So you have performed some differential gene expression experiments and have discovered a (few) non-coding RNAs that are of conspicuous interest… What now? Unless you are lucky and someone else has already characterised your needle in a haystack, odds are little is known about this transcript. You might be tempted to paste that .fasta file into mfold and say: “Look! It folds into an RNA secondary structure!” yet this won’t tell you much, besides that your RNA might look like a Christmas tree in February. This video explains how you can find out which regions of your RNA transcript of interest might be responsible for its biological function.
Category Archives: Smithy’s structures
Ever so often, you stumble across a magnificent work of science. This was the case for me a few weeks ago when this work popped up in my news feed. The authors investigate how a genomic locus that is the strongest risk factor for artherosclerosis produces a regulatory non-coding gene that regulates other genes associated to the disease.
They used stable over-expression and knock-down approaches to investigate the role of distinct ANRIL (a long non-coding RNA, aka lncRNA) isoforms in several key mechanisms of atherogenesis. They show that this gene guides epigenetic effector complexes to specific genomic loci.
Through what molecular mechanism you ask? None other than via endogenous transposable elements–ALUs specifically–that have been harnessed through evolution to perform regulation of gene expression in our genomes. FYI, repetitive elements compose ~46% of the human genome, 20% of which are ALUs.
Last year, the massive ENCODE consortium disclosed that over 80% of the human genome appears to be functional through several detailed biochemical experiments. Their findings fuelled an already heated debate regarding the biological pertinence of similar findings. Many old-school biochemists and proponents of the “selfish” DNA hypothesis (who I collectively refer to as junk DNAy-sayers) dismiss the use of such data to support the notion that the majority of the genome is functional.
Amidst the nit-picking, bickering, and refutations, one logical argument stands out that somewhat confounds the ENCODE findings: the lack of detectable evolutionary conservation. Indeed, the statement that > 80% of the human genome sequence is biologically functional lies in stark contrast to the fact that < 9% of it is observed to be conserved throughout mammalian evolution. But is this estimate really accurate? Continue reading
The basics are up and running.