MicroRNA molecules are a part of the complex machinery of gene expression that builds proteins from the blueprints encoded in DNA. This machinery determines levels of specific proteins in a cell. By doing so it steers cell processes, and is in turn steered by the structures and activities of those proteins. A cell is an enormously intricate feedback loop.
Individual differences in longevity exist for entities living in very similar environments, and these differences have to arise from some collection of mechanisms - such as the differences in gene expression between individuals. Here researchers move from checking global gene expression levels to checking microRNA levels in much the same way: to see if they can find correlations between specific microRNA molecules and individual longevity. No amazing results yet, but these are early days:
In the round worm Caenorhabditis elegans, genetically identical animals exhibit large differences in their lifespan with associated declines in motor skills and pathogen resistance. We have previously shown that aging behavioral phenotypes in individual worms are associated with statistically significant changes in gene expression. We hypothesized that the distinct age dependent gene expression profiles that exist between genetically identical individuals are likely to be mediated through variations in gene regulatory networks. miRNAs represent likely candidates for mediating some of this variation in expression as they are known modulators of gene expression, which have been shown to act to facilitate the robustness of such networks.
We measured the abundance of 69 miRNAs expressed in individual animals at different ages [and] found that miRNA abundance was highly variable between individual worms raised under identical conditions and that expression variability generally increased with age. To identify expression differences associated with either reproductive or somatic tissues, we analyzed wild type and mutants that lacked germlines. miRNAs from the mir-35-41 cluster increased in abundance with age in wild type animals, but were nearly absent from mutants lacking a germline, suggesting their age-related increase originates from the germline. Most miRNAs with age-dependent levels did not have a major effect on lifespan, as corresponding deletion mutants exhibited wild-type lifespans. The major exception to this was mir-71, which increased in abundance with age and was required for normal longevity. Our genetic characterization indicates that mir-71 acts at least partly in parallel to insulin/IGF like signals to influence lifespan.