end of the telomere
* Telomerase complementary C&C to specific telomeric DNA seq. Using telomerase RNA as a
template, telomerase catalyses the formation of phosphodiester bonds* between (incoming)
deoxyribonucleotides (& existing 3’ OH group of existing DNA overhang) elongating the 3’overhang
* Telomerase translocates along telomeric end from 5’ to 3’ to elongate the overhang
* In germ & stem cells: allow them to continuously undergo cell division & will not undergo apoptosis
to pass on genetic info to daughter cells for many generations

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8
Q

What are some non-coding sequences in humans?

A

Telomeres
Centromeres

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9
Q

Definition of cancer

A

Uncontrolled Cell Division & spread of abnormal cells due to dysregulation of cell cycle

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10
Q

Define proto-oncogenes

A

Gene that codes for proteins involved in normal cell
division (always establish in given context that gene
was previously normal)

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11
Q

Define Tumour Suppressor Gene

A

Gene that codes for proteins that inhibits cell division,
helps prevent uncontrolled cell division by (i) Cell
Cycle arrest, (ii) DNA repair, (iii) Apoptosis

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12
Q

What genes undergo Gain in Function mutation in Cancer & what are the traits of GIF mutations?

A

Proto-oncogenes

  1. Gene product produces is hyperactive OR excessive
  2. Only Single Mutation in 1 allele is needed
  3. Dominant mutation involved
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13
Q

What genes undergo Loss of Function mutation in Cancer & what are the traits of LoF mutations?

A

TSG

  1. Gene product produced is non-functional OR insufficient/not produced
  2. Mutations in BOTH allele is needed (aka 2 mutates)
  3. Recessive mutation involved
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14
Q

Outline the development of cancer (8)

A
  • [Effect of agent] Carcinogen increases chances of DNA damage and mutations in the genes which
    control regulatory checkpoints of the cell cycle in a single cell
  • Loss-of-function mutation of TSG in BOTH alleles of ‘__’ causes inability to inhibit cell cycle, repair
    damaged DNA and promote apoptosis → potential cancerous cells not removed
  • Gain-in-function mutation of POG in just 1 alleles of ‘__’→ oncogenes will result in overexpression
    of proteins or production of hyperactive/degradation resistant proteins → uncontrolled cell division to
    form primary tumour
  • [Development] Loss of contact inhibition enables cells to grow into a tumour
  • Genes coding for telomerase are activated → cells can divide indefinitely
  • Angiogenesis occurs within the tumour so that the blood vessels formed can transport oxygen and
    nutrients for its growth
  • [Spread] Resulting in the formation of a malignant tumour capable of metastasizing to other parts of
    body to form secondary tumours
  • Cancer is multi-step process that takes time as it takes years to accumulate these mutations.
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15
Q

Why is cancer a disease of old age? What are some risk factors?

A

Cancer is multi-step process that takes time as it takes years to accumulate these mutations.

Risk factors includes: smoking (carcinogens), excessive ionising radiation (like X-ray)

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16
Q

What are some cell division checkpoints?

A

M Checkpoint (M for Mitosis)

G1/G2 checkpoint

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17
Q

How Dysregulation of the checkpoints of cell division may lead to cancer? (3)

A

Dysregulation of (any 1 checkpoint)
o M checkpoint dysregulated → any cell with chromosomes that are not attached to spindle
fibres continues into metaphase & anaphase to produce genetically mutant cells
o G1/G2 checkpoint dysregulated → damaged DNA not repaired → cells continue into M phase
→ accumulating mutations
o Leading to uncontrolled cell division

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18
Q

How does oncogenes cause cancer?

A

Mutated form of proto-oncogene → excessive
production of the protein products OR oncogene
codes for a protein with increased activity / more
resistant to degradation ➔ uncontrolled cell division

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19
Q

How does mutated TSG cause cancer?

A

Mutated form of TSG → no functional gene products
formed → unable to stop cell cycle to allow repair any
damaged DNA, unable to activate DNA repair
mechanism to repair damaged DNA thus

accumulation of mutations, unable to initiate
apoptosis → cell with potential to cause cancer not removed

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20
Q

What is the Ras gene? How is it mutated in Cancer?

A

A gene involved in cell-signaling for normal cell division. Ras (protein) gene product helps activate downstream molecules to eventually cause cell division.

Mutation → constitutively active ras protein → bind
irreversibly to GTP → increasing frequency of cell
division even in absence of growth factors

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21
Q

What is the a specific gene example of TSG? How is it involved in cancer?

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A

p53 gene (master gene for cell division control)

Mutation → p53 gene products no longer act as
Activator that upregulate genes involved in (i) cell
cycle arrest, (ii) DNA repair, (iii) Apoptosis

22
Q

What is a sign that the cancer is turning malignant?

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A

Loss of contact-inhibition with excessive angiogenesis

In late stages: metastasis happens causing secondary tumours to be formed elsewhere

23
Q

What are the types of GENE mutations?

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A

SAID
Substitution
Addition
Inversion
Deletion

24
Q

What are some impacts of gene mutations?

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A

Frame-shift mutation
Silent mutation
Missense mutation
Nonsense mutation

25
What does it mean to have a Silent mutation? How does silent mutation happen?
Point mutation that does not lead to ∆ in a.a seq [S] explained by: 1. Degeneracy of the Genetic code: change in codon can still code for the same a.a. 2. Point mutation happened in non-coding region
26
What does it mean to have a nonsense mutation? What are the results?
Point mutation that leads to premature STOP codon This causes the polypeptide to be terminated earlier
27
What are the stop codons?
Mnemonic: - U Are Good (UAG) - U Are Awesome (UAA) - U Good & Awesome (UGA)
28
How can the Chr structure be mutated?
Translocation* Deletions Duplications Inversions
29
What are some Chromosomal Mutations?
Chromosomal STRUCTURE Chromosomal NUMBER
30
What is the case-example of a chromosomal number mutation? What are its typical symptoms?
Trisomy 21 (Down Syndrome) Short stature, low IQ, facial features
31
Define non-disjunction of chromosomes (2)
1. Homologous chromosomes do not move properly to opposite poles during meiosis I OR 2. When sister chromatids fail to separate properly to opposite poles during meiosis II.
32
Where & when can non-disjunction happen to result in errors like Trisomy 21?
1. During mitosis (RARE) 2. During Meiosis I 3. During Meiosis II
33
When does nondisjunction of Chr causes more deleterious effect?
In meiosis I end upwith 2x N+1, 2x N-1 (vs in Meiosis II end up with 2x N, 1x N+1, 1x N-1)
34
Describe how does Promoters work (3)
Serve as recognition site for binding of RNA pol, GTFs to initiate transcription * TATA box- determines precise transcription start site * CAAT & GC boxes- improves efficiency of promoter by recruiting GTFs & RNA pol to promoter
35
Describe how enhancer region work (2)
Allow STFs called Activators bind to it → (spacer DNA bends → allowing activator to bind to RNA pol & GTFs) → promoting formation of TIC * May also recruit Histone Acetyltransferase & CRC to decondense chromatin →...
36
Describe how Silencers work
Allow binding STF called Repressors → (spacer DNA bends → allowing repressor to bind to RNA pol & GTFs) → preventing assembly of TIC at promoter * May also recruit histone Deacetylase & CRC to condense chromatin → …
37
Describe how does Chromatin Remodeling Complexes work
Protein complexes that temporarily alter nucleosome structure UPREGULATE: ✓ DNA less tightly wound around histones → allow RNA Pol, GTF to access promoter → promote assembly of TIC → frequency of transcription increase DOWNREGULATE: × DNA more tightly wound around histones → … → f(transcription) falls
38
What is so special about DNA methylation? Describe how does it regulate gene activity.
ONLY for selected cytosine Addition of Methyl group to selected cytosine residues on DNA [DNA Methyltransferase] Mainly DOWNREGULATE × Prevents GTF from accessing promoter → prevent assembly of TIC × Recruit CRCs, DNA Deacetylase & Repressors → prevent assembly of TIC & transcription (chromatin condenses)
39
Describe how histone Deactylation & Acetylation work
Deacetylation by histone deacetylase removes Acetyl group from histones Histone Acetyltransferase does the opp. of adding × Removal of acetyl groups → restoring tighter electrostatic interaction btwn DNA & histones → reducing accessibility of promoter → prevent binding of GTP, RNA pol → prevent formation of TIC ✓ Histone Acetyltransferase…
40
What are methods of regulation at genomic level
CDH Chromatin remodelling complex DNA methylation Histone Deacetylation
41
What are the ways of regulation at Transcriptional Level
PES Promoter (proximal CE) Enhancer (distal CE) Silence (distal CE)
42
How does addition of 5' cap regulate post-transcriptionally? (3)
Allows cell to recognise mRNA ✓ Act as Signal to export mRNA out of nucleus ✓ Stabilize & Protect growing mRNA from Degradation by Ribonucleases
43
Describe how splicing of introns act to regulate at post-transcriptional level (2)
✓ Spliceosome splice introns & join exons → allowing mRNA to produce functional proteins ✓ Alternative Splicing: allowing 1 gene to produce mature mRNA with diff combi of exons to produce diff proteins
43
How does polyadenylation regulate ____ level? Describe how it works (3)
post-transcriptional level ✓ Addition of 3’ Poly A Tail → act as a Signal to export Mature mRNA out of nucleus ✓ Stabilize & Protect Mature mRNA from degradation by ribonucleases ✓ Interact with initiation factors & 5’ cap for initiation of translation
44
What are the post-transcriptional level regulation?
CSP 5' cap addition splicing introns polyadenylation
45
What are the ways translational level regulation happens?
1. T1/2 of mRNA 2. Formation of TIC regulation
46
Describe how is the mRNA t1/2 regulated?
Longer poly A tail = longer t1/2 ✓ Ribonuclease remove poly A tail until it reaches critical length where it triggers removal of 5’ cap by another ribonuclease
47
How is the formation of Translation Initiation Complex regulated? what level is this?
Translational level * Translation Repressor bind to (i) 5’ cap, (ii) 5’ UTR, (iii) 3’ UTR → prevent small ribosomal subunit from binding to 5’ cap of mRNA → prevent formation of TIC * Phosphorylation can activate ETIFs * Anti-sense RNA complementary to mRNA synthesized to block translation OR target it for degradation by ribonucleases
48
What are the post-translation regulation methods?
1. Quality = Covalent Modification to form functional proteins 2. Quantity of the proteins (gene products) via Phosphorylation AND Degradation of proteins by Proteasome
49
Describe all the ways that post-translation regulation happens
1. Covalent Modification to form functional proteins ✓ C.mod like Glycosylation, Disulfide bond formation make proteins functional in GA, RER 2. Regulate Protein Activity by Phosphorylation ✓ Phosphorylation activates proteins → functional & active 3. Protein Degradation ✓ Ubiquitin ligase tags proteins with Ubiquitin protein → tagged will enter Proteasome → enzymes of proteasome hydrolyse protein into small peptides ✓ Which is then further hydrolysed to a.a by enzymes in cytosol

H2 Biology (20 decks)

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