NIH Common Fund song & video contests

“We want to know whether our future baby’s health is based on genes or the environment.” This is a concern shared by a lot of would-be parents for sure, and is the question posed to Dr. M. Elizabeth Ross at the beginning of this short video. The video, made by the labs of Dr. Ross and Dr. Christopher E. Mason at Weill Cornell Medical College is part of a competition sponsored by the NIH to commemorate the 10th anniversary of the Common Fund.

Logo for the NIH Common Fund 10-Year Commemoration Song & Video Competitions

The video takes a tongue-in-cheek approach to explaining an NIH-funded project investigating the role of epigenetic changes in birth defects. The contest ends tomorrow, May 9, and the results will be determined by the number of “Likes” the videos receive on YouTube.

To vote for this or any of the other amazing videos (and songs), check out the contest page here.

 

What makes a Nature Genetics paper?

largecoverIn the editorial published in the current issue of Nature Genetics, we draw attention to the development and implementation of community standards for biomedical publications. We also note that we will be discussing our own standards—interactively with the community, we hope—on this blog.

The goal is two-fold. First, we’d like to better communicate to researchers what we’re looking for in specific sub-fields (eg: genomic associations, cancer studies, epigenetics, evolutionary genetics, data analysis, etc) to more clearly answer the question “what makes a Nature Genetics paper?” Second, we want you to help us update what a Nature Genetics paper should be. Are there criteria we should be applying that we’re not? Don’t be shy. Obviously, we love to hear what we’re doing right, but it’s much more helpful to learn what we’re doing wrong.

So, to start off, I’m asking you: What makes a Nature Genetics paper? What should make a Nature Genetics paper? Send me your questions about our editorial processes or your comments/suggestions either in the comments to this post, by email (brooke.laflamme [at] us.nature.com) or on Twitter (@Brooke_LaFlamme). We will post contributions without name attribution unless you specify that you want to be named. For reasons of editorial responsibility we will need to record your name and affiliation offline. Questions and comments will be answered by staff on our editorial team in future posts.

 

 

 

 

New non-coding RNAs keep stem cells stemmy

Human embryonic stem cells. Image adapted from Russo E (2005) Follow the Money—The Politics of Embryonic Stem Cell Research. PLoS Biol 3(7): e234. doi:10.1371/journal.pbio.0030234

Human embryonic stem cells. Image adapted from Russo E (2005) Follow the Money—The Politics of Embryonic Stem Cell Research. PLoS Biol 3(7): e234. doi:10.1371/journal.pbio.0030234{credit}Nissim Benvenisty{/credit}

Stem cells are increasingly being used to develop new disease treatments and to understand the basic biology of a number of diseases. However, one of the questions that still needs to be answered regarding stem cells is how they manage to stay in a pluripotent state, instead of differentiating into other cell types. Understanding how pluripotency is maintained has important implications for the optimization of stem cell-based therapies and to the understanding of disease states such as cancer than involve an aberrant undifferentiated state.

Earlier this week in Nature Genetics, Piero Carninci, Alistair Forrest and colleagues (including the FANTOM consortium) reported the identification of a new class of non-coding RNAs that appear to be important for maintaining pluripotency. They name these new RNAs “Non-annotated stem transcripts (NASTs),” since they previously had no known or predicted function. In fact, nearly none of them had even been identified as transcripts before this analysis.

The authors found that NASTs tend to be transcribed from long-terminal repeat (LTR) retrotransposon families, suggesting an important role for this particular “junk DNA”.  To figure out what they actually did in the cell, the group knocked down specific NASTs in mouse stem cells carrying a reporter for nanog (a marker of the pluripotent state). Basically, if the NAST in question is important for maintaining pluripotency, knocking it down should reduce the reporter expression (in this case, they’d glow less green under UV light). They tested 77 NASTs, 25 of which affected the expression of the nanog reporter. They confirmed that these NASTs affected pluripotency by also checking the expression of other marker genes.

In a press release, Dr. Carninci had this to say about the study:

“Our work has just begun to unravel the scale of unexpected functions carried out by retrotransposons and their derived transcripts in stem cell biology. We were extremely surprised to learn from our data that what was once considered genetic ‘junk’, namely ancient retroviruses that were thought to just parasite the genome, are in reality symbiotic elements that work closely with other genes to maintain iPS and ES cells in their undifferentiated state. This is quite different from the image given by textbooks that these genomic elements are junk.” 

As we delve deeper and deeper into our genome, we continue to find unique functions for “junk DNA”, which we’ve known isn’t actually junk for some time. Studies such as this one, that integrate data from a variety of sources and add functional data to test in silico predictions, will surely yield more exciting discoveries about our genomes.

 

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