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Home | Pregnancy Timeline | News Alerts |News Archive Nov 11, 2013

 

Fly eye color varies based on the level of RNA editing. Red eyes, left, suggest a lot of editing, while white eyes suggest little. Credit: Reenan lab/Brown University.


Researchers at the Georgia Institute of Technology and Emory University have demonstrated that compacting chromatin is essential to embryonic stem cell differentiation. Embryonic stem cells (ESCs) express several different types of H1 subtypes, and ESCs that fail to express these H1 subtypes show reduced chromatin compaction and impaired differentiation. The diminished differentiation capacity of these genes seems to derived from the inability of these cells to properly silence particular genes.

Yuhong Fan, assistant professor in the Georgia Tech School of Biology said, “While researchers have observed that embryonic stem cells exhibit a relaxed, open chromatin structure and differentiated cells exhibit a compact chromatin structure, our study is the first to show that this compaction is not a mere consequence of the differentiation process but is instead a necessity for differentiation to proceed normally,”

 







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Edited RNA + invasive DNA add individuality

An enzyme that edits RNA may loosen gene control over invasive snippets of DNA and affect how genes are turned on and off. In fruit flies, this newly understood mechanism appears to contribute to differences in individual eye color and life span.

The story of why we are all so different lies deep within the mixing and matching of DNA through breeding. A new study shows how a molecular mechanism for individual variation found in fruit flies uses components operating in a wide variety of species, including humans.


The newly found mechanism is based in a genetic oddity. Nearly all genomes — humans, fruit flies, even corn and rice — constantly grapple with parasitic snippets of genes called “transposons.”

These snippets copy themselves, move around, and embed themselves within DNA.

Left unchecked, transposons can alter genetic instructions, usually for the worse, sometimes for the better.

But other genes don’t leave transposons unchecked. They “look” for the tell-tale double-stranded RNA associated with transposons, chop the strands up, using the pieces to “silence” or "turn off" these invasions.


In a new paper published in Nature Communications, scientists reveal how an enzyme called ADAR, edits double-stranded RNAs in humans, flies, and many other creatures, by loosening the system that keeps “Hoppel” transposons silenced in fruit flies. Transposons are silenced by being tightly wound around tiny balls of material called chromatin. ADAR loosens the tightly wound RNA of the "silenced"  Hoppel transposons in fruit flies — allowing the gene to become active.

As the amount of ADAR varies from one individual to another, the amount of jailbreaking from chromatin prisons varies too. After realizing an abundance of ADAR reduces silencing in flies — and a lack of ADAR means widespread silencing — the researchers measured two levels of ADAR activity: in life span and in eye color.

The study was focused on fruit flies, ADAR, and the double-stranded RNA of the Hoppel transposon, but the ability of RNA editors to loosen the silencing of at least some transposons may be a source of individual variation in humans and other species too, said Brown University biologist Robert Reenan, senior author of the new study published online. Editing of double-stranded RNA — or a lack of editing — has already been linked to diseases in people, including amyloid lateral sclerosis and, specifically in the case of ADAR, Aicardi-Goutières syndrome.


“ADAR in humans functions the same way it does in flies, and double-stranded RNAs are made in humans the same way. They are all generic, off the shelf staples of our biological toolkit. This is not anything that is particular to flies.”

Robert A. Reenan, professor of biology, Department of Molecular Biology, Cell Biology and Biochemistry, Brown University


Many of Reenan’s studies focus on ADAR’s editing activity in the development of the nervous system, this investigation began years ago when lead author and then graduate student Yiannis Savva happened to overexpress ADAR in fruit fly salivary gland cells and found some ADAR bound to an unexpected site on chromosome four.

Reenan recalled: “I told him that’s either an artifact or it will be the centerpiece of your thesis.”

Various tests revealed that the chromosome four site was home to several Hoppel transposons and double-stranded RNA.

Savva and Reenan were curious about what business ADAR had with the transposon. Through years of experiments, they moved the transposons to gene locations where they normally weren’t found — and always subsequently found ADAR. Deleting the double-stranded RNA from chromosome four caused ADAR to disappear.

Savva and his collaborators then measured silencing of tranposons with varying levels of ADAR and found that the more ADAR there was, the less silencing of genes there was.

In collaboration with Stephen Helfand, an expert on the biology of aging, the team found that a reduction of ADAR increased fruitfly life span.

“As a loss of [gene] silencing has been associated with aging in Drosophila and other organisms, we performed lifespan analyses on [low-ADAR] adults and wild-type controls and found a ~20-percent increase in the median life span of [low-ADAR] males and females,” the authors wrote in Nature Communications.

Later they looked at eye color, using natural (wild-type) flies and those where ADAR activity was either artificially curtailed or excessively active. Natural or wild-type flies have eyes that run from red to white with various blends in between, reflecting the amount of silencing of their eye color gene. In flies with excessive ADAR, there was little gene silencing and eyes were red much more frequently. In the ADAR-hamstrung flies, virtually all of the eyes were white (reflecting a lot of silencing of the red color gene).

Ultimately, Savva said, ADAR appears to be allowing transposons like Hoppel to exercise their capacity to regulate gene expression, even though they are really just uninvited guests in the genome.

Said Savva:“What ADAR does is fine tune this regulatory network. In cells where you have ADAR, the network is activated. In cells where you don’t it’s silenced. It provides dynamic control.”

In other words, some of the differences among us may be apparent in the eyes of flies.

Abstract
Heterochromatin formation drives epigenetic mechanisms associated with silenced gene expression. Repressive heterochromatin is established through the RNA interference pathway, triggered by double-stranded RNAs (dsRNAs) that can be modified via RNA editing. However, the biological consequences of such modifications remain enigmatic. Here we show that RNA editing regulates heterochromatic gene silencing in Drosophila. We utilize the binding activity of an RNA-editing enzyme to visualize the in vivo production of a long dsRNA trigger mediated by Hoppel transposable elements. Using homologous recombination, we delete this trigger, dramatically altering heterochromatic gene silencing and chromatin architecture. Furthermore, we show that the trigger RNA is edited and that dADAR serves as a key regulator of chromatin state. Additionally, dADAR auto-editing generates a natural suppressor of gene silencing. Lastly, systemic differences in RNA editing activity generates interindividual variation in silencing state within a population. Our data reveal a global role for RNA editing in regulating gene expression.

In addition to Savva, Reenan, and Helfand, authors on the paper are James Jepson, Yoah-Jen Chang, Rachel Whitaker, Brian Jones, Nian Jiang, and Guyu Du of Brown; Georges St. Laurent of Brown and the St. Laurent Institute; and Michael Tackett and Phillipp Kapranov of the St. Laurent Institute.

The National Institute on Aging (grants: AG16667, AG24353, AG25277) and the Ellison Medial Foundation funded the research.

Editors: Brown University has a fiber link television studio available for domestic and international live and taped interviews, and maintains an ISDN line for radio interviews. For more information, call (401) 863-2476.

Original press release:http://news.brown.edu/pressreleases/2013/11/eyes