:: Posted by American Biotechnologist on 06-24-2013
Intergenic DNA, or junk DNA as its more colloquially known, was once thought of as “extra” DNA strands that play no role in the transcriptional process. However, in recent years, it has been shown that Junk DNA is actually transcribed into Junk RNA which is not tranlasted into protein (unlike their non-junk counterparts). In fact, researchers have demonstrated that Junk RNA is actually created by upstream transcription which occurs when the transcriptional process moves both upstream and downstream from the DNA promoter region. Since coding RNA is created from the downstream process, upstream transcription results in non-translatable RNA.
In a new study published in Nature this week, researchers at MIT described a mechanism by which cells initiate but then halt the copying of RNA in the non-protein coding direction while allowing the downstream activity to continue unhindered. In this model, the poly-A-tail, along with a factor known as U1 snRNP, work together to halt the upstream copying of RNA and actually chop up “Junk RNA” before it becomes too long.
For further reading see MIT biologists reveal how cells control the direction in which the genome is read
:: Posted by American Biotechnologist on 03-28-2012
A hidden and never before recognized layer of information in the genetic code has been uncovered by a team of scientists at the University of California, San Francisco (UCSF) thanks to a technique developed at UCSF called ribosome profiling, which enables the measurement of gene activity inside living cells — including the speed with which proteins are made.
By measuring the rate of protein production in bacteria, the team discovered that slight genetic alterations could have a dramatic effect. This was true even for seemingly insignificant genetic changes known as “silent mutations,” which swap out a single DNA letter without changing the ultimate gene product. To their surprise, the scientists found these changes can slow the protein production process to one-tenth of its normal speed or less.
:: Posted by American Biotechnologist on 09-28-2010
The Harvard Medical School Blog, it takes 30, recently wrote a post on the controversy surrounding microRNA’s mechanism of action. In a nutshell, the controversy surrounds whether or not microRNAs act by inhibiting mRNA translation or mRNA stability. The studies involved used what may be considered not so robust methodologies which may have clouded the accuracy of their results.
In any event, the issue is quite interesting for anyone involved in transcriptional/translational research and the post does a good job of sizing up the debate. Below is a short snippit from the post itself:
A recent paper from the Bartel and Weissman groups (Guo et al. Mammalian microRNAs predominantly act to decrease target mRNA levels, Nature 466 835-40, PMID: 20703300) provides an interesting snapshot of the journey of a field from consensus to controversy to (one day?) consensus again.
At issue is the question of how microRNAs — small RNAs that control gene expression — have their effect. Clearly they bind specifically to messenger RNAs that carry a short target sequence; clearly, the overall result is that a reduced amount of protein is expressed from the targeted mRNA. But is the translation of the mRNA blocked, or is the mRNA itself destabilized, or both? The answer could affect everything from the way you measure an miRNA effect to the way you think about choosing targets for therapeutic applications. And the consensus in the field seems to be swinging fairly hard — or has swung, depending on who you talk to — from one extreme (the main effect is on translation) almost all the way to the other (most, but not all, of the effect is due to mRNA destabilization).
For more information see the It takes 30 blog from the Department of Systems Biology @ Harvard Medical School