Telomeres and Aging - Page-by-Page Notes

Page 1

  • Telomeres and Aging

Page 2

  • Learning objectives:
    • Explain the genetic factor in cell aging via telomere shortening with every cell division.
    • Explain how telomerase can reverse telomere shortening in cancer, germ cells, and stem cells.

Page 3

  • Core concepts:
    • Telomere shortening contributes to aging by reducing replicative capacity; telomerase extends telomeres in cells where it is active (germ, stem, many cancer cells).
    • Telomerase is a ribonucleoprotein that uses an RNA template to add telomere repeats.

Page 4

  • End Replication Problem:
    • Linear chromosomes are not fully replicated by DNA polymerase; 5' ends are not completely copied, leading to progressive shortening.

Page 5

  • Replication dynamics:
    • Leading strand synthesized continuously; lagging strand synthesized discontinuously as Okazaki fragments; RNA primers required.

Page 6

  • RNA primer removal and gaps:
    • Removal of RNA primers leaves gaps between fragments; ends are not fully replicated.

Page 7

  • Primer removal consequences:
    • Gaps persist between Okazaki fragments until ligation.

Page 8

  • Ligase:
    • Ligase seals nicks to form a continuous strand.

Page 9

  • End gaps:
    • Each round of replication leaves 50-200\text{ bp} unreplicated at the 5' end.

Page 10

  • Circular DNA:
    • Most bacterial DNA is circular; circular genomes have no ends and thus no end replication problem.

Page 11

  • Telomeres as a temporary solution:
    • Telomeres consist of non-coding repeats of \text{TTAGGG} in humans.
    • They protect coding regions and help prevent loss of genetic information, replicative senescence, and apoptosis; chromosome ends are not treated as breaks.

Page 12

  • Implications of telomere shortening:
    • Telomere length correlates with proliferative capacity and finite replicative life span (mortal).

Page 13

  • Possible outcomes of telomere shortening:
    • Senescence, apoptosis, or limited proliferation.

Page 14

  • Senescence and Hayflick limit:
    • Normal cells stop dividing when telomeres reach a critical length; Hayflick limit defines this replicative cap; prevents proliferation of damaged cells.

Page 15

  • Telomere shortening as a driver of aging:
    • Shortened telomeres contribute to aging through progressive tissue decline and cell loss.

Page 16

  • Telomerase activity distribution:
    • Active in germ cells, gametes, epidermal stem cells, hair follicle stem cells, some immortalized cells, and the majority of cancer cells.
    • Inactive in most somatic/differentiated/post-mitotic cells.

Page 17

  • Telomerase composition:
    • Telomerase is a ribonucleoprotein enzyme complex.

Page 18

  • Telomerase mechanism basics:
    • Telomere repeat sequence: \text{TTAGGG} repeats; telomere overhang with a 5' to 3' orientation; telomerase extends the 3' end.

Page 19

  • Telomere extension concept:
    • Telomerase adds repeats to the 3' end, creating a longer overhang; gaps remain if extension is incomplete.

Page 20

  • Telomerase RNA template:
    • Telomerase uses its RNA component as a template to extend the telomere.

Page 21

  • Continued extension and synthesis:
    • After extension, DNA polymerase synthesizes the complementary strand with help of RNA primers; ligase seals.

Page 22

  • Resulting telomere length:
    • Extended telomere length achieved through coordinated telomerase extension and conventional replication.

Page 23

  • Telomerase activity in cells:
    • Activity is observed in cells that are immortal or far from replicative senescence.

Page 24

  • Stem vs. somatic cells:
    • Embryonic stem cells: longer telomeres + active telomerase.
    • Somatic cells: shorter telomeres + inactive telomerase.

Page 25

  • Why do we age?
  • Telomere dynamics contribute to aging; telomere shortening leads to senescence and functional decline.

Page 26

  • Key relationships:
    • Telomeres regulate replicative capacity; telomerase maintains telomere length; cancer links telomere maintenance to uncontrolled division and apoptosis pathways.

Page 27

  • Resources:
    • The Science of Aging: https://www.youtube.com/watch?v=BkcXbx5rSzw
    • End Replication problem: https://www.youtube.com/watch?v=5emqrkIvlTY
    • Telomerase: https://www.youtube.com/watch?v=i6nE6gUp2cw