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ScienceWeek
CELL BIOLOGY: A SINGLE CELL LIVING 250 MILLION YEARS?
The following points are made by Christopher R. Brodie (American Scientist 2005 Nov-Dec):
1) What is the oldest living thing on Earth? A Madagascar radiated tortoise given to the Tongan royal family by Captain James Cook in the 1770s was at least 188 years old when it died in 1965. A creosote bush in the California desert has been dated at approximately 12,000 years. The King's lomatia plant in Tasmania is estimated to be at least 44,000 years old and is still growing (although it does not seem to be able to reproduce sexually). But the age of these organisms may be dwarfed by the apparent age of a recently discovered living bacterium: 250 million years.
2) In 2000, a research team described the isolation of a dormant but living bacterium from pockets (inclusions) of fluid trapped inside 250-million-year-old salt crystals buried half a kilometer deep in New Mexico. The bacterium was named Bacillus (later, Virgibacillus) species 2-9-3, and the report elicited strong skepticism from many quarters. Biological chemists doubted that nucleic acids could remain pristine over such time periods. Even had the bacterium hibernated as a hardy spore, its DNA surely would have broken down over 250,000 millennia, if not from the barrage of ultraviolet light during its long-ago residence on the surface, then from naturally occurring terrestrial radiation over the Earth's evolution. Geologists questioned the age of the fluid inclusions, arguing that certain features of the Salado Formation (the source of the halite crystal) suggested that flaws in the rock had permitted the intrusion of more recent fluid (which, by inference, had carried more recent bacteria into the ancient rock).
3) Geneticists pointed out that one of the bellwether genes that the group had sequenced -- one that encodes the so-called 16S ribosomal subunit -- was far too similar to its counterpart in another strain of bacteria. According to this critique, either the "ancient" bacterium was actually a contaminant, or its descendants had inexplicably failed to change in the past 250 million years.
4) But the research group that discovered the bacterium has followed up the original report with publications that seek to counter each of these criticisms. In 2002, the group reported their calculation that the degree of genetic damage caused by normal traces of radioactive potassium-40 in the surrounding rock was not great enough to rule out a quarter-billion years of bacterial survival. In April of 2005, an enlarged group of researchers reported a test of the idea that inclusions in the salt crystals were newer than the surrounding rock. The results suggest the crystals that formed around pockets of fluid (and presumably bacteria) were created on or near the surface instead of far underground.
5) Many questions remain. Would not organic molecules crucial to life, including DNA, spontaneously degrade in 250 million years even in the absence of ionizing radiation? Do the older and nonviable inclusion pockets contain the remains of expired microbes? And, perhaps most interestingly of all, what is the mechanism? How do these ancient organisms manage to survive so long?[1-3]
References (abridged):
1. Vreeland RH, Rosenzweig WD, Lowenstein T, Satterfield C, Ventosa A. Fatty acid and DNA analyses of Permian bacteria isolated from ancient salt crystals reveal differences with their modern relatives. Extremophiles. 2005 Aug 30
2. Vreeland RH, Straight S, Krammes J, Dougherty K, Rosenzweig WD, Kamekura M. Halosimplex carlsbadense gen. nov., sp. nov., a unique halophilic archaeon, with three 16S rRNA genes, that grows only in defined medium with glycerol and acetate or pyruvate. Extremophiles. 2002 Dec;6(6):445-52.
3: Maughan H, Birky CW Jr, Nicholson WL, Rosenzweig WD, Vreeland RH. The paradox of the "ancient" bacterium which contains "modern" protein-coding genes. Mol Biol Evol. 2002 19(9):1637-9
American Scientist http://www.americanscientist.org
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Related Material:
CELLULAR SENESCENCE, CANCER, AND AGING
The following points are made by A. Krtolica et al (Proc. Nat. Acad. Sci. 2001 98:12072):
1) Multicellular organisms have evolved mechanisms to prevent the unregulated growth and malignant transformation of proliferating cells. One such mechanism is "cellular senescence", which arrests proliferation (essentially irreversibly) in response to potentially oncogenic events. Cellular senescence appears to be a major barrier that cells must overcome to progress to full-blown malignancy.
2) Cellular senescence was first described as a process that limits the proliferation of cultured human fibroblasts ("replicative senescence"). Proliferating cells progressively lose telomere DNA, and short telomeres, which are potentially oncogenic, elicit a senescence response. In addition, DNA damage, expression of oncogenes, and supraphysiological mitogenic signals also cause cellular senescence. Cellular senescence is controlled by tumor suppressor genes and seems to involve a checkpoint that prevents the growth of cells at risk for neoplastic transformation. In this regard, cellular senescence is similar to apoptosis. However, whereas apoptosis kills and eliminates damaged or potential cancer cells, cellular senescence involves a stable arrest of growth.
3) Cellular senescence is also thought to contribute to aging, although how it does so is poorly understood. In addition to arresting growth, senescent cells show changes in function. Because senescent cells accumulate with age, they may contribute to age-related declines in tissue function. If so, cellular senescence may be an example of "antagonistic pleiotropy". Aging phenotypes are thought to result from the declining force of natural selection with age. Consequently, traits selected to maintain early life fitness can have unselected deleterious effects late in life, a phenomenon termed "antagonistic pleiotropy". The senescence-induced growth arrest may suppress the development of cancer in young organisms. The functional changes, by contrast, may be unselected consequences of the growth arrest and thus compromise tissue function as senescent cells accumulate.
Proc. Nat. Acad. Sci. http://www.pnas.org
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Related Material:
AGING, LIFESPAN, AND SENESCENCE
Notes by ScienceWeek:
Our knowledge of the basis of senescence of cells, tissues, and organisms (including humans) has entered a new phase in recent decades because of the new vistas opened by molecular biology. Model systems have started to provide insights, and one important approach has been the identification of genes that determine the lifespan of an organism. The very existence of genes that when mutated can extend lifespan suggests to many researchers that one or a few processes may be critical in aging, and that a slowing of these processes may slow aging itself.
The following points are made by L. Guarente et al (Proc. Nat. Acad. Sci. 1998 95:11034):
1) In the budding yeast Saccharomyces cerevisiae, aging results from the asymmetry of cell division, which produces a large mother cell and a small daughter cell arising from the bud. Much of the macromolecular composition of the daughter cell is newly synthesized, whereas the composition of the mother cell grows older with each cell division. It has been shown that mother cells of this yeast species divide a relatively fixed number of times, and exhibit a slowing of the cell cycle, cell enlargement, and sterility. Analysis of *ribosomal DNA in old cells reveals an accumulation of *extrachromosomal ribosomal DNA of discrete sizes, apparently representing a cumulative fragmentation of chromosomal ribosomal DNA. The authors suggest it will be of great interest to assess the generality of this process as an aging mechanism.
2) In Caenorhabditis elegans, the *neurosecretory system regulates whether animals enter the reproductive life cycle or arrest development at a primitive *diapause stage. Developmental arrest is apparently induced by a *pheromone and involves behavioral and morphological changes in many tissues of the animal, with the lifespan becoming 4 to 8 times longer than that of the normal 3-week lifespan of fully developed animals. Declines in pheromone concentration induce recovery to reproductive adults with normal metabolism and lifespan. Genes that regulate the function of the C. elegans diapause and the neuroendocrine aging pathway have been identified, and at least one of these genes codes for an *insulin-like receptor apparently involved in metabolism. The authors suggest that if the association of longevity and diapause is general, it is possible that *polymorphisms in the human insulin receptor-signaling pathway genes and related gene *homologues may underlie genetic variation in human longevity.
3) In plants, there is a large range of lifespans in the various plant kingdoms. Certain tree species live for well over a century, whereas other plants complete their life cycle in a few weeks. The "yellowing" of leaves is often referred to in the plant literature as leaf senescence or the "senescence syndrome" -- referring to the process by which nutrients are mobilized from the dying leaf to other parts of the plant to support their growth. The senescence syndrome is characterized by distinct cellular and molecular changes, with the chloroplast the first part of the cell to undergo disassembly (producing the "yellowing"). In many plant species, certain hormones can either enhance or delay senescence. Although the genes that are expressed during the plant senescence syndrome (as well as ways to manipulate such senescence) have been identified, much remains to be done to understand the molecular basis of aging in plants. For example, nothing is known about the signal transduction pathways that lead to altered gene expression during senescence, or how plant hormones such as *cytokinin influence senescence. But there are now many tools to explore this process. The authors conclude: "It remains to be seen whether common mechanisms link the aging process in diverse organisms."
Proc. Nat. Acad. Sci. http://www.pnas.org
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Notes by ScienceWeek:
ribosomal DNA: A ribosome (not to be confused with riboZYME) is a small particle, a complex of various ribonucleic acid component subunits and proteins that functions as the site of protein synthesis. The term "ribosomal DNA" refers to the gene or genes that code for the RNA in ribosomes. In other words, the term "ribosomal DNA" does not refer to any DNA in ribosomes (there is no DNA in ribosomes).
extrachromosomal: In general, this refers to anything outside of chromosomes, and in this case to DNA fragments unincorporated into chromosomal DNA.
neurosecretory system: In general, all neural systems contain both neurons that themselves secrete chemical messengers and neurons that signal special secretory cells to secrete chemical messengers. A neurosecretory pathway is a delineated signaling system that involves such a resultant secretion.
diapause: In general, this refers to any programmed period of suspended development in invertebrates.
pheromone: In general, a chemical substance which, when released into an animal's surroundings, influences the development or behavior of other individuals of the same species.
insulin: A protein hormone that promotes uptake by body cells of free glucose and/or amino acids, depending on target cell type.
polymorphisms: A genetic polymorphism is a naturally occurring variation in the normal nucleotide sequence of the genome within individuals in a population. Variations are denoted as polymorphisms only if they cannot be accounted for by recurrent mutation and occur with a frequency of at least about 1 percent.
homologues: In general, the term "homologous" means having the same structure. But the term has special uses in genetics and evolution biology.
cytokinin: A group of plant growth substances. They are chemically identified as derivatives of the purine base adenine. They stimulate cell division and determine the course of differentiation. They work synergistically with other plant hormones called "auxins".
ScienceWeek http://scienceweek.com
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