bio aging final exam Intracellular processes.txt

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bio aging final exam Intracellular processes.txt
2012-12-12 14:58:35
bio aging final exam INTRACELLULAR processes

bio aging final exam INTRACELLULAR processes
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  1. Weismann hypothesis related to cells
    • Germ cells immortal
    • somatic cells mortal
  2. Leonard Hayflick
    • human DIPLOID FIBROBLASTS: showed declining rate of cell division, discrediting Alexis Carrel's immortal somatic cell exp.
    • NOT all cell types have Hayflick limit thou: intestinal epithelial cells, blood precursor cells, basal cells giving rise to keratinocyes can divide infinitely
  3. Cell Cycle
    • G-1: Cytoplasmic growth occurs (PROTEIN SYNTHESIS)
    • S-phase: synthesis of DNA and duplication of nuclear chromosomes
    • G-2: Cell COMMITTED to cell division (Also protein synthesis)
    • M: Mitosis or meiosis
    • G-0: Terminal differentiation (NO Further cell division)
  4. *Hayflick Senescence definition
    • Called senescence during: Last three periods of growth of diploid fibroblasts
    • Phase I: Increasing Growth rates over time (Log phase)
    • Phase II: Consistant Growth Rates over time (stationary phase)
    • Phase III: Declining growth Rates over time (Lag phase- senescent culture), genes synthesized at lower rate, p53 shows increased activity
  5. *Diploid Fibroblasts in vitro cell growth good biomarker for senescence
    • 1. Cells from YOUNG donors undergo more pop. doubling vs. OLD donors
    • 2. Cells from accelerated aging patients (w/Werner's or Hutchinson-Gilford) showed LOWER proliferation potential vs. healthy
    • 3. Population doubling for embryonic cells from different vertebrate species CORRELATED with maximum species lifespans
    • 4. Cells from liquid nitrogen 'remember' how many cell division remain
  6. Objections to in vitro growth as biomarker for senescence
    • 1. Phase III cells have heterogeneity in # of pop. doublings they can do
    • 2. Declining growth rates in fibroblasts may be due to differentiation
    • 3. Growth of REDUCED oxygen conditions can INCREASE # of pop. doublings of in vitro
    • 4. Cancer or other normal cells can proliferate without limit, NO relation to Mortality rates
    • 5. Loose Correlations b/w species longevity and in vitro pop. doubling suggest cell growth rates are consequence of longevity vs. a cause
    • 6. Telomerase in determinig proliferative potential is evidence AGAINST in vitro cell proliferation potential
  7. Telomeres
    • First recognized by McClintock & Muller, and as role in cell division by Olovnikov
    • Present in all vertebrate chromosomes (not in Dros. and other invertebrates)
    • Not present in circular chromosomes of mitochondria, chloroplasts and prokaryotes
    • 5'-TTAGGG-3' and its compliment 5'-CCCTAA-3'
  8. Telomerase
    • Lengthens telomeres to prevent chrom shortening with cell division
    • Absent from most somatic human cells (including fibroblasts)
    • Present in most cancers
    • Bodnar inserted into epithelial and fibroblasts and showed NO decline of cell divisions
    • Geron corp. would like to see telomerase added to every cell type
  9. Lipofuscin and waste accumulation theory
    • Produced: as consequence of free radical oxidation of membrane lipids
    • Postmitotic cells Accumulate lipofuscin: neurons, cardiac cells, skeletal muscle cells
    • Waste accumulation Theory: May be a good biomarker of aging
  10. Controlled cell death (apoptosis)
    • important feature of development: apoptosis of skin ridges
    • and aging: cell death mechanism thought to be response to increased DNA damage levels
    • seem to be a mechanism to control growth of cancer cells: thru p53 tumor suppressor gene