Author: Ines Alvarez-Garcia

PLOS Biology at ASCB 2013: Open for Cell Biology

ASCB meet editorsAt PLOS Biology, we strongly believe that we are open for a reason: our aim is to publish high quality research in areas of broad significance, ensuring that it reaches the widest possible audience without any barriers to access. Cell biology is an area of research that we believe should be as openly available as possible by being published in an open access, CC-BY journal, with associated data being mineable and reusable.

PLOS Biology publishes cell biology research of exceptional significance, originality, and relevance that informs research in its field and influences thinking beyond. We encourage you to consider PLOS Biology as a high visibility outlet for your future research. We are interested in all areas of cell biology. To get a taste of the research in cell biology that we have recently published, check out the links below to access the latest research in this field.

I will be attending the 2013 American Society of Cell Biology annual meeting in New Orleans next week together with my colleagues from PLOS ONE, and while there I very much look forward to meeting with our Academic Editors, authors, and reviewers in the cell biology research community.

If you are also attending the meeting and would like to find out more about how to publish in an Open Access journal, please visit us at the PLOS booth, number 211, where you can meet me and my PLOS colleagues. PLOS Biology is organizing a ‘meet the editor’ session on Monday, December 16, from 12-1pm – so do come by then. Alternatively, you can email me at plosbiology[at]plos.org to arrange a time to chat.

Looking forward to meeting you in New Orleans!

 

OA logo

 

 

If you are interested in cell biology, you might want to read the following research articles – all Open Access and available to read to all:

 

The Circadian Clock Coordinates Ribosome Biogenesis. Céline Jouffe, Gaspard Cretenet, Laura Symul, Eva Martin, Florian Atger, et al. (2013)

 

Molecular Remodeling of Tip Links Underlies Mechanosensory Regeneration in Auditory Hair Cells. Artur Indzhykulian, Ruben Stepanyan, Anastasila Nelina, Kateri Spinelli, Zubair Ahmed, et al. (2013)

 

A Meiosis-Specific Form of the APC/C Promotes the Oocyte-to-Embryo Transition by Decreasing Levels of the Polo Kinase Inhibitor Matrimony. Zachary Whitfield, Jennifer Chisholm, R. Scott Hawley, Terry Orr-Weaver (2013)

 

Dynactin Subunit p150pGlued Is a Neuron-Specific Anti-Catastrophe Factor. Jacob Lazarus, Armen Moughamian, Mariko Tokito, Erika Holzbaur (2013)

 

Partial Inhibition of Adipose Tissue Lipolysis Improves Glucose Metabolism and Insulin Sensitivity Without Alteration of Fat Mass. Amandine Girousse, Geneviève Tavernier, Carine Valle, Cedric Moro, Niklas Mejhert, et al. (2013)

 

Strigolactone Can Promote or Inhibit Shoot Branching by Triggering Rapid Depletion of the Auxin Efflux Protein PIN1 from the Plasma Membrane. Naoki Shinohara, Catherine Taylor, Ottoline Leyser (2013)

 

Molecular Composition and Ultrastructure of the Caveolar Coat Complex. Alexander Ludwig, Gillian Howard, Carolina Mendoza-Topaz, Thomas Deerinck, et al. (2013)

 

HDAC4 Reduction: A Novel Therapeutic Strategy to Target Cytoplasmic Huntingtin and Ameliorate Neurodegeneration. Michal Mielcarek, Christian Landles, Andreas Weiss, Amyaouch Bradaia, et al. (2013)

 

Anthranilate Fluorescence Marks a Calcium-Propagated Necrotic Wave That Promotes Organismal Death in C. elegans. Cassandra Coburn, Erik Allman, Parag Mahanti, Alexandre Benedetto, et al. (2013)

 

Front Matter

No Question about Exciting Questions in Cell Biology. Tom Pollard (2013).

 

Deducing Protein Function By Forensic Integrative Cell Biology. Bill Earnshaw (2013). In press.

 

Category: Announcement, Cell biology, Conference, Open access, PLOS Biology | 1 Comment

microRNAs: targeting seeds of destruction

Modified logo wth textA central dogma of biology goes like this: the DNA of genes is copied (‘transcribed’) to make messenger RNA (mRNA), and mRNA is then translated to make protein. Well, that’s what my textbooks used to say when I was a biology student.

This dogma remained unchallenged for decades, in fact until 1993, when Victor Ambros and colleagues identified a tiny RNA transcript in a worm. The worm was called C. elegans and the tiny transcript, lin-4. Without encoding any protein, this small RNA turned out to have a potent effect in the cells of  C. elegans – it could recognize and pair with  a complementary mRNA and prevent it from being translated into protein. Biologists call this effect ‘gene silencing‘.

It took several years before another of these tiny, silencing transcripts was found, and then the floodgates opened. In the years that followed, scientists discovered that these so-called microRNAs were present in lots of other animals and in plants too.

So how do these microRNAs work? Just 22 nucleotides long, these tiny transcripts control what proteins are made in a cell by preventing their translation from mRNAs. When a microRNA pairs with an mRNA, through complementary base pairing, the mRNA is destroyed or not translated.  But given how tiny microRNAs are, how do they find the right target to pair with and silence?  Early attempts to answer this question relied on computer programs but these tended to generate endless lists of targets, many of which turned out to be false.

So several years ago, Stephen Cohen and colleagues set about the laborious task of trying to answer this question. Their work culminated in a groundbreaking paper published in PLOS Biology, entitled Principles of MicroRNA–Target Recognition.

Using genetic tools and experimental approaches available to them in the model organism, Drosophila, Cohen and co discovered that miRNA targets can be divided into two overall categories: those that pair with just the 5′ end of microRNAs and those that additionally need to pair with its other end – the 3′ end.  Surprisingly, they also discovered that pairing with the 5′ end sometimes relied on so-called seed sites that consist of just seven or eight bases complementary to the microRNA 5′ end. The finding that so little sequence complementarity is needed revealed that microRNAs have many more target sites than had been previously imagined.  Indeed, Cohen and colleagues estimated that the Drosophila fly genome has about 100 sites for every microRNA in its genome.  That’s alot of targets, and this work hinted at the likelihood that microRNAs regulate many, many protein-coding genes by silencing their mRNAs.
With its discovery of how microRNAs accurately pair with their targets, this article had a far reaching impact on the field of microRNA biology and gene regulation. As PLOS Biology Editorial Board Member Avinash Bhandoola explains, this work offered“an important set of insights essential to the microRNA field”, including the development of computational tools better equipped to predict true microRNA targets.

Indeed, over the years, research on microRNAs has uncovered that these tiny regulators are involved in many key biological processes.

collection logoSee the Tenth Anniversary PLOS Biology Collection or read the Biologue blog posts highlighting the rest of our selected articles.

 

 

 

ResearchBlogging.org
Brennecke J, Stark A, Russell RB, & Cohen SM (2005). Principles of microRNA-target recognition. PLoS biology, 3 (3) PMID: 15723116

Category: Bioinformatics, Biology, Developmental biology, Genetics, Molecular biology, PLOS Biology | Tagged | Leave a comment