Mechanisms of Interspecies Senescence Research Paper

Pages: 3 (954 words)  ·  Bibliography Sources: 3  ·  File: .docx  ·  Level: College Senior  ·  Topic: Death and Dying  (general)


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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Young cells would therefore be defined as containing genomic material that is being actively maintained in a generally silenced state through promotion of histone H3 lysine 27 methylation and histone deacetylation (Rando and Chang, 2012, p. 52-53). Accordingly, the Polycomb group repressors and sirtuins (deacetylases) are found to be associated with the chromatin in young cells. In contrast, old cells can be discriminated young ones by the accumulation of DNA damage, the loss of associated sirtuins, and the replacement of Polycomb group proteins by those from the trithorax group. The trithorax group expresses proteins that function to trimethylate histone H3 at lysine 4, a marker for gene activation. The overall effect of this transition from a young chromatin state to an aged one, and the loss of robust silencing machinery, is an increase in transcriptional noise being generated.

TOPIC: Research Paper on Mechanisms of Interspecies Senescence the Assignment

In summary, senescence appears to be a regulated process responsive to the cellular and nuclear machinery that controls chromatin structure. This theory is supported by cloning experiments that rely on somatic nuclear transfer and the improbable immortality of Hydra species. Although oxidative damage remains a popular explanation for the aging process, unless the damage cannot be overcome by the cellular repair machinery, it appears unlikely that it will directly influence aging unless it damages genes involved in maintaining a silenced chromatin state.

Works Cited

Bosch, Thomas C.G. (2009). Hydra and the Evolution of Stem Cells. Bioessays, 31, 478-486.

Metcalfe, Neil B. And Alonso-Alvarez, Carlos. (2010). Oxidative stress as a life-history constraint: The role of oxygen species in shaping phenotypes from conception to death. Functional Ecology, 24, 984-996.… [END OF PREVIEW] . . . READ MORE

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How to Cite "Mechanisms of Interspecies Senescence" Research Paper in a Bibliography:

APA Style

Mechanisms of Interspecies Senescence.  (2012, May 2).  Retrieved July 27, 2021, from

MLA Format

"Mechanisms of Interspecies Senescence."  2 May 2012.  Web.  27 July 2021. <>.

Chicago Style

"Mechanisms of Interspecies Senescence."  May 2, 2012.  Accessed July 27, 2021.