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• W1869698906 abstract "In this issue of Molecular Cell, Kil et al., 2015Kil I.S. Ryu K.W. Lee S.K. Kim J.Y. Chu S.Y. Kim J.H. Park S. Rhee S.G. Mol. Cell. 2015; 59 (this issue): 651-663Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar provide evidence for self-sustained circadian oscillations of the hyperoxidation of the mitochondrial Peroxiredoxin, PrxIII, and cytosolic release of mitochondrial H2O2, which might constitute one biochemical output coupling metabolic changes and transcriptional-based core clocks. In this issue of Molecular Cell, Kil et al., 2015Kil I.S. Ryu K.W. Lee S.K. Kim J.Y. Chu S.Y. Kim J.H. Park S. Rhee S.G. Mol. Cell. 2015; 59 (this issue): 651-663Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar provide evidence for self-sustained circadian oscillations of the hyperoxidation of the mitochondrial Peroxiredoxin, PrxIII, and cytosolic release of mitochondrial H2O2, which might constitute one biochemical output coupling metabolic changes and transcriptional-based core clocks. In mammals, work over the last 20 years has established the presence of an intracellular circadian clock based on a negative autoregulatory transcriptional-translational feedback loop in which CLOCK:BMAl1 activate transcription of the Period and Cryptochrome genes, the protein products of which repress CLOCK:BMAL1, and thereby their own expression (Mohawk et al., 2012Mohawk J.A. Green C.B. Takahashi J.S. Annu. Rev. Neurosci. 2012; 35: 445-462Crossref PubMed Scopus (1365) Google Scholar). In contrast, S. elongatus uses a post-translational oscillator comprised of KaiA, KaiB, and KaiC, which together are necessary and sufficient for circadian rhythmicity in vitro in the presence of ATP (Nakajima et al., 2005Nakajima M. Imai K. Ito H. Nishiwaki T. Murayama Y. Iwasaki H. Oyama T. Kondo T. Science. 2005; 308: 414-415Crossref PubMed Scopus (789) Google Scholar). What about a mammalian autonomous non-transcriptional clockwork? In 2011, O’Neill and Reddy reported that in red blood cells (RBCs) hyperoxydation (sulfinylation, -SO2) of peroxiredoxin (Prxs) (see Figure 1) undergoes oscillations that fulfill all the criteria of a bona fide circadian rhythm (O’Neill and Reddy, 2011O’Neill J.S. Reddy A.B. Nature. 2011; 469: 498-503Crossref PubMed Scopus (589) Google Scholar). As RBCs are anucleated, these oscillations proved the existence of a non-transcriptional-based circadian rhythm in mammals. Similar Prx daily rhythms were found in a variety of eukaryotes, cyanobacteria, and archaea, making it the first evolutionarily conserved circadian rhythm marker (Edgar et al., 2012Edgar R.S. Green E.W. Zhao Y. van Ooijen G. Olmedo M. Qin X. Xu Y. Pan M. Valekunja U.K. Feeney K.A. et al.Nature. 2012; 485: 459-464PubMed Google Scholar). As to the mechanism, the presence of Prxs oscillations in C. elegans and N. crassa that lack sulfiredoxin (Srx), the enzyme reducing sulfinylated Prx (see Figure 1), indicated that Prx-SO2 reduction is at least in some cases dispensable for the cycle to occur. Rhee and colleagues then described an Srx-independent mechanism for the RBCs Prx-SO2 oscillations, in which sulfinylation is caused by hemoglobin autoxidation-dependent H2O2 generation, and its rhythm imprinted by selective proteasomal degradation of PrxII-SO2 over reduced enzyme (Cho et al., 2014Cho C.S. Yoon H.J. Kim J.Y. Woo H.A. Rhee S.G. Proc. Natl. Acad. Sci. USA. 2014; 111: 12043-12048Crossref PubMed Scopus (91) Google Scholar). As to the 24 hr period, these authors suggested that it could be imparted by the rhythmic oxygen supply to tissue, which fails to explain maintenance of this period in cultured RBCs. Rhee and colleagues now propose an Srx-dependent mechanism for the rhythmic sulfinylation of mitochondrial PrxIII (Kil et al., 2015Kil I.S. Ryu K.W. Lee S.K. Kim J.Y. Chu S.Y. Kim J.H. Park S. Rhee S.G. Mol. Cell. 2015; 59 (this issue): 651-663Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar) (Figure 2). As PrxIII is predicted to contribute to the degradation of 90% of mitochondrially produced H2O2, its inactivation by hyperoxidation, which reflects an important scavenging workload, eventually leads to an overflow of H2O2 in the cytosol that triggers the slow import of Srx and the resetting of PrxIII scavenging capacity. Except for the mitochondrial supply of H2O2, the rhythmic phenomenon appears totally independent of transcriptional clocks. A key point of the model is the temporal dissociation between completion of a PrxIII sulfinylation threshold at which H2O2 is released and Srx-dependent sulfinic acid reduction, which is expected to imprint an oscillatory pattern on Prx sulfinylation in the presence of a constant supply of H2O2. Such a self-sustained nature of the PrxIII cycle could be easily tested in isolated mitochondria led to respire in a constant environment. However, what about the influence of the H2O2 supply parameter? Knowledge that the magnitude of Prx hyperoxidation is proportional to the amount of H2O2 removed, itself a function of H2O2 levels, indicates that any changes in the levels and timing of the supply of mitochondrial H2O2 will influence the self-sustained PrxIII-SO2 oscillations. To appreciate this parameter, we must consider the sources of mitochondrial H2O2 that differ in the tissues in which the redox clockwork is present. As previously shown by Rhee and colleagues, in adrenal gland (AG), mitochondrial H2O2 is produced as by-product of CYP11B1 catalytic activity during corticosteroid (CS) synthesis, which is stimulated by the circadian pituitary release of ACTH (Kil et al., 2012Kil I.S. Lee S.K. Ryu K.W. Woo H.A. Hu M.C. Bae S.H. Rhee S.G. Mol. Cell. 2012; 46: 584-594Abstract Full Text Full Text PDF PubMed Scopus (125) Google Scholar). In this case, the release of H2O2 into the cytosol serves to establish a negative feedback loop of CS synthesis by inhibiting mitochondrial import of the CYP11B1-substrate cholesterol through activation of the p38 MAPK. Here, ACTH must dictate the circadian rhythm of CS release, but the PrxIII/system is essential as the negative limb of the loop. Predictably, the PrxIII/Srx system will also be essential for rhythm recovery after AG unscheduled stress stimulation, and even for buffering the mitochondrial release of harmful H2O2 levels, since the intensity and timing of the feedback look is expected to be proportional to the amount of H2O2 produced by CYP11B1. In the heart and BAT, in which oxidative metabolism is very high, the respiratory source becomes important. It is therefore important in these cases to consider respiration rate rhythmicity, which is under control of a BMAL1-CLOCK-dependent control of the mitochondrial SIRT3 deacetylase through NAD+ levels (Peek et al., 2013Peek C.B. Affinati A.H. Ramsey K.M. Kuo H.Y. Yu W. Sena L.A. Ilkayeva O. Marcheva B. Kobayashi Y. Omura C. et al.Science. 2013; 342: 1243417Crossref PubMed Scopus (447) Google Scholar). In these tissues, the PrxIII/Srx system must adapt to the predicted oscillatory respiratory production of H2O2, and as in the AG, might become important under stress, i.e., cardiotonic exercise or ambient temperature drop, by buffering excess release of mitochondrial H2O2. The heart and brown adipose tissue (BAT) raise the question of the purpose of daily mitochondrial H2O2 release. Given the known signaling role of H2O2, such a cyclic release of H2O2 should alter in a timely fashion not only transcriptional clock regulators, many of which (such as REV-ERBβ and the PER2:CRY1 heterodimer complex) are thiol-redox sensitive, but also the multitude of thiol-redox regulatory factors, as nuclear receptors, kinases, phosphatases, and transcription factors that are also or not involved in circadian regulation. In this regard, Kil et al., 2015Kil I.S. Ryu K.W. Lee S.K. Kim J.Y. Chu S.Y. Kim J.H. Park S. Rhee S.G. Mol. Cell. 2015; 59 (this issue): 651-663Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar show that activation of the p38 MAPK in the AG and BAT oscillates with a phase and period identical to that of PrxIII-SO2, which also indicates the oscillatory release of H2O2 into the cytosol. The predicted reciprocal interplay between the PrxIII/Srx system and local transcriptional clocks might allow synchronization between local metabolic activity and systemic circadian regulation. If indeed this is the case, the presence of the PrxIII/Srx clockwork in AG, heart, and BAT, and not in the liver, might indicate a fundamental difference between the signals of food intake and physiological activity with regards to their integration by systemic clockwork mechanisms. Many other great questions are raised by the study of Kil et al., 2015Kil I.S. Ryu K.W. Lee S.K. Kim J.Y. Chu S.Y. Kim J.H. Park S. Rhee S.G. Mol. Cell. 2015; 59 (this issue): 651-663Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar, such as the possible regulation of the PrxIII/Srx clockwork by PrxIII acetylation and phosphorylation, which are known to change its sensitivity to sulfinylation. A central question in H2O2 signaling is the origin of specificity, given the promiscuous nature of H2O2 and its ubiquitous signaling effects. As initially proposed by Carl Nathan with the concept of “specificity of another kind,” H2O2 might in fact operate as a superimposed co-signal of lesser specificity that integrates cellular activities by recruiting, timing, and tuning signaling pathways in accordance with the metabolic state of the cell (D'Autreaux, B. and Toledano, M.B. (2007)D'Autreaux B. Toledano M.B. Nat. Rev. Mol. Cell Biol. 2007; 8: 813-824Crossref PubMed Scopus (2481) Google Scholar). The temporal segregation of H2O2 release into cytosol during one half of the day now provides strong support for this concept. We are indebted to Isaac Edery for critical review of the manuscript. This work was funded by a grant from ANR ERRed, InCA PLBIO INCA_5869 to M.B.T. and a VLM grant to A.D.-M. Circadian Oscillation of Sulfiredoxin in the MitochondriaKil et al.Molecular CellJuly 30, 2015In BriefKil et al. show that the coordinated import and degradation of Srx provide the basis for sulfiredoxin oscillation and consequent PrxIII-SO2 oscillation in mitochondria and likely result in a daily rhythm of H2O2 release, which regulates various cell signaling pathways. Full-Text PDF Open Archive" @default.
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• W1869698906 title "Keeping Oxidative Metabolism on Time: Mitochondria as an Autonomous Redox Pacemaker Animated by H2O2 and Peroxiredoxin" @default.
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