Open Reading Frame: cancer metabolism, bird flu diversity & antibiotic resistance

Posted by Biome on 22nd August 2014 - 0 Comments


Open Reading Frame brings together a selection of recent publication highlights from elsewhere in the open access ecosystem. This week we take a look at the past few weeks in biology.

 

Duck crop_Wikimedia_Mallard2Why do birds have more types of flu?
Raising the spectre of ‘bird flu’ is a perennial media favourite for a slow news day, but it does reflect the real role that wild bird populations play as reservoirs for a diverse set of influenza viruses; viruses that have the potential to be spread to humans. But what makes avian influenza more varied than its human counterpart? This question is addressed in a new study that models the evolution and transmission of flu in these two populations, with the help of almost 40 years of sequence data from bird flu viruses. The results show that the higher diversity is likely a combination of two things: the relatively short lifespan of birds when compared to humans, and the increased potential for survival of influenza viruses in water, allowing for indirect environmental transmission in addition to direct bird-to-bird spread. As well as helping us understand the spread of the virus, the results suggest that environmental decontamination may be a necessary part of avian influenza control.
Benjamin Roche et al. PLOS Biology

 

Warburg effect is involved in cancer migration
In recent years increasing attention has been given to a metabolic feature of proliferating cancer cells. The Warburg effect, as it is known, describes the tendency of cancer cells to consume glucose at an abnormally high rate, which they do so anaerobically even in the presence of oxygen. Attention has been largely focused on its role in cancer proliferation, but less in regard to cellular migration – another important aspect of tumour growth and spread. A study of this in the NCI-60 panel of cancer cell lines first uses a genome-scale computational model of their cellular metabolism to demonstrate that these cells do exhibit the Warburg effect and that it is associated with migratory behaviour. Subsequently, experimental knockdown of genes predicted from this model to interfere with the Warburg effect in several cases did successfully reduce cell migration. The authors claim that drugs to inhibit migratory behaviour may be promising candidates for future cancer treatments, side-stepping some of the side effects of existing cancer drugs.
Keren Yizhak et al. Molecular Systems Biology

 

Face symmetry, child_Flickr_Eliza AdamSymmetrical face, healthy child?
A substantial body of research supports the idea that humans use facial symmetry as a criterion for selecting sexual partners. If true, it is assumed that this is because symmetry reflects underlying physiological health; healthy genes, symmetrical face. This idea is tested in a new study, utilising data from a long-term study of children growing up in south-west England. Over 5000 children aged 15-16 had their facial symmetry measured using computer software. This measure of symmetry was correlated with the actual health of these children – data which was regularly collected throughout their lives. The symmetry of these children’s faces had no correlation with their health. This is in contrast to a number of previous studies that have found such a correlation in humans; notably though, this new study has a much larger sample size and more reliable measurements of health than previous research. This suggests that if these children’s parents did subconsciously assess each other for the symmetry of their faces, it was not in the hope of having healthy children.
Pound et al. Proceedings of the Royal Society B

 

ETosis: the extracellular phagocyte trap
The innate immune system is one part of the defence against infection in organisms across the whole spectrum of animal and plant life, whereby immune cells and other mechanisms that offer general protection against threats are utilised, rather than specific responses to particular pathogens. In the last decade one new mechanism of innate immunity, named ETosis, has been discovered in vertebrate immune systems. In this process inflammatory cells release chromatin – the complex of DNA and proteins that package DNA – outside the cell to trap bacteria, fungi and viruses at the cost of cell death. For the first time a new study  searches for the existence of ETosis in invertebrate animals. The authors examined crab immune cells and found that they too could be stimulated to release their chromatin in response to infection, both in isolated immune cells and living crabs, successfully trapping bacteria. Moreover, they also found this response in a mussel and a sea anemone species. The latter is an acoelomate – a evolutionary branch of animals lacking a body cavity – which suggests that the mechanism predates the evolution of the coelom, making it an extremely ancient form of immune defence.
Calum T. Robb et al. Nature Communications

 

E coli crop_Flickr_James JoelTag-team genes that assist antibiotics
Many hands are (rightly) being wrung over the need for the development of more and better antibiotics to control the rapid spread of antibiotic-resistant bacteria. Parallel to these efforts, strategies are being tested to get more out of the antibiotics we already have. One is the introduction to bacteria (via phage) of genes whose expression will help antibiotic delivery: membrane transporters, say, or genes that suppress the bacterial stress response. Even better, a combinations of these genes is often much more effective than each gene is alone, but discovering the combinations that work is a laborious and time-consuming process. A new paper now describes a rapid screening protocol (called CombiGEM) that barcodes and quickly identifies pairs of genes whose interaction should improve antibiotic efficacy. In follow-up tests, the effect of certain gene pairs increases the lethality of the antibiotic ceftriaxone to multi-resistant NDM-1 E. coli by one or two orders of magnitude. It’s a promising proof-of-principle for another approach to overcoming antibiotic resistance.
Allen A Cheng et al. PNAS

 

Counting the cost of retractions
Research articles that are retracted following the discovery of misconduct can cause considerable damage to the scientific process. Beyond this damage though, retracted articles will also have wasted much of the funding underlying the research; a particular concern when this money comes from taxpayers. New research attempts to estimate this cost by utilising an online database of all grants funded by the NIH (the primary funder of biomedical research in the USA). By linking grant numbers to retracted articles, the authors identified 149 papers based on research funded by the NIH between 1992-2012 that were eventually retracted due to misconduct. On average, each of these retracted articles received $392,000 in NIH funds, although in one extreme case a grant of $3.6 million dollars resulted in just one, eventually retracted, paper. In total, $123 million dollars of funding was spent on research reported in these retracted articles. Not an insubstantial sum, but the authors do point out that this represents less than 0.03 percent of the total NIH budget over these 20 years.
Stern et al. eLife

 

Written by Christopher Foote, Executive Editor for the BMC Series, Kester Jarvis (@Kestererer), Senior Editor for BMC Biology, and Tim Sands, Executive Editor for the BMC Series.