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      Circadian transcription factor BMAL1 regulates innate immunity against select RNA viruses

      Author(s): , , , ,
      Publication date Created:
      Publication date (Print):
      Journal: Innate Immunity
      Publisher: SAGE Publications

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          Abstract

          BMAL1 (brain and muscle ARNT-like protein 1, also known as MOP3 or ARNT3) belongs to the family of the basic helix-loop-helix (bHLH)-PAS domain-containing transcription factors, and is a key component of the molecular oscillator that generates circadian rhythms. Here, we report that BMAL1-deficient cells are significantly more susceptible to infection by two major respiratory viruses of the Paramyxoviridae family, namely RSV and PIV3. Embryonic fibroblasts from Bmal1-/- mice produced nearly 10-fold more progeny virus than their wild type controls. These results were supported by animal studies whereby pulmonary infection of RSV produced a more severe disease and morbidity in Bmal1-/-mice. These results show that BMAL1 can regulate cellular innate immunity against specific RNA viruses.

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          NIH Image to ImageJ: 25 years of image analysis.

          Lynda C. Schneider, Wayne S Rasband (2013)
          For the past 25 years NIH Image and ImageJ software have been pioneers as open tools for the analysis of scientific images. We discuss the origins, challenges and solutions of these two programs, and how their history can serve to advise and inform other software projects.
          Article 0 comments Cited 4147 times – based on 0 reviews     Review now
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            Coordinated transcription of key pathways in the mouse by the circadian clock.

            Satchidananda Panda, Marina P. Antoch, Brooke H. Miller … (2002)
            In mammals, circadian control of physiology and behavior is driven by a master pacemaker located in the suprachiasmatic nuclei (SCN) of the hypothalamus. We have used gene expression profiling to identify cycling transcripts in the SCN and in the liver. Our analysis revealed approximately 650 cycling transcripts and showed that the majority of these were specific to either the SCN or the liver. Genetic and genomic analysis suggests that a relatively small number of output genes are directly regulated by core oscillator components. Major processes regulated by the SCN and liver were found to be under circadian regulation. Importantly, rate-limiting steps in these various pathways were key sites of circadian control, highlighting the fundamental role that circadian clocks play in cellular and organismal physiology.
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              Disruption of the Clock Components CLOCK and BMAL1 Leads to Hypoinsulinemia and Diabetes

              Biliana Marcheva, Kathryn Moynihan Ramsey, Ethan D Buhr … (2010)
              The molecular clock maintains energy constancy by producing circadian oscillations of rate-limiting enzymes involved in tissue metabolism across the day and night1–3. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis, and while rhythmic control of insulin release is recognized to be dysregulated in humans with diabetes4, it is not known how the circadian clock may affect this process. Here we show that pancreatic islets possess self-sustained circadian gene and protein oscillations of the transcription factors CLOCK and BMAL1. The phase of oscillation of islet genes involved in growth, glucose metabolism, and insulin signaling is delayed in circadian mutant mice, and both Clock 5,6 and Bmal1 7 mutants exhibit impaired glucose tolerance, reduced insulin secretion, and defects in size and proliferation of pancreatic islets that worsen with age. Clock disruption leads to transcriptome-wide alterations in the expression of islet genes involved in growth, survival, and synaptic vesicle assembly. Remarkably, conditional ablation of the pancreatic clock causes diabetes mellitus due to defective β-cell function at the very latest stage of stimulus-secretion coupling. These results demonstrate a role for the β-cell clock in coordinating insulin secretion with the sleep-wake cycle, and reveal that ablation of the pancreatic clock can trigger onset of diabetes mellitus.
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                Author and article information

                Journal
                Title: Innate Immunity
                Abbreviated Title: Innate Immun
                Publisher: SAGE Publications
                ISSN (Print): 1753-4259
                ISSN (Electronic): 1753-4267
                Publication date Created: November 24 2016
                Publication date (Print): December 05 2016
                Volume: 23
                Issue: 2
                Pages: 147-154
                Article
                DOI: 10.1177/1753425916681075
                PubMed ID: 27913791
                SO-VID: 40ba0c63-e270-42f7-be00-59ca30eeb9dc
                Copyright © © 2016
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