Reviewing Negligible Senescence in Sea Urchins
Among the sea urchins can be found some of the few species to exhibit negligible senescence, an apparent lack of the obvious features of degenerative aging. By studying negligibly senescent species and the differences in their biochemistry, researchers hope to learn more about the mechanisms that drive aging. As this review notes, the data uncovered to date in sea urchins looks quite similar to the situation for long-lived and negligibly senescent clam species such as Arctica islandica:
Aging in humans and other animals is a well-defined process characterized by a progressive functional decline and increasing mortality over time. However, there are a number of different animals that show negligible senescence, with no increase in mortality rate or decrease in fertility, physiological function, or disease resistance with age. Studying these animals may suggest effective defenses against the degenerative process of aging, and sea urchins provide an ideal model to investigate mechanisms of longevity and negligible senescence.Different species of sea urchins exhibit very different natural lifespans, and some have extreme longevity and negligible senescence. For example, the red sea urchin Strongylocentrotus franciscanus is one of the earth's longest living animals, living in excess of 100 years with no age-related increase in mortality rate or decline in reproductive capacity. In contrast, Lytechinus variegatus has an estimated lifespan of only 4 years, while the most widely studied species of sea urchin, S. purpuratus, has an estimated maximum lifespan of more than 50 years. Comparisons between long-, intermediate-, and short-lived species may provide insight into mechanisms involved in lifespan determination and negligible senescence. Thus, sea urchins represent an interesting alternative model for aging research.
Studies to date have demonstrated maintenance of telomeres, maintenance of antioxidant and proteasome enzyme activities, and little accumulation of oxidative cellular damage with age in tissues of sea urchin species with different lifespans. Gene expression studies indicate that key cellular pathways involved in energy metabolism, protein homeostasis, and tissue regeneration are maintained with age. Taken together, these studies suggest that long-term maintenance of mechanisms that sustain tissue homeostasis and regenerative capacity is essential for indeterminate growth and negligible senescence, and a better understanding of these processes may suggest effective strategies to mitigate the degenerative decline in human tissues with age.
" Maintenance of telomeres in tissues of species with different lifespans suggests a lack of telomere-directed senescence in sea urchins. Although the levels of telomerase activity were not quantified in the tissues of species used in these studies, it is interesting to note that TRF length was inversely correlated with life expectancy such that short-lived L. variegatus had the longest mean TRF length. This suggests that telomere length is not a determinant of maximum lifespan of sea urchin species and is consistent with the observation that average telomere length across species does not generally correlate with interspecific variation in maximum lifespan"
Interesting and similar to a report I read about starfish clones living far longer. I also notice they fell into the same trap about telomeres, given that it isn't about having longer Telomeres (mice have long telomeres)that dictates lifespan.
The frequently made misconception about telomeres is that telomere length defines or causes aging, it does not. An organism’s telomere length has little to do with how long it lives or how fast it ages. People often point out, some animals, such as mice, have long telomeres and a short lifespan, while other animals, such as humans, have much shorter telomeres but longer lifespan.
To clarify, Telomere theory doesn’t suggest that telomere length controls aging, in fact telomere length is irrelevant to aging. It is the change in telomere length that controls cell aging. The key isn't how long your telomeres are at birth, but how much your telomeres have shortened relative to that starting length. It's this shortening that changes gene expression.
Changes in telomere lengths from birth to old age in mice and other animals show clearly that telomere shortening – or rather, the way in which shortening telomeres cause changes in gene expression – is a primary driver of aging of the cell and therefore the organism.
Interesting article though and just reinforces support that telomeres are far more important to aging than some dismiss them and shows once again that researchers often fall into the same misunderstandings people make about telomere biology.