Logical Biology 5(1): 89-91, 2005

SHORT COMMUNICATION

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LETTER TO THE EDITOR

 

Searching for the Deep Root and

Fundamental Mechanism of Biotic Aging

 

Shi V. Liu

 

Eagle Institute of Molecular Medicine

Research Triangle Park, North Carolina, USA

 

E-mail: SVL@logibio.com

 

(Received 2005-03-11; accepted 2005-03-18 on condition *)

(Published online 2005-03-18)

 

HIGHLIGHT

 

Biotic aging is an ancient topic and has captured human interest for long time.  However, our current understanding of biotic aging may be very limited because it is restricted to only the eukaryotic world of life.   This letter urges researchers and readers to pay attention to the study on prokaryotic aging because it may help to reveal the deep root and fundamental mechanism of biotic aging.

 

KEY WORDS

 

Aging, Eukaryotic aging, Prokaryotic aging, Cell aging, Evolution

 

 

Dear Editor:

 

I am very delighted to see that aging once again became a focal point in scientific publication as reflected by the special issue of Cell, Reviews on Aging (Vol. 120. No. 4, Feb. 25, 2005).  However, I am a little disappointed to see that current studies on biotic aging are still largely confined within the eukaryotic world.  This situation is evident from the contents of the 11 reviews in this special issue of Cell because they all addressed aging in eukaryotic organisms, especially multicellular organisms.  Aging in prokaryotic organisms was mentioned only in one review but no real insight was given (8).

The evolutionary tree of biotic aging as depicted right now goes deep only to unicellular eukaryotic yeast and back only to 1 billion years ago (6).  However, with recent highlight on bacterial aging (5, 10), we may need to re-examine our perceptions on biotic aging.  If aging also occurs in prokaryotic world, as predicted by theoretical analyses (13, 15-17) and indicated by experimental observations (1, 16, 18, 19, 22), then our search for the root of biotic aging should go even deeper.

Facing such a challenge and opportunity, we may particularly need to re-evaluate the validity and suitability of some dominant theories of biotic aging that are based on or related to only the eukaryotic features.  These include disposable soma model of aging (9), the mitochondria link for aging (2), and the telomere shortening hypothesis (3, 20).  In my opinion, some of these theories more likely explain the consequences rather than identify the fundamental causes of biotic aging. We should also realize that some proposed aging mechanisms such as the endocrine regulation of aging (7), the sex and death connection (21), and the tumor suppression and longevity (4) may only address the superficial manifestations of aging and have an even limited applications because they are specific to more complex biotic features that exist only in the even higher forms of eukaryotic life.

The discovery of prokaryotic aging and, more importantly, the revised view of bacterial/cell life (13, 15-17) ends a long-standing dichotomy in biology and ushers in a unification of all life forms under some common fundamental principles (11).  This unification of biology also eliminates a major road block against finding common and fundamental cause and mechanism for biotic aging across the divisions of phylogenetic domains or kingdoms.  A hypothesis which links DNA aging with cell aging and combines genetics with epigenetics is proposed (12).  This hypothesis may serve as a new theoretic framework for studying aging from molecular level to the cell/organismal level.  This conceptual paradigm shift, along with a methodological paradigm shift in cell age-synchronization (14), should lead future study on biotic aging into a deep level and result in productive outcome.

 

REFERENCES

1.         Ackermann, M., S. C. Stearns, and U. Jenal. 2003. Senescence in a bacterium with asymmetric division. Science 300:1920.

2.         Balaban, R. S., S. Nemoto, and T. Finkel. 2005. Mitochondria, oxidants, and aging. Cell 120:483-95.

3.         Bodnar, A. G., M. Ouellette, M. Frolkis, S. E. Holt, C. P. Chiu, G. B. Morin, C. B. Harley, J. W. Shay, S. Lichtsteiner, and W. E. Wright. 1998. Extension of life-span by introduction of telomerase into normal human cells. Science 279:349-52.

4.         Campisi, J. 2005. Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. Cell 120:513-22.

5.         Ferber, D. 2005. Microbiology: Immortality dies as bacteria show their age. Science 307:656.

6.         Guarente, L., and F. Picard. 2005. Calorie Restriction- the SIR2 Connection. Cell 120:473-82.

7.         Kenyon, C. 2005. The plasticity of aging: insights from long-lived mutants. Cell 120:449-60.

8.         Kirkwood, T. B. 2005. Understanding the odd science of aging. Cell 120:437-47.

9.         Kirkwood, T. B., and R. Holliday. 1979. The evolution of ageing and longevity. Proc. R. Soc. Lond. B. Biol. Sci. 205:531-546.

10.       LDC. 2005. Microbiology: Unequal fission. Science 307:1015-1016.

11.       Liu, S. V. 2005. It is a high time to unify biology under common life principles. Logical Biology 5.

12.       Liu, S. V. 2005. Linking DNA aging with cell aging and combining genetics with epigenetics. Logical Biology 5:51-55.

13.       Liu, S. V. 2000. Logical fallacies and methodological mistakes in microbiology - An overview. Logical Biology 1:25-31.

14.       Liu, S. V. 2004. Method and apparatus for producing age-synchronized cells. US patent US6767734B.

15.       Liu, S. V. 2004. Prokaryotic aging: Breaking through the “cell cycle” limitation. Logical Biology 4:1-6.

16.       Liu, S. V. 1999. Tracking bacterial growth in liquid media and a new bacterial life model. Science in China 42:644-654.

17.       Liu, S. V. 2000. What is bacterial life? Logical Biology 1:5-16.

18.       Liu, S. V., and J. J. Zhang. 2004. Age synchronization of Caulobacter crescentus and implications for prokaryotic aging study. Logical Biology 4:7-15.

19.       Liu, S. V., and J. J. Zhang. 2004. Crossband in Caulobacter’s stalk is a cell reproduction remnant and bacterial age indicator. Logical Biology 4:16-27.

20.       McEachern, M. J., A. Krauskopf, and E. H. Blackburn. 2000. Telomeres and their control. Annu Rev Genet 34:331-358.

21.       Partridge, L., D. Gems, and D. J. Withers. 2005. Sex and death: what is the connection? Cell 120:461-72.

22.       Stewart, E. J., R. Madden, G. Paul, and F. Taddei. 2005. Aging and death in an organism that reproduces by morphologically symmetric division. PLoS Biol 3:295-300.

 

 

* This manuscript was accepted on the condition that it becomes eligible for Logical Biology to publish when author finally agrees to publish it after failure in seeking publication in “traditional” journals.  The current publication is the exact version submitted to Cell on March 11th, 2005.  The only changes made are the layout and the reference styles.  Cell discussed the letter editorially and concluded that “at this time your letter does not seem appropriate to consider for the journal.”