Fight Aging!

A great deal of research into fundamental mechanisms associated with aging and the way in which metabolism determines variations in natural longevity has been carried out - and is still carried out - using yeast cells. The phenomenon of enhanced health and longevity with calorie restriction exists in yeast, for example, and involves similar mechanisms to those found in mammals. It is not the only common point of reference.

Yeasts are not animals, but rather forms of fungus, or at least belong to various branches of that large taxonomy. But what about the kingdom of plants? Plants age, and that fact can be investigated, and the mechanisms compared with those of mammals. Yet their cells are are arguably more different from ours than are those of yeast, so can the study of aging in plants be expected to yield anything that is of practical value when it comes to intervening in mammalian aging to extend healthy life? There are researchers who think so, and this open access paper serves as an overview of some of their arguments, with pointers to other papers in a recent issue of the Journal of Ecology:

Plants do not count... or do they? New perspectives on the universality of senescence

Surprisingly, little is known about the general patterns, causes and consequences of whole-individual senescence in the plant kingdom. There are important differences between plants and most animals, including modular architecture, the absence of early determination of cell lines between the soma and gametes, and cellular division that does not always shorten telomere length. These characteristics violate the basic assumptions of the classical theories of senescence and therefore call the generality of senescence theories into question.

Most classical theories of senescence were developed with an implicit general animal or explicit human bias in mind. In spite of taxonomic biases, understandably driven by an anthropocentric interest in delaying death and improving life quality at advanced ages, the claim has been made that senescence is universal. Hamilton stated that senescence should occur even 'in the farthest reaches of almost any bizarre universe'. His assertion is of broad interest to evolutionary biologists in general and plant ecologists in particular because (i) it suggests the existence of a universal rule of ecology and evolution that is yet to be tested, and (ii) it obviously suggests that plants are not immune from senescence.

The universality of senescence rests on the assumption that the wear-and-tear of life is cumulative and inescapable over an organism's life span because time flows only in one direction. Yet, plants show extreme plasticity, being able to retrogress to juvenile stages under specific conditions. Chen et al. recently showed that the genetic and physiological activity of grafted stems of Sequoia sempervirens is the same as that in juveniles and very distinct from that of ungrafted adults. Plants have been historically considered as populations of modules in a continuous state of renewal and replacement, allowing continuous whole-plant rejuvenation. The relationship between leaf senescence, module senescence and whole-plant senescence remains largely unexplored, and yet full of potential. For instance, many species (e.g. the orchid Spiranthes spiralis) completely renew their photosynthetic and below-ground storage tissues annually. These species are potentially in a state of 'perpetual somatic youth'.

The field of senescence is by historical inertia dominated by research on humans. The main emphasis of research into senescence to date has been on whether and how humans can slow it down, and even postpone it. We argue that there are at least three reasons why human demographers, animal ecologists and plant population ecologists should work together.

First, all three parties are currently asking the same questions, although perhaps with different terminology. Human demographers are interested in how cultural background and migration affect population dynamics and senescence rates, whereas animal and plant population ecologists are interested in maternal effects and dispersal.

Second, senescence is a phenomenon caused by evolutionary processes, and the comparative method has previously proved useful in ascertaining the ecological and physiological processes necessary for its evolution. Research that ignores taxonomic boundaries will advance our understanding of evolutionary senescence.

Thirdly, for decades, animal demographers have been developing robust statistical tools to explore the evolution of senescence that account for differences between individuals within populations with imperfect long-term data. All of these techniques could prove useful in the plant world too, particularly in the examination of long-lived species. Furthermore, we argue that the transfer of knowledge between these research factions should be tri-directional. For instance, the work by Caswell & Salguero-Gómez [introduces] a novel method for quantifying selection gradients on age and stage in plants that is equally applicable to the analyses of data from humans and the rest of the animal kingdom.

I would argue that continuous renewal seen in some plant species is similar in relevance to the exceptional regeneration of hydra, or the strange life cycle of the jellyfish Turritopsis Dohrnii - by which I mean interesting, but not of any great relevance to human aging. Plants and hydra and jellyfish all lack the complex structures that higher animals possess. We can't just regenerate everything or throw away the majority of our body or regress back to earlier life stages because we have minds and other systems that are bound to the physical structure and specific existing cells of our nerve and brain tissue. Becoming complex seems to have the attached cost of a loss of regenerative capacity, except when it comes to our germ cells and early embryos, which seem quite capable of rejuvenation when needed. But then they are not possessed of complex structures, and arguably have more in common with the hydra than with an adult individual.