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Evolution: RNA Silencing Sheds Light on the RNA World

Intro: “These findings provide a link between RNA silencing and the earliest mechanisms of RNA transcription – perhaps shedding light on both the origins of RNA replication (and therefore life) and the evolution of RNA silencing“.

By PLoS Biology: RNA silencing – also known as RNA interference* – is an intriguing phenomenon in which short, double-stranded RNA “triggers” can prevent the expression of specific genes. First discovered in plants, RNA interference is now recognized as a widespread, if not ubiquitous, phenomenon, and it is causing great excitement as an experimental technique for selectively blocking gene expression.

The mechanisms of RNA silencing have been intensively studied. One important step is the formation of single-stranded RNA pieces (called siRNAs) from the double-stranded triggers. In “lower” organisms – including plants, protozoa, fungi, and nematode worms – it also involves an enzyme – called RNA-dependent RNA polymerase – that can generate a strand of RNA using existing RNA as a template. This means that it can create double-stranded RNA from single-stranded pieces of RNA. By doing this, it generates more triggers and so amplifies the effect of RNA silencing. Paula Salgado and her colleagues have studied the structure of one such polymerase, called QDE-1, and found that it provides clues to the earliest stages of evolution.

When a gene is transcribed and translated to generate a protein, the process begins with a DNA-dependent RNA polymerase. Like QDE-1, DNA-dependent RNA polymerases generate strands of RNA – the difference is that they use a DNA template to do it. The RNA they generate is called messenger RNA and is in turn used as the template for building a protein out of amino acids. The structures of DNA-dependent RNA polymerases have been described previously, so that the authors of this study could compare them with their new structure of QDE-1.

What they found was a remarkable similarity.

Continued at “RNA Silencing Sheds Light on the RNA World
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A related post from Monday, October 02, 2006:

RNA Interference: Nobel prize for genetic discovery goes to Mello and Fire

From BBC News (UK): Two US scientists have been awarded the Nobel Prize for medicine for their pioneering work in genetics.

The work of Dr Andrew Fire (Stanford University School of Medicine: homepage) and Dr Craig Mello (University of Massachusetts: homepage) could lead to new treatments for a range of illnesses, including viral infections and cancer.

They discovered a phenomenon called RNA interference, which regulates the expression of genes.

…The Nobel citation, issued by Sweden’s Karolinska Institute, said: “This year’s Nobel Laureates have discovered a fundamental mechanism for controlling the flow of genetic information.”…

…Scientists have speculated that the mechanism developed hundreds of millions of years ago as a way to protect organisms against invading viruses, which sometimes create double-stranded RNA when they replicate. [Evolution, Umass, Laureate, Science]

*Info on RNA interference:

RNA interference (also called “RNA-mediated interference”, but abbreviated RNAi) is a cellular mechanism for the targeted destruction of RNA molecules. RNAi involves double-stranded ribonucleic acid (dsRNA) that can specifically interfere with the expression of genes with sequences that are complementary to the dsRNA. RNAi is a form of post-transcriptional gene silencing in which an antisense RNA strand targets a complementary gene transcript such as a messenger RNA for cleavage by a ribonuclease. RNAi has been shown to be a common cellular process in many eukaryotes. The ribonuclease-containing multi-protein complex (RISC) that is involved in RNAi-mediated transcript cleavage is conserved across the eukaryotic domain, as is the enzyme Dicer that processes dsRNA to the short (about 24 nucleotides long) forms that can be used to specifically target complementary gene transcripts for destruction. [More]

John Latter / Jorolat
Evolution Research:
http://evomech5.blogspot.com/




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