Deiodinase type-3 establishes the period of circannual interval timing in mammals
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PROVIDER: PRJNA1144448 | ENA |
REPOSITORIES: ENA
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Project description:Animals respond to environmental cues to time phenological events, but the intrinsic mechanism of circannual timing remains elusive. We used advanced transcriptomic sequencing and high frequency resolution during the initiation, maintenance and recovery of circannual timing for Siberian hamster energy balance to delineate the molecular architecture of a neuroendocrine seasonal clock. Three distinct phases of transcript changes were identified, and deiodinase type-3 (Dio3) expression was activated during the initiation phase. Targeted mutation of Dio3 resulted in a shortening of the circannual interval timer period. Hamsters that exhibit a form of naturally occurring disruption in Dio3 eliminated circannual interval timing. Our work demonstrates that the evolutionary conserved changes in hypothalamic tanycytes expression of Dio3 is critical for timing seasonal life history traits in chordates.
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2023-01-02 | GSE208236 | GEO
Project description:The three isoenzymes of iodothyronine deiodinases (DIO1-3) are membrane-anchored homo-dimeric selenoproteins which share the thioredoxin fold structure. Several questions regarding their catalytic mechanisms still remain open. Here, we addressed the roles of several cysteines which are conserved among deiodinase isoenzymes and asked whether they may contribute to dimerization and reduction of the oxidized enzyme with physiological reductants. We also asked whether amino acids previously identified in DIO3 play the same role in DIO1. Human DIO1 and 2 were recombinantly expressed in insect cells with selenocysteine replaced with cysteine (DIO1U126C), or in COS7 cells as selenoprotein. Enzyme activities were studied by radioactive deiodination assays with physiological reducing agents and recombinant proteins were characterized by mass-spectrometry. Mutation of Cys124 in DIO1 prevented reduction by glutathione, while 20 mM dithiothreitol still regenerated the enzyme. Protein thiol reductants, thioredoxin and glutaredoxin, did not reduce DIO1U126C. Mass-spectrometry demonstrated the formation of an intracellular disulfide between the side-chains of Cys124 and Cys(Sec)126. We conclude that the proximal Cys124 forms a selenenyl-sulfide with the catalytic Sec126 during catalysis, which is the substrate of the physiological reductant glutathione. Mutagenesis studies support the idea of a proton-relay pathway from solvent to substrate that is shared between DIO1 and DIO3.
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Project description:Abstract The metabolic syndrome is a cluster of conditions that predispose for diabetes and cardiovascular disease. Nine metabolic syndrome patients were recruited to 48 workouts of interval training. At the end of the study, all patients significantly reduced their risk of cardiovascular disease (in terms of VO2max, blood pressure and plasma lipid). Exercise-induced transcriptional changes may provide new mechanistically insights in the area of improved health by exercise. Aim: Determine whether transcriptional changes occurred in the blood cells of patients after the exercise program. We hypothesized that significantly altered biological processes in blood would include a set of genes at least partly responsible for the improvement seen in this patient group after the exercise programme. Methods: Blood from five patients were collected in PAXgene tubes pre and post the exercise period. RNA was extracted and run on microarrays. Results: Gene set enrichment analysis revealed twelve significantly enriched biological processes and molecular functions that were up-regulated post exercise. Seven processes and functions were down-regulated (nom p-value <0.05). Exercise induced a down-regulation of plasma mRNA- and protein levels of arginase-I and vWf, which might explain improved risk profile and endothelial function of the metabolic syndrome patients. Conclusion: After the exercise period was completed, the metabolic syndrome patients had decreased transcription of genes associated with blood clotting and steroid metabolism. Arginase-I was decreased post exercise, which may explain the previous reported improved NO-availability and endothelial function. Keywords: aerobic capacity, cardiovascular disease, microarray, arginase, blood clotting
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