Life and Death of Cells and Organisms

Factors of aging
Proliferation (telomere shortening), Cell replacement (removal of senesecent cells), DNA damage & repair(mutations), Energy & metabolism (free radicals)
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Post-mitotic cells
Cells reach a mature differentiated state and do not divide
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Sources of damage
Intrinsic and extrinsic sources
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Imperfect repair of DNA damage
Accumulation of oncogenic mutations which cause mitotic cells to express hyperplastic or neoplastic phentotypes
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Cerebral cortex neurons
Not replaced if the cells die
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Fat cells
Replaced at a rate of 10% per year in adults
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Cells replacement rate
Cells with a high turn over rate are linked with the conditions they survive in.
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Stem cells divison
In protective niche; divide a finite number of times; remain quiescent most of the time
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Peak cell divisions time
Night, as there is less stresses at this time
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Resting phase of cells replication
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Enzyme that maintains the telomere ends of chromosomes
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Human telomerase reverse transcriptase (hTERT)
Ectopic exression leads to immortal cell growth in culture
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Telomerase complex
Subunits: TERT, TERC, DKC1, TEP1.
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A reverse transcriptase, creates DNA from RNA
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Naked chromosome
Looks like DNA damage, cells will try to repair it by joining to another chromosome
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Types of Single strand issues
Base excision, miss-match excision & nucleotide excision
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Genome size and damage
The larger the genome, the increase in likelihood of mutation, increased chance of cancer development.
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Oxygen metabolism
Base excision repair
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Replication infidenlity
Mismatch repair
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UV light
Nucleotide excision repair
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Recombinational repair
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UV light, mutagens
Translesion synthesis
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UV light, Oxygen, EMS
Avoidance/reversal of damage
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Damage in BRCA-2
Causes breast and ovarian cancer due to damaged repair by homologous recombination
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Damage in Werner syndrome
Causes premature aging, cancers and genome instability. Damage in accessory 3' exonuclease and DNA helicase
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Inherited damage
Cells in the colon lining pass on damaged during replication. Leads to epigenetic alterations.
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Ettor-correcting processes, required for enhanced specificity.
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DNA polymerase proofreading
3'->5' proofreading exonuclease domain, check each nucleotide during DNA synthesis and excise mismatch nucleotides.
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DNA polymerase delta
Enzyme involved in DNA replication and repair. Consist of 4 subunits: POLD1, POLD2, POLD3, POLD4. Used for leading and lagging strand synthesis.
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The removal of an amine group from a molecule of amino acid.
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Base excision repair
Repairs damaged DNA throughout the cell cycle. It is responsible primarily for removing small, non-helix-distorting base lesions from the genome. The related nucleotide excision repair pathway repairs bulky helix-distorting lesions.
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Miss-match excision repair
Strand specific. Uses a parental template. Newly synthesised lagging-strand DNA transiently contains nicks, directs mismatch proofreading systems to the appropriate strand. Uses 6 enzyme mechanisms.
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Nucleotide excision repair
Repairs damage caused by UV radiation. Has three pathways NER, base excision repair (BER) and DNA mismatch repair (MMR)
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BER pathway
Recognise specific non-bulky lesions in DNA. Repaired by specific glycosylases.
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UV DNA damage
Results in bulky DNA adducts. Recognition leads to the removal of a short single - stranded DNA segment that contains the lesion.
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Xeroderma pigmentosum (XP)
Genetic disorder (autosomal recessive), decreased ability to repair DNA damage caused by UV light. Development of skin cancer by 10 years old. 9 specific mutations. There is no cure. Vitamin D supplementation is required.
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Double strand breaks
Caused by ionising radiation, anticancer drugs. Repaired by Non-homologous end-joiningor non-homologous end-joining.
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Non-homologous end-joining
Break ends are directly ligated without the need for a homologous template
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Homology directed repaire
Repair directed repair to DNA lesions. most common is Non-homologous end-joining. Needs a homologue piece of DNA to be present.
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System used to create targeted double strand breaks. Uses RNA guided cleavage of a specific site of DNA. This is a donor template, creates a blunt ends. Uses natural DNA-repair mechanisms to insert novel genes.
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DNA damage checkpoints
Opportunity to stall cell divisions such as effective DNA repair. Blocking cells before mitosis.
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Mutations of genes greatly increase lifetime risk to develop canceras. Misregulation and alteration increases risks of cancer,
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Ageing and food
less food-> less energy required -> less mutations
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Conserved Ser/Thr kinase regulates cell growth and responds to environmental cues . TORC1 is sensitive to rapamycin leads to increase in autophagy, TORC2 is not, leads to increase in cell growth.
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A deacetylase, type of protein post-translation modification regulated acetylases and deacetylase. Links with cell longevity.
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Naturally regulated mechanism of the cell that disassembles unnecessary components. Allows for orderly degradation or recycling cellular components
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Anatomical joining of two individuals. Led to the transfer of ageing processes (impaired cognition or neurogenesis) or rejuvenation (increased neurogenesis). Transfer life into the old subject from the young and reversed.
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Card 2


Cells reach a mature differentiated state and do not divide


Post-mitotic cells

Card 3


Intrinsic and extrinsic sources


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Card 4


Accumulation of oncogenic mutations which cause mitotic cells to express hyperplastic or neoplastic phentotypes


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Card 5


Not replaced if the cells die


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