Last week, Cell Press announced a new open-access, online-only journal, Cell Reports. According to the new journal's editor, Boyana Konforti, Cell Reports "will publish high-quality papers across the entire life sciences spectrum" and will focus on "shorter, single-point articles … in addition to longer articles." Konforti shares more details on the new journal — including how its editorial board is composed of up-and-coming young investigators "who will be the new leaders in their respective fields," and what authors can expect when submitting manuscripts — in this Cell Press video:
In a paper published online in advance in Cell Metabolism this week, researchers at the Yale School of Medicine and elsewhere shows that the "deletion of the mammalian INDY homolog [mindy] mimics aspects of dietary restriction and protects against adiposity and insulin resistance in mice." By creating a mindy-knockout mouse, the team found that loss of the INDY homolog "promotes mitochondrial biogenesis and energy expenditure" and protects the animal "from diet- and age-associated insulin resistance."
Over in Cell, investigators at Harvard Medical School and New York University School of Medicine "present a unifying hypothesis about how messenger RNAs, transcribed pseudogenes, and long noncoding RNAs 'talk' to each other using microRNA response elements as letters of a new language." Further, the team suggests that that competing endogenous RNA activity governed by such language "forms a large-scale regulatory network across the transcriptome, greatly expanding the functional genetic information in the human genome."
A trio of researchers at the Fundamental Research on Matter's Institute AMOLF in the Netherlands reports its engineering of an E. coli lac repressor-regulated genetic module, with which it "measured tradeoffs in fitness between environments [to] predict the competition between regulatory phenotypes." The team shows that "regulatory evolution in adverse environments is delayed at specific boundaries in the phenotype space of the regulatory LacI protein," though that constraint can be relieved by mutation, in which case "adaptation proceeds toward the optimum, yielding LacI with an altered allosteric mechanism that enables an opposite response to its regulatory ligand." Overall, the AMOLF team says that its results demonstrate that "regulatory evolution can be understood in terms of tradeoff optimization theory."