Genome-wide views of aging gene networks
2015-01-13Genome-wide views of aging gene networks
paper
Stuart Kim in Molecular Biology of aging
More info for Table 1
"C:\Sync\cnio\2014\2014\11-04-2014d1017\Expanded aging microarray study table 11-04-2014d1017.xlsx"
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Table 1 lists 75 publications that use gene arrays to study aging involving diverse organisms (yeast, worms, flies, mice, rats, monkeys, and humans) and many tissues (including brain, muscle, kidney, liver, blood, eye prostate, and heart)
Possible sources of data to compare healthy and disease or aged networks 09-26-2014d1648
There is a list of gene expression publications in old and young mice in this paper (Table 1 pg 3)
Genome-wide views of aging gene networks
for c elegans
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genes that act in the insulin-like signaling path-
way such as daf-2, age-1, and daf-16
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This result shows that the mechanisms responsible for long life in insulin-like signaling mutants may be similar to those responsible for long life in dauers
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both aging and oxidative sress caused an increase in expression of purine biosynthesis, heat shock, antioxidant, and innate immune response genes
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Bahar et al. (2006) have recently provided evidence for a global change in the robustness of the transcriptional network as a function of age
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Bahar et al. used RT-PCR to measure expression of a set of randomly
chosen genes in single cardiomyocytes in young and old mice. They
found that in young mice, cardiomyocytes typically express genes at sim-
ilar levels, but that in old mice, individual cells have varying levels of gene
expression.
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Aging caused by a global increase in tran-
scriptional noise is a new and exciting potential mechanism for cellular
senescence.
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A long-held view is that accumulation of somatic mutations plays a key role in decreasing cellular function in old age
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there may be sites in the genome that are exceptionally prone to DNA damage, based on chromatin accessibility and GC content
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Resveratrol (3, 4', 5-trihydroxystilbene) is a plant-derived polyphe-
nolic compound that has been shown to extend the life span of yeast,
worms, ?ies and mice (Howitz et al. 2003; Wood et al. 2004; Viswanathan
et al. 2005).
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they showed that resveratrol counteracted the changes in gene expression caused by the high calorie diet
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These results suggest that c elegans aging may be caused by the presence of unfolded proteins in the ER
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A popular hypothesis is that accumulation of oxidative damage is a major cause of aging
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Zahn et al. (2006) have discovered genetic pathways that
show common age regulation in kidney, brain, and muscle
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only a very small fraction of wild mice achieve their maximal life span of 3 years
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the median life span in the United States was 47 years in 1900
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Of the five genetic pathways that were age-regulated in human, one (the electron transport chain genes) showed similar age regulation in the other three species
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expression of the electron transport chain may be a particularly interesting biomarker for aging because it scales with life span in species that are distantly related
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finally, an unsolved challenge is to develop new ways to analyze entire gene networks that can explain how similar genomes (such as mouse and human) give rise to organisms with vastly different life spans.