Induction of cellular senescence in immortalized cells by human chromosome 1

Article Abstract:

Aging is a process undergone not only by individuals, but also by body cells when they are grown under controlled conditions in the laboratory. Under such circumstances, some human cells divide a finite number of times, then show signs of aging, and die. Tumor cells, on the other hand, grow indefinitely and are called immortal. What it is that limits a cell's life span is not known, but there are two main theories. The error catastrophe theory holds that mutations and random damage, accumulating over time, eventually destroy the cell's ability to replicate. The genetic theory states that senescence (growing old) is genetically programmed, and it receives support from the finding that hybrids, or mixtures, of mortal and immortal cells do, in fact, age, suggesting that senescence is dominant over immortality. Fibroblast (connective tissue) cells with a known, finite, life span were fused with immortal cells and allowed to replicate. The majority (15/27) of the hybrids formed in the above manner showed signs of aging, as measured by standard cell culture techniques. Twelve hybrids, however, were immortal, and their chromosomes were examined to see whether the loss of senescence could be due to a chromosomal structure different from the cells that died. In all the immortal hybrids, human chromosome number 1 was missing. To see whether immortality was a direct result of the absence of chromosome 1, or whether the presence of this chromosome had induced aging in the cells with a finite life span, additional hybrids were made which contained chromosome 1. These cells grew old. In hybrids that were immortal, no chromosome 1 could be detected. These results were consistent with the hypothesis that human chromosome 1 contains a gene that regulates senescence. It is likely, however, that several genes control this process in the normal cell. (Consumer Summary produced by Reliance Medical Information, Inc.)

Tumors

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Expression of a zinc finger gene in HTLV-I and HTLV-II-transformed cells

Article Abstract:

Entry of a foreign molecule, or antigen, into the body stimulates the immune system to assume a defensive role. When the T cell, a type of white blood cell involved in the immune response, becomes activated, it begins to replicate and assume the identity of an activated T cell. Viruses can enter T cells and transform them into malignant agents by altering their genetic codes. Two retroviruses active in this regard are HTLV-I and HTLV-II (human T cell leukemia virus types I and II), associated with leukemia. Research on the mechanisms controlling T cell proliferation after infection by these viruses revealed that a gene designated as 225 (a zinc finger gene) appeared consistently in all the cell lines that had been transformed by HTLV-I or HTLV-II. Such zinc finger regions have been identified in other proteins that regulate transcription, one step in the DNA replication process. The structure of the protein expressed by this region is presented. Although the exact function of 225 is not known, evidence suggests that it may send a proliferative message to the cell, and then play a regulatory role in gene expression. This is the only transcription factor whose expression is activated in all cells that have been transformed by these two viruses. As such, it may be an important regulator of malignant transformation if retroviruses cause its production to become aberrant. (Consumer Summary produced by Reliance Medical Information, Inc.)

Molecular biology, HTLV infections, Retrovirus infections

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Mechanisms and evolution of aging

Article Abstract:

Aging would seem to be contrary to natural selection, but studies on the Caenorhabditis elegans have shown definite genetic influence. 'Age' mutations found so far indicate that the extension of life span by stress-response genes is more likely than truncation by biological-clock genes.

Cover Story, Oxidation, Physiological, Physiological oxidation, Stress (Physiology)

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