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1. As far as any scientist can tell, Lobsters show no signs of aging and when they die, it seems to be of extrinsic causes like predation.  In his encyclopedic work, Longevity, Senescence, and the Genome, Finch (1990) devotes an entire chapter to "negligible senescence" in lobsters, Quahog clams, tortoises and bristlecone pines.   Of course, we are not suggesting that lobsters are impervious to death,and in fact their constant growth probably limits their lifespan at some point.  But for dramatic effect we choose the word 'immortal', and think the term is not too inappropriate:  Single cell lines which do not age are refferred to as 'immortal', as is the more primitive multi-cellular organism Hydra.  

See also:

Cellular senescence not observed in sponges, corals and lobsters.

Animals that are immortal or long-lived animals with "negligible senescence"

This excellect explanation of the Telomere Position Effect and its role in human aging is offered by the Telomolecular team at this URL:

Position effect is a term used to describe an event in which a gene's behavior is affected by its location on the chromosome. The changes in behavior can be expressed in various ways, such as differences in the appearance and function of cells (phenotype), relay of instructions from the gene, and in doubling time of the dividing cells. Position effects have been reported in insects, plants, yeast and mice, and more recently in human cells. The findings that TPE exists in human cells offer clues to cellular aging. In the experiments reported in Science magazine, investigators used a human cancer cell line called HeLa to investigate TPE and the relation between gene activity and telomere length. HeLa cells, which are "immortal," contain telomerase that lengthens the telomere, enabling the cells to keep dividing. In the experiments, investigators introduced into the cell a gene called luciferase (the gene that makes fire flies glow), linked to DNA. Luciferase, called a reporter gene whose location is identified in the cell by its luminescence, was inserted near a telomere. Its luminescence compared to that of the reporter inserted at internal sites of the chromosome. To test if telomere length influences gene silencing, the investigators then elongated the telomere by telomerase, and examined telomere positional effect on luciferase. The results showed that luciferase near the telomere produced 10 times less luminescence than luciferase located at internal sites in the chromosome. Increasing the length of the telomere further increased TPE, resulting in an additional two- to 10-fold decrease in luminescence. These experiments showed that the proximity of a telomere to a gene silences the gene: when the telomere is lengthened, and the gene is located further away from the critical end of the telomere, it is silenced even more. TPE is meaningful and consistent with experimentation. Old cells fail to produce key enzymes and proteins essential in tissue repair, they divide very slowly, and eventually reach cell senescence and die. However, cells treated to produce the telomerase enzyme divide indefinitely in an energetic fashion, produce the proteins that young cells produce, and repair internal cell damage while preventing genomic instability. Young cells show an incredible resistance to oxidative damage, glycation, and cell mutations of all kind that old cells do not. Because young cells replicate vigorously, demonstrate superior cell signaling, produce important proteins (such as collagen and elastin in the skin), and have more rapid cell function, they are able to maintain tissues and vital organs in a way that old cells cannot.

Matsumura, Hayflick.  Senescent human diploid cells in culture: survival, DNA synthesis and morphology. 1979.

Matsumura, Hayflick.  DNA Synthesis in the human diploid cell strain WI-38 during in-vitro aging: an autoradiography study. 1979.

We believe that this will first arrive in the form of a drug or natural supplement - a molecule small enough to penetrate the somatic cell walls in the human body, which has the ability to activate the dormant gene which lies in each of our somatic cells and codes for hTERT, the catalytic component of telomerase.  This was the gene that Geron used (by inserting an extra, non-dormant copy) to immortalize the now famous cells.  The challenge of delivering that small molecule to every single cell in the body would be conveniently met by the cardiovascular system - a system designed to carry out just that type of delivery. Its perfection will come in the far more advanced ability to periodically extend telomeres to precise lengths appropriate to the tissue those cells inhabit.

Aging selected for its own sake

Aging is a specific biological function rather than the result of a disorder in complex living systems: biochemical evidence in support of Weismann’s hypothesis

The programmed death phenomena, aging and the Samurai law of biology

The Evolution of Aging

So could HGPS be 'cured' with telomerase activation of cells throughout the body?  Not really in the sense that this would not address the underlying, and devastating, failure of each cell to build a secure membrane inside the nucleus.  But, in theory it should greatly ameliorate the symptoms in as much as it was successfull in allowing the compensating cells to hyperproliferate without aging, that is, without losing telomere length.  Even better would be the development of a viral gene therapy technique one day that could somehow fix the mutation or override it with a healthy copy of the LMNA gene.

In this case, however, it might also be attributed to some cells whose DNA damage has triggered a senescence response, which is a damage control cell response similar to the p53 'aptopsis' response intended at haulting the division lest the damage spread further.

See also:

Opresko PL et al., Coordinate action of the helicase and 3' to 5' exonuclease of Werner syndrome protein

Orren DK et al.,  The Werner syndrome helicase/exonuclease (WRN) disrupts and degrades D-loops in vitro