The mechanisms involved in aging appear to be conserved from Hydra to humans. Hydra immortality depends on an ability to maintain three distinct populations of stem cells, and the same could be concluded with respect to the germ cells and somatic nuclear material for more complex metazoans. The mechanism that appears to be common among all metazoans is the epigenetic control of gene silencing, such that a robust silencing activity is associated with young cells and increased transcriptional noise associated with aged cells. This essay details current theories that attempt to explain metazoan senescence.
Mechanisms of Interspecies Senescence
Senescence
The nature of human experience has impelled us throughout time to ponder mortality and immortality. Today, biologists are actually beginning to provide answers to what were formally purely philosophical and religious questions. What follows is a discussion of the mechanisms underlying biological mortality and immortality, otherwise known as senescence.
In terms of biological immortality, the cnidarian Hydra stands out. Some hydra species have been shown to survive indefinitely under laboratory conditions, by relying on asexual reproduction (Bosch, 2009, p. 484). Bosch suggests that asexual budding confers an evolutionary advantage to Hydra, because it provides a mechanism for generating enough offspring to survive competition and predation pressures from other species. Rapid asexual budding, in turn, requires cells to proliferate continuously. In other words, the stem cell populations in Hydra, which give rise to the various cell types required to make a complete organism, appear to be immortal. This is consistent with recent research findings that suggest accelerated aging (progeria) in humans is due in part to defects in the stem cell populations.
The progeny of Hydra stem cells differ from their counterparts in more complex metazoans, as well (Bosch, 2009, p. 481). For example, ectodermal epithelial cells have been shown to retain the capacity for transdifferentiation into a variety of other cellular phenotypes. For example, these cells can change their shape, function, and interactions with other cells within the organism. Differentiation is therefore a normal process in Hydra development, but commitment to a specific cellular phenotype is not. In contrast, phenotypic commitment is a part of normal development for bilateral metazoans. It should be noted though, that the three stem cell populations that give rise to all the cellular phenotypes in Hydra are not capable of transdifferentiation and are therefore committed to a specific cellular phenotypes.
The ability of the Hydra stem cell progeny to differentiate seems to depend on epigenetic reprogramming (Bosch, 2009, p. 481), which suggests that the maintenance of a pluripotent, undifferentiated stem cell state, and thus biological immortality, also depends on maintenance of a defined epigenetic state. The epigenetic connection between biological immortality and mortality appears to extend to all metazoans. In the nematode Caenorhabditis elegans, the maintenance of a stem cell population depends in part on maintaining a specific epigenetic state (Rando and Chang, 2012, p. 47-51). In Drosophila, the epigenetic reprogramming of disc imaginal cells, which give rise to adult structures like legs and wings, can be induced by tissue fragmentation and regeneration. In addition, the cloning of mammals has depended on the ability to reprogram the epigenetic state of germ and somatic cells. This was accomplished as early as 1952 by transferring the nuclear material of a somatic cell to an enucleated oocyte.
The aging process in all metazoans therefore seems to be selectively controlled in terms of cellular phenotype. The stem cells in Hydra are essentially immortal, and the same could be argued for the germ cells and the nuclear material of somatic cells in worms, flies, mice, and humans. In addition, most metazoan somatic cells appear to retain the capacity to reset to a pluripotential state, although there are some exceptions to this rule. Exceptions include cells exposed to significant levels of reactive oxygen species (ROS). In fact, cellular senescence, and thus aging, was believed to be the result of primarily the accumulation of DNA damage due to reactive oxygen species (for example see: Metcalfe and Alonso-Alvarez, 2010). However, the ability of somatic cells to become rejuvenated after transfer to an oocyte suggests this theory is flawed (Rando and Chang, 2012, p. 51-52).
Recent research efforts have provided additional support for the theory that epigenetics determines aging and cellular senescence. Gene products that are involved in establishing a repressive chromatin structure, or silenced state, have been linked in a positive manner with longer life spans in C. elegans and D. melanogaster (Rando and Chang, 2012, p. 52). The association between gene products controlling chromatin silencing has been supported by experiments in mice. Due to the highly conserved nature of the chromatin silencing machinery, the same genes are expected to be associated with human longevity as well.
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