dDOR Is an EcR Coactivator that Forms a Feed-Forward Loop Connecting Insulin and Ecdysone Signaling

SummaryBackgroundMammalian DOR was discovered as a gene whose expression is misregulated in muscle of Zucker diabetic rats. Because no DOR loss-of-function mammalian models are available, we analyze here the in vivo function of DOR by studying flies mutant for Drosophila DOR (dDOR).ResultsWe show that dDOR is a novel coactivator of ecdysone receptor (EcR) that is needed during metamorphosis. dDOR binds EcR and is required for maximal EcR transcriptional activity. In the absence of dDOR, flies display a number of ecdysone loss-of-function phenotypes such as impaired spiracle eversion, impaired salivary gland degradation, and pupal lethality. Furthermore, dDOR knockout flies are lean. We find that dDOR expression is inhibited by insulin signaling via FOXO.ConclusionThis work uncovers dDOR as a novel EcR coactivator. It also establishes a mutual antagonistic relationship between ecdysone and insulin signaling in the fly fat body. Furthermore, because ecdysone signaling inhibits insulin signaling in the fat body, this also uncovers a feed-forward mechanism whereby ecdysone potentiates its own signaling via dDOR

Mechanisms of Modulation of Mitochondrial Architecture

Mitochondrial network architecture plays a critical role in cellular physiology. Indeed, alterations in the shape of mitochondria upon exposure to cellular stress can cause the dysfunction of these organelles. In this scenario, mitochondrial dynamics proteins and the phospholipid composition of the mitochondrial membrane are key for fine-tuning the modulation of mitochondrial architecture. In addition, several factors including post-translational modifications such as the phosphorylation, acetylation, SUMOylation, and o-GlcNAcylation of mitochondrial dynamics proteins contribute to shaping the plasticity of this architecture. In this regard, several studies have evidenced that, upon metabolic stress, mitochondrial dynamics proteins are post-translationally modified, leading to the alteration of mitochondrial architecture. Interestingly, several proteins that sustain the mitochondrial lipid composition also modulate mitochondrial morphology and organelle communication. In this context, pharmacological studies have revealed that the modulation of mitochondrial shape and function emerges as a potential therapeutic strategy for metabolic diseases. Here, we review the factors that modulate mitochondrial architecture

Characterizing Dust-Radiation Feedback and Refining the Horizontal Resolution of the MarsWRF Model Down to 0.5 Degree

Acknowledgments Once again, our warmest thanks go to the PlanetWRF development team for providing the MarsWRF model free of charge to us and their proactive attitude in general. We would also like to thank two anonymous reviewers and the Associate Editor Dr Claire Newman for their several detailed and insightful comments and suggestions that helped to significantly improve the quality of the paper. We would like to acknowl- edge the support of this work by funding from the United Arab Emirates University (UAE University). Also, we are deeply grateful to High-Performance Computing, Division of Information Technology, UAE University, for the valuable access to the computational resources required for this work. We thank IT engineers Asma AlNeyadi, Anil Thomas, and Nithin Damodaran for their professional assistance and support in technical questions. M.-P. Z. has been partially funded by the AEI (MDM-2017-0737, Unity of Excellence “María de Maeztu” - Centro de Astro- biología (CSIC-INTA)) and the Spanish Ministry of Science and Innovation (PID2019-104205GB-C219). Finally, we declare that there are no real or perceived conflicts of interests for any author.Peer reviewedPublisher PD

Fully Interactive and Refined Resolution Simulations of the Martian Dust Cycle by the MarsWRF Model

Acknowledgments: First of all, our warmest thanks go to the PlanetWRF development team for providing the MarsWRF model free of charge to us and their proactive attitude in general. We thank Andy Heaps, National Centre for Atmospheric Science (NCAS), Department of Meteorology, University of Reading, UK, for his helpful advice regarding the data visualization using cf‐Python. We would also like to thank Michael Mischna, Alexandre Kling, and the Associate Editor Claire Newman for their several detailed and insightful comments and suggestions that helped to significantly improve the quality of the paper. M. P. Z. acknowledges the partial support by the Spanish State Research Agency (AEI) project MDM‐2017‐0737 Centro de Astrobiología (CSIC‐INTA), Unidad de Excelencia María de Maeztu. Internally, we would like to express our greatest thanks to the High‐Performance Computing, Division of Information Technology, United Arab Emirates University. Our particular thanks go to Asma AlNeyadi, Anil Thomas, and Nithin Damodaran for their intensive and continuous support in technically demanding questions. Also, we would like to thank the Digitization Unit, UAEU Libraries, for the digitization of auxiliary data on the observational record of the atmospheric T15 temperature and vertical weighting functions of Viking/IRTM. In addition, we thank UAEU Libraries for their assistance in making supporting data of this article available online. In particular, we are grateful to Digitization Technician Shireen M. Wolied, Fadl M. Musa/Digital Library Service, and Student Muhammad Abdul Rahim Sami Ullah. Funding Information: United Arab Emirates University (UAEU). Grant Number: 21R033‐NSS Center 7‐2017 Spanish State Research Agency (AEI). Grant Number: MDM‐2017‐0737Peer reviewedPublisher PD

Breaking up is hard to do: RalA, mitochondrial fission and cancer

The small GTPases RalA and RalB are activated downstream of oncogenic Ras. While activation of RalA is critically important for tumor initiation and growth of Ras-driven cancers, the highly similar small GTPase RalB is implicated in cell survival and metastasis. This difference in function between these two related proteins maps to the C-terminus, a 30 amino acid region that regulates subcellular localization and contains several potential phosphorylation sites. Here we discuss our recent evidence that phosphorylation by the mitotic kinase Aurora A promotes RalA relocalization to mitochondrial membranes, where it recruits the effector RalBP1 and the large dynamin-related GTPase Drp1 to promote mitochondrial fission. As upregulation of both RalA and Aurora A have been observed in human tumors, and phosphorylation of RalA at the site targeted by Aurora A promotes tumorigenesis, it is possible that regulation of mitochondrial fission is one mechanism by which RalA promotes cancer

Are Slope Streaks Indicative of Global-Scale Aqueous Processes on Contemporary Mars?

Acknowledgments We acknowledge the editorial board of Reviews of Geophysics for inviting the submission of this review article. We extend our gratitude to the efforts of the handling editor and the reviewers. We thank NASA, JPL‐Caltech, JPL/Goddard, University of Arizona, Malin Space Science systems, Arizona State University, USGS, ESA/DLR/FU Berlin, and Google Earth for providing various satellite images, maps, and JMARS software free of charge. The paper is theoretical, and no new data have been generated during the work. All the used satellite images of Mars can be rendered on JMARS software using the image ID provided in the respective figure captions, and the image sources have also been duly acknowledged in the respective figure captions. The maps in various figures have been created using ArcGIS version 10.4 (http://desktop.arcgis.com/en/arcmap/latest/get‐started/setup/arcgis‐desktop‐quick‐start‐guide.htm). Although we have cited all the previous research results used in the paper, we here acknowledge the efforts of all those researchers in providing the essential inputs for our study. A. B. acknowledges the Swedish Research Council for supporting his research in cold arid environments. L. S. acknowledges the German Academic Exchange Service (DAAD) for her PhD scholarship.Peer reviewedPublisher PD