CSHL 2008, Session II: Telomeres

OK, on to the telomeric part of the session:

Brad Johnson talked about G-quadruplex structures, which often form at telomeres, and suggested that they may be connected to gene expression in cellular senescence.

Robert Marciniak presented evidence that the telomeres act as a “genotoxic clock.” In his model, repair of DNA damage at telomeres results in telomere shortening — so that even in non-dividing cells, the lifetime exposure to DNA damaging agents will be reflected in telomere length.

Liz Blackburn reviewed even more evidence that peripheral blood leukocyte telomere length is associated with psychological stress and the risk of CVD. This story is evolving into an explanation for immune senescence and the increased susceptibility of the elderly to diseases of various kinds. The model goes roughly as follows: Signal input → brain → hormones → negative outputs including shorter telomeres → immune dysfunction → disease impact

Ursula Muñoz-Najar examined TIFs (telomere dysfunction-induced foci) in aging mice, as well as mice eating high-fat, CR or control diets. Both aging and high-fat diets are associated with increased TIFs, but — fortunately for the mice — this is reversible when the mice are shifted to a lower-calorie, lower-fat diet. Resveratrol had similar effects on TIFs: in mice on a high-fat diet, RSV could reduce TIF levels to that of mice on control diets. To the extent that TIFs are a legitimate biomarker of aging, these findings are consistent with (now questioned) reports that resveratrol can extend the healthspan of mice fed an unhealthy diet.

Session index:


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