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Official websites use. Share sensitive information only on official, secure websites. We show that SOCE-deficient mice accumulate pathological amounts of lipid droplets in liver, heart and skeletal muscle. SOCE is crucial to induce mobilization of fatty acids from lipid droplets, lipolysis and mitochondrial fatty acid oxidation. SOCE-deficient cells upregulate lipophagy that protects them against lipotoxicity. Our data provide evidence for an important role of SOCE in lipid metabolism. Patients with loss-of-function mutations in ORAI1 , the best characterized member of the ORAI family, or in STIM1 suffer from an autosomal-recessive disease syndrome named CRAC channelopathy that is characterized by severe immunodeficiency, muscular hypotonia and anhidrotic ectodermal dysplasia Lacruz and Feske, The cellular mechanisms underlying disease pathogenesis in different tissues are incompletely understood. In the absence of SOCE, cells display impaired lipolysis, and upregulate lipophagy that protects them from lipotoxicity. As reported previously, only a small fraction of skeletal myofibers in Orai1 R93W mice contain markedly swollen mitochondria with abnormal cristae structure McCarl et al. Because Orai1 R93W mice die perinatally, we established a tamoxifen-inducible mouse model in which Stim1 and Stim2 genes can be deleted in all tissues of adult animals to abolish SOCE. Histologies of their heart muscle, skeletal muscle and liver revealed the accumulation of pathological amounts of LDs when compared to tamoxifen injected Cre-negative littermates Figure 1C. Collectively these findings suggest that SOCE has a conserved role in controlling lipid homeostasis in mice and humans both in vivo and vitro. G98R mutation shows LD deposition arrow. H Dashed boxes indicate regions shown at higher magnification in the right panels. Nuclei were counterstained with DAPI. Lipid catabolism in cells depends on mitochondria, and reduced mitochondrial function leads to triglyceride accumulation in muscle and liver Petersen et al. Opening of UCP2, which is controlled by fatty acids and other factors, results in the reduction of the mitochondrial membrane potential MMP and of ROS production and thus prevents mitochondrial damage Brand and Esteves, Consistent with reduced UCP2 expression, we observed higher numbers of damaged mitochondria as suggested by increased colocalization of mitochondria and acidic vesicular compartments lysosomes in fibroblasts of SOCE-deficient patients Figure 2G. Similar results were found using the pH sensitive MitoKeima reporter Katayama et al. Images show cells at low left and high right magnification. To assess the function of the ETC in mitochondria of SOCE-deficient cells, we measured the hyperpolarization rate of the MMP after treatment of cells with oligomycin, which inhibits the ATP synthase and thus traps protons in the intermembrane space. Whereas basal mitochondrial superoxide levels were slightly, but not statistically significantly increased in SOCE-deficient cells Figure 2K and 2L , the rate of superoxide production after ATP synthase inhibition with oligomycin was significantly reduced in the absence of SOCE, indicative of lower electron-transport rate by the ETC Figure 2K and 2M. Direct analysis of O 2 consumption rate revealed normal or moderately reduced basal respiration in patient fibroblasts, but a significant decrease in the maximal respiration rate in SOCE-deficient patient cells compared to controls Figure S2C. Expression of both genes was reduced in patient fibroblasts when cultured in high-glucose medium, and this difference became more pronounced when cells were cultured in OA-containing medium followed by starvation in 2 mM glucose medium Figure 2Q and 2R. To assess mitochondrial fatty acid oxidation FAO , we measured cellular O 2 utilization of fibroblasts cultured in OA-containing medium with or without subsequent starvation. The CPT1 inhibitor etomoxir, which inhibits fatty acid transport into the mitochondria, was used to estimate the contribution of FAO to total mitochondrial respiration. Starvation induced a drastic increase in etomoxir-sensitive mitochondrial respiration in control, but not in SOCE-deficient patient cells Figure 2S. Taken together, our data show that SOCE controls expression of several key mitochondrial enzymes including uncoupler proteins, ETC components and enzymes involved in fatty acid oxidation and thereby regulates mitochondrial function and FAO. Isoproterenol was again unable to rescue this defect Figure 3E. The lipolysis defect was not dependent on the saturation of the fatty acid nutrient, as SOCE-deficient cells cultured with palmitic acid PA instead of OA also showed impaired free glycerol release upon starvation when compared to control cells Figure 3F. Representative histograms left and quantification of 3 repeat experiments right. Data are representative of 3 repeat experiments. Representative Western blots top and normalized ratios of phospho-HSL to total HSL expression bottom from 5 repeat experiments see Methods for details. We observed a small, but visible reduction in HSL phosphorylation on Ser in SOCE-deficient NIH3T3-L1 cells when cultured in high-glucose medium, which became more pronounced when cells were cultured in OA followed by starvation in the presence or absence of isoproterenol. In addition to conventional lipolysis, LDs can also be targeted for lysosomal hydrolysis through lipophagy Singh et al. Immunoblots for the autophagosome marker microtubule-associated protein light chain 3 LC3 in cells maintained in the presence or absence of lysosomal protease inhibitors revealed consistently higher steady-state levels of LC3-II and increased autophagic flux measured as the amount of LC3-II degraded in lysosomes in patient cells, suggesting higher rates of autophagy in the absence of SOCE Figure 4A and 4B. Consistent with the immunoblot data, SOCE-deficient cells had significantly higher content of autophagosomes and autolysosomes Figure 4C and 4D. As in human fibroblasts, the higher content of autophagic compartments in muscles of knock-in mice was a result of higher number of autolysosomes, further supporting an increase in autophagic flux in these animals Figure S3H. B LC3-II steady-state levels left and autophagic flux right calculated by densitometric analysis of immunoblots. C Images of representative cells. Total protein degradation rates E and percentage of lysosomal protein degradation and macroautophagy-dependent degradation 3-methyladenine 3-MA sensitive in cells treated without or with 10 mM 3-MA for the duration of the chase. Representative images of merged channels. Boxed area at higher magnification middle and detail of lipid droplets right show colocalized pixels in white. J and K ATG7 knockdown causes lipotoxicity. Despite marked upregulation of autophagy in SOCE-deficient cells, we found that protein is not favored as targeted cargo, as proteolysis of long-lived proteins was reduced in the absence of SOCE Figure 4E and this reduction was preferentially due to decreased 3-Methyladenine 3-MA -sensitive proteolysis macroautophagy Figure 4F. Analysis of the LDs that accumulate in the skeletal muscle from Orai1 R93W knock-in mice also revealed that a significantly higher percentage of LDs in these animals had morphological features previously attributed to active lipophagy Figure S3I—S3K Singh et al. To assess the functional importance of increased lipophagy in SOCE-deficient cells, we ablated expression of autophagy-related protein 7 ATG7 , which is essential for autophagosome formation, using specific short-hairpin RNA. Taken together, these results suggest that the increase in lipophagy in SOCE-deficient cells may compensate for the loss of conventional lipolysis and serve as a protective mechanism against lipotoxicity. Mammals adapt to prolonged fasting by activating lipolysis in their adipose tissues, thereby releasing fatty acids into the circulation Finn and Dice, To adjust to the abundance of fatty acids, the liver and other organs reprogram their metabolism by transcribing genes involved in fatty acid utilization. Alternatively, cells were cultured in medium containing 0. Alternatively, cells were cultured in 0. Fasting results in increased fatty acid levels in the serum and induces reprogramming of tissue metabolism Cahill, In this study, we provide evidence for an important role of SOCE in the lipid metabolism of mammalian cells. The physiological signal initiating SOCE and lipolysis at the cellular level and in vivo remains to be investigated. Collectively, our data support an important role of SOCE in orchestrating the fasting response at the transcriptional level to promote lipid utilization. Fatty acids are actively transported into the mitochondrial matrix where they are broken down during beta-oxidation to supply the TCA cycle with acetyl-CoA. Clinically, a decline in mitochondrial function is associated with triglyceride accumulation in the skeletal muscle and heart Petersen et al. We observed impaired mitochondrial function in SOCE-deficient cells, which showed reduced expression and function of ETC complexes CI and CIV and consequently reduced proton pumping, electron transport, O 2 consumption and oleic acid oxidation. Furthermore, SOCE-deficient cells had reduced levels of UCP2, a proton transporter in the inner mitochondrial membrane, whose opening prevents mitochondrial damage Berardi and Chou, ; Brand and Esteves, Consistent with reduced UCP2 expression, we observed a higher MMP and more mitochondria undergoing degradation in acidic compartments. SOCE-deficient cells showed marked upregulation of autophagy, preferentially of lipid droplets, i. Our data indicates that this marked upregulation of autophagy favors lipids as predominant cargo. Lipophagy upregulation occurs during starvation and in response to lipid challenges in multiple cell types and failure to do so contributes to steatosis in common liver disorders Dolganiuc et al. Increased lipophagy appears to be protective in SOCE-deficient cells as blockage of autophagy makes these cells more vulnerable to lipotoxicity. We propose that increased lipophagy in SOCE-deficient cells is an attempt by SOCE-deficient cells to compensate for impaired conventional lipolysis and an attempt to provide the remaining functional mitochondria with FFA for beta oxidation and energy production. Part of the beneficial effect of upregulated autophagy in SOCE-deficient cells could also originate from the role of this process in organelle quality control, in particular of mitochondria. The effects of deleting these genes on lipid metabolism in Drosophila have been attributed to alterations at the neurological, adipose tissue and cellular level. In this study, we describe a cell intrinsic role for SOCE in the regulation of lipid metabolism at both the functional and transcriptional level. These findings may contribute to a better understanding of the pathogenic mechanisms behind common metabolic diseases and underscore SOCE-dependent signaling as a potential novel therapeutic target for the treatment of disorders of lipid metabolism. More detailed methods can be found in Supplemental Experimental Procedures. Orai1 R93W knock-in mice McCarl et al. All animal experiments were conducted in accordance with institutionally approved protocols. RC, described in Maus et al. R91W described in Feske et al. Human dsRed-LC3 plasmid Boland et al. Oleic acid OA and palmitic acid PA , both from Sigma Aldrich, were dissolved in chloroform, chloroform was evaporated and fatty acids were conjugated to bovine serum albumin BSA. TCA cycle function was measured as described Abramov et al. Respiration of intact patient cells was measured using a Seahorse XF24 analyzer Seahorse Bioscience or the respiratory chain enzyme activity in muscle biopsies from patients Table S1 was measured as described Gempel et al. FAO was analyzed using either a Seahorse XF24 analyzer or by incubation of cells with 14 C-labeled oleic acid followed by analysis of 14 CO 2 as previously described Huynh et al. Lipolysis was analyzed with a colorimetric assay F, Sigma to measure the free glycerol content or a fluorescent quantification kit MAK, Sigma to measure the FFA content in the extracellular medium. To test lipotoxicity, cells were stained with propidium iodide PI and analyzed by flow cytometry. Cells were loaded with Fura-2 and analyzed as described Maus et al. TEM was conducted as described McCarl et al. DF was conducted using confocal microscopy or fluorescence microscopy with deconvolution. Immunoblot and immunofluorescence procedures and antibodies can be found in Supplemental Experimental Procedures. We thank Drs. Deng and M. Ramasamy for assistance with FAO experiments. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Conflict of interest statement: S. The remaining authors declare no conflict of interest. Supplemental Information includes Supplemental Experimental Procedures , eight figures, two tables and three videos that can be found with this article online at xxxxxx. This section collects any data citations, data availability statements, or supplementary materials included in this article. As a library, NLM provides access to scientific literature. Cell Metab. Published in final edited form as: Cell Metab. Find articles by Mate Maus. Find articles by Mario Cuk. Find articles by Bindi Patel. Find articles by Jayson Lian. Find articles by Mireille Ouimet. Find articles by Ulrike Kaufmann. Find articles by Jun Yang. Find articles by Rita Horvath. Find articles by Hue-Tran Hornig-Do. Find articles by Zofia Chrzanowska-Lightowlers. Find articles by Kathryn J Moore. Find articles by Ana Maria Cuervo. Find articles by Stefan Feske. Issue date Mar 7. PMC Copyright notice. The publisher's version of this article is available at Cell Metab. Open in a new tab. Download video file 1. Download video file 4. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. 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