Pro n Eu Flashcards
What are tell-tale signs of a Prokaryote? [4]
- No membrane-bound organelles
- Has nucleoid instead of a nucleus
- Has circular DNA a./w small amt of histone-LIKE proteins
- Has 70S ribosomes (vs 80s)
Why must the genome in eukaryote be so compact? [3]
- Make long molecule of DNA more compact to fit in nucleus
- To prevent entanglement → prevent DNA breakage or damage → prevent cancer
- Regulation of gene expression → DNA wound around histones prevents GTFs and RNA pol access
to genes that are not needed to be expressed
What are some genomic regulation in Eu [4]
- Chromatin Remodelling Complexes
- DNA Methylation
- Histone (De)acetylation
- Gene amplification
What are the MAIN role of telomeres? [4]
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
What are the other roles of Telomeres (3)
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
In Cancer, other than proto-oncogenes and Tumour Suppressor Gene mutations, what is another reason that cancer are “immortal”?
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.
How does telomerase work? (4)
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
What are some non-coding sequences in humans?
Telomeres
Centromeres
Definition of cancer
Uncontrolled Cell Division & spread of abnormal cells due to dysregulation of cell cycle
Define proto-oncogenes
Gene that codes for proteins involved in normal cell
division (always establish in given context that gene
was previously normal)
Define Tumour Suppressor Gene
Gene that codes for proteins that inhibits cell division,
helps prevent uncontrolled cell division by (i) Cell
Cycle arrest, (ii) DNA repair, (iii) Apoptosis
What genes undergo Gain in Function mutation in Cancer & what are the traits of GIF mutations?
Proto-oncogenes
- Gene product produces is hyperactive OR excessive
- Only Single Mutation in 1 allele is needed
- Dominant mutation involved
What genes undergo Loss of Function mutation in Cancer & what are the traits of LoF mutations?
TSG
- Gene product produced is non-functional OR insufficient/not produced
- Mutations in BOTH allele is needed (aka 2 mutates)
- Recessive mutation involved
Outline the development of cancer (8)
- [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.
Why is cancer a disease of old age? What are some risk factors?
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)
What are some cell division checkpoints?
M Checkpoint (M for Mitosis)
G1/G2 checkpoint
How Dysregulation of the checkpoints of cell division may lead to cancer? (3)
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
How does oncogenes cause cancer?
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
How does mutated TSG cause cancer?
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
What is the Ras gene? How is it mutated in Cancer?
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
