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Báo cáo y học: "Transcriptional (dys)regulation and aging in Caenorhabditis elegans"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Minireview cung cấp cho các bạn kiến thức về ngành y đề tài: Transcriptional (dys)regulation and aging in Caenorhabditis elegans. | Minireview Transcriptional dys regulation and aging in Caenorhabditis elegans Zachary Pincus and Frank J Slack Address Department of Molecular Cellular and Developmental Biology Yale University New Haven CT 06520 USA. Correspondence Frank J Slack. Email frank.slack@yale.edu Published 16 September 2008 Genome Biology 2008 9 233 doi 10.1186 gb-2008-9-9-233 The electronic version of this article is the complete one and can be found online at http genomebiology.com 2008 9 9 233 2008 BioMed Central Ltd Abstract A circuit of transcription factors has been discovered in Caenorhabditis elegans that could provide a link between laboratory-defined intracellular longevity pathways gene dysregulation and the process of normal aging. The fact that single-gene mutations can prolong an organism s lifespan might seem unlikely but many geronto-genes have been identified in model organisms that when knocked out or over- or underexpressed increase or decrease lifespan in the laboratory environment. These genes largely assort into several now-familiar pathways 1 2 many of which converge on the insulin insulin-like growth factor I IGF-I signaling pathway which in Caenorhabditis elegans includes daf-2 an insulin IGF-I receptor homolog age-1 which encodes a phosphatidylinositol 3-OH kinase PI3K at the top of the DAF-2-activated signaling cascade and daf-16 a forkhead-family transcription factor that is inactivated by this cascade. Nevertheless it is unclear whether the activities of these longevity pathways are modulated during normal aging and as such their role in the process of senescent decline in wild-type individuals is uncertain. Several pathways with longevity phenotypes in knockout animals may not be relevant to normal aging these include the insulin IGF-1 pathway the endoplasmic reticulum stress response mediated by the sirtuin SIR-2.1 and mitochondrial electron transport 3 . Because of this many researchers in the field suspect that aging is primarily driven by accumulation of