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Unsaturation of very-long-chain ceramides regulates hypoxia response by modulating ethylene signaling in Arabidopsis

ABSTRACT: Lipid remodeling is crucial for hypoxic tolerance in animals, whilst little is known about the hypoxia-induced lipid dynamics in plant cells. Here we performed a mass spectrometry-based analysis to survey the lipid profiles of Arabidopsis rosettes under various hypoxic conditions. We observed that hypoxia caused a significant increase in total amounts of phosphatidylserine, phosphatidic acid and oxylipins, but a decrease in phosphatidylcholine (PC) and phosphatidylethanolamine (PE). Particularly, significant gains in the polyunsaturated species of PC, PE and phosphatidylinositol, and losses in their saturated and mono-unsaturated species were evident during hypoxia. Moreover, hypoxia led to a remarkable elevation of ceramides and hydroxyceramides. Depletion of ceramide synthases LOH1, LOH2, and LOH3 enhanced plant sensitivity to dark submergence (DS), but displayed more resistance to submergence under light than wild type. Consistently, levels of unsaturated ceramide species (22:1, 24:1, and 26:1) predominantly declined in the loh1, loh2, and loh3 mutants under DS. Evidence that C24:1-ceramide interacted with recombinant CTR1 protein in vitro, enhanced ER-to-nucleus translocation of EIN2-GFP and stabilization of EIN3-GFP in vivo, suggests a role of ceramides in modulating ethylene signaling. The DS-sensitive phenotypes of loh mutants were rescued by a ctr1-1 mutation. Thus, our findings demonstrate that unsaturation of very-long-chain ceramides is a protective strategy for hypoxic tolerance in Arabidopsis.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE59719 | GEO | 2016/07/24

SECONDARY ACCESSION(S): PRJNA256034

REPOSITORIES: GEO

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Unsaturation of very-long-chain ceramides regulates hypoxia response by modulating ethylene signaling in Arabidopsis

Project description:Lipid remodeling is crucial for hypoxic tolerance in animals, whilst little is known about the hypoxia-induced lipid dynamics in plant cells. Here we performed a mass spectrometry-based analysis to survey the lipid profiles of Arabidopsis rosettes under various hypoxic conditions. We observed that hypoxia caused a significant increase in total amounts of phosphatidylserine, phosphatidic acid and oxylipins, but a decrease in phosphatidylcholine (PC) and phosphatidylethanolamine (PE). Particularly, significant gains in the polyunsaturated species of PC, PE and phosphatidylinositol, and losses in their saturated and mono-unsaturated species were evident during hypoxia. Moreover, hypoxia led to a remarkable elevation of ceramides and hydroxyceramides. Depletion of ceramide synthases LOH1, LOH2, and LOH3 enhanced plant sensitivity to dark submergence (DS), but displayed more resistance to submergence under light than wild type. Consistently, levels of unsaturated ceramide species (22:1, 24:1, and 26:1) predominantly declined in the loh1, loh2, and loh3 mutants under DS. Evidence that C24:1-ceramide interacted with recombinant CTR1 protein in vitro, enhanced ER-to-nucleus translocation of EIN2-GFP and stabilization of EIN3-GFP in vivo, suggests a role of ceramides in modulating ethylene signaling. The DS-sensitive phenotypes of loh mutants were rescued by a ctr1-1 mutation. Thus, our findings demonstrate that unsaturation of very-long-chain ceramides is a protective strategy for hypoxic tolerance in Arabidopsis. Arabidopsis Affymetrix GeneChip arrays were probed with RNAs isolated from leaves of untreated plants (controls) and plants upon hypoxia under light submergence for 48 h.

2016-07-24 | E-GEOD-59719 | biostudies-arrayexpress

Liver-specific ceramide reduction alleviates steatosis and insulin resistance in alcohol-fed mice

Project description:Alcohol’s impairment of both hepatic lipid metabolism and insulin resistance (IR) are key drivers of alcoholic steatosis, the initial stage of alcoholic liver disease (ALD). Pharmacologic reduction of lipotoxic ceramide prevents alcoholic steatosis and glucose intolerance in mice, but potential off-target effects limit its strategic utility. Here, we employed a hepatic-specific acid-ceramidase (ASAH) overexpression model to reduce hepatic ceramides in a Lieber-DeCarli model of experimental alcoholic steatosis. We examined effects of alcohol on hepatic lipid metabolism, body composition, energy homeostasis and insulin sensitivity as measured by hyperinsulinemic-euglycemic clamp. Our results demonstrate that hepatic ceramide reduction ameliorates the effects of alcohol on hepatic lipid droplet accumulation by promoting VLDL secretion and lipophagy, the latter of which involves ceramide cross-talk between the lysosomal and lipid droplet compartments. We additionally demonstrate that hepatic ceramide reduction prevents alcohol’s inhibition of hepatic insulin signaling. These effects on the liver are associated with a reduction in oxidative stress markers and are relevant to humans, as we observe peri-lipid droplet ASAH expression in human ALD. Together, our results suggest a potential role for hepatic ceramide inhibition in preventing ALD.

2020-07-08 | GSE139015 | GEO

Removing a Double Bond from Ceramides Ameliorates Insulin Resistance and Hepatic Steatosis

Project description:Ceramides contribute to the lipotoxicity that underlies diabetes, hepatic steatosis, and heart disease. By genetically engineering mice, we deleted the enzyme dihydroceramide desaturase-1 (DES1) which inserts a conserved double bond into the backbone of ceramides and other predominant sphingolipids. Ablation of DES1 from whole animals, or tissue-specific deletion in the liver, and/or adipose tissue resolved hepatic steatosis and insulin resistance in mice caused by leptin deficiency or obesogenic diets. Mechanistic studies revealed new ceramide actions that promoted lipid uptake and storage and impaired glucose utilization, none of which could be recapitulated by (dihydro)ceramides that lacked the critical double bond. These studies suggest that inhibition of DES1 may provide a means of treating hepatic steatosis and cardiometabolic disorders.

2020-01-30 | GSE132056 | GEO

Ethylene modulates the dynamics of translation via GCN2 and EIN2 in Arabidopsis under submergence

Project description:General translational repression is predicted as a key process to reduce energy consumption under hypoxia. We have previously showed that mRNA loading onto polysome is reduced in Arabidopsis under submergence. Here, we showed that plant stress activated GCN2 (general control nonderepressible 2) can phosphorylate eIF2a (Eukaryotic Initiation Factor 2a) in Arabidopsis under submergence, and this process is reversible after desubmergence. Compared to the wild-type, the reduction in polysome loading during submergence was less severe in the gcn2 mutant. Transgenic lines overexpressing GCN2 had more ATP and conferred better tolerance under submergence, suggesting that GCN2 might modulate the dynamics of translation to adjust the energy homeostasis under hypoxia. Interestingly, GCN2-eIF2a signaling was activated by ethylene under submergence. However, GCN2 activity was not affected in ein2-5 and eil1ein3 under submergence, suggesting that GCN2 activity was regulated by noncanonical ethylene signaling. In addition, the polysome loading was retained in both ein2-5 and etr1-1 under submergence, implying that ethylene modulated the dynamic translation under submergence via EIN2 and GCN2. Notably, our NGS analysis also demonstrated that EIN2 and GCN2 regulated the translation of 23 core hypoxia genes as well as 53% translational repressed genes under submergence. On the other hand, EIN2 and GCN2 also affected the expression of genes involved in hypoxic response, ethylene response, biotic stress and negative regulation of cytokinin signaling. Taken together, these demonstrated that entrapped ethylene triggers GCN2 and EIN2 to ensure the translation of stress required proteins under submergence and also provide a step stone for future investigation how eukaryotic cells modulate the translation to response for the changeable environments.

2022-06-08 | GSE149414 | GEO

Jasmonate Regulates Plant Responses to Reoxygenation through Activation of Antioxidant Synthesis

Project description:Submergence induces hypoxia in plants; exposure to oxygen following submergence, termed reoxygenation, produces a burst of reactive oxygen species. The mechanisms of hypoxia sensing and signaling in plants have been well studied, but how plants respond to reoxygenation remains unclear. Here, we show that reoxygenation in Arabidopsis thaliana involves rapid accumulation of jasmonates (JAs) and increased transcript levels of JA biosynthesis genes. Application of exogenous methyl jasmonate improved tolerance to reoxygenation in wild-type Arabidopsis; also, mutants deficient in JA biosynthesis and signaling were very sensitive to reoxygenation. Moreover, overexpression of the transcription factor gene MYC2 enhanced tolerance to post-hypoxic stress and myc2 knockout mutants showed increased sensitivity to reoxygenation, indicating that MYC2 functions as a key regulator in the JA-mediated reoxygenation response. MYC2 transcriptionally activates members of the VITAMIN C DEFECTIVE (VTC) and GLUTATHIONE SYNTHETASE (GSH) gene families, which encode rate-limiting enzymes in the ascorbate and glutathione synthesis pathways. Overexpression of VTC1 and GSH1 in the myc2-2 mutant suppressed the post-hypoxic hypersensitive phenotype. The JA-inducible accumulation of antioxidants may alleviate oxidative damage caused by reoxygenation, improving plant survival after submergence. Taken together, our findings demonstrate that JA signaling interacts with the antioxidant pathway to regulate reoxygenation responses in Arabidopsis.

2017-08-25 | GSE93393 | GEO

Altered lipid metabolism in the aging kidney identified by three layered omic analysis

Project description:Aging-related diseases and their comorbidities affect the life quality of a constantly growing proportion of our population. Age-associated changes of kidney structure and function are considerable contributors to the dramatically increased incidence of chronic kidney disease world-wide which has been identified to be a prominent cardiovascular risk factor. In order to detect molecular mechanisms involved in kidney aging we analyzed gene expression profiles of kidneys from adult and aged wild-type mice by a three-layered omics strategy. To this end, transcriptomic, proteomic and targeted lipidomic profiles of young and aged mice were generated and integrated. Transcriptome and proteome analyses revealed differential expression of genes involved primarily in lipid metabolism and immune response. Additional lipidomic analyses uncovered significant age-related differences in the total amount of phosphatidylethanolamines, phosphatidylcholines and sphingomyelins as well as in subspecies of phosphatidylserines and ceramides, while total ceramide levels remained unchanged. By integration of these datasets we identified Aldh1a1, a key enzyme in vitamin A metabolism specifically expressed in the medullary ascending limb, as one of the most prominent upregulated proteins in old kidneys. Moreover, ceramidase Asah1 was highly expressed in aged kidneys, consistent with a decrease in ceramide C16. In summary, our data suggest that changes in lipid metabolism are involved in the process of kidney aging and in the development of chronic kidney disease. 14 weeks females (4 replicates); 96 weeks females (5 replicates)

2015-10-30 | E-GEOD-74463 | biostudies-arrayexpress

Aging stress and ceramide dependent RNA sequencing expression profiling depends on ceramide synthase 6

Project description:The bioactive sphingolipid ceramide, generated by ceramide synthase, is an adaptive stress effector induced in response to various stress stimuli such as aging. In fact, ceramide synthase (CerS) was first discovered in yeast as a longevity assurance gene (LAG1), as the reduced ceramide generation consequent to LAG1 deletion increased longevity. There are six homologues of mammalian LAG1/ceramide synthases (CerS1-6) that generate ceramides with different fatty acid chain lengths with distinct functions and hydrophobicity. Ceramide can be metabolized by sphingosine kinase 1 or 2 for the generation of pro-survival sphingosine 1-phosphate (S1P), which enhances immune cell egress to the blood stream, activating immune function. Ceramide is known to induce mitophagy and cell death. Here we investigated the role of this sphingolipid pathway in immune function, specifically T cell functions, via high throughput expression profiling.

2021-01-01 | GSE148498 | GEO

Effect of Hypoxia in Severe Preeclampsia through Epigenetic Regulation

Project description:Though the pathophysiology of preeclampsia (PE) is unclear worldwide, placental hypoxia has been implicated in the pathologic processes of PE.In this study, we profiled the transcriptome in BeWo and JEG-3 cells cultured in hypoxic condition or normal ones based on the RNA sequencing dataset. After filtered the low-quality ones, the RNA readers was aligned to human genome hg19 by TopHat and then assembled by Cufflinks. The expression value of each transcript was calculated and consequently differentially expressed genes were screened out. CD39 and ZDHHC14 were found to have both different mRNA in hypoxic cells and abnormal methylation level in severely preeclamptic placentas. The mRNA expression of CD39 and ZDHHC14 in placental tissues were analyzed using qRT-PCR. The differential methylated regions (DMRs) of CD39 and ZDHHC14 were confirmed by MassARRY EppiTYPER. The effect of hypoxia on trophoblast cells was detected with western blotting and enzyme linked immunosorbent assay. The results showed CD39 and ZDHHC14were significantly lower in severe PE placenta, hypoxia significantly reduced the expression of CD39 and ZDHHC14 and the secretion of CD39 in trophoblast cells. Therefore, we believed hypoxia plays an important role in the processes of severe PE via decreasing the expression of CD39 and ZDHHC14 by changing their methylation level in placenta.

2017-08-27 | GSE72437 | GEO

Identification of hypoxia-regulated genes in the liver of common sole (Solea solea) fed different dietary lipid contents

Project description:Hepatic transcriptome of sole fed low and high lipid dietary content in the early response to hypoxic stress. Characterization of the hepatic transcriptome of S. solea in order to assess the molecular mechanisms underlying the effects of dietary lipid content on hypoxia tolerance in common sole. S. solea individuals (8 month post-hatching) were fed for two month with commercial diets containing either 11% lipids or 20% lipids. Before hypoxia challenge stress, 38 individuals (19 from each dietary group) were randomly pooled in a single tank (1 m3) and left undisturbed and unfed for 48 h. The hypoxia challenge consisted then in a decrease of water oxygenation from 100 % to 10 % within one hour, followed by a slower descent at 2 % hr-1 to 4%. As fish lost their equilibrium, they were removed and sampled. Thirty six individuals (18 from each dietary group) were also sampled in normoxic conditions, resulting in 4 experimental groups: Normoxia low-lipid, Normoxia high-lipid, Hypoxia low-lipid, Hypoxia high-lipid. The experimental design was therefore a 2-way full factorial design between two juvenile dietary lipid contents and two oxygen concentration conditions.

2013-10-07 | E-GEOD-44579 | biostudies-arrayexpress

Disrupted lipid homeostasis in the absence of the transcriptional activator mga2 results in a failure to activate SREBPs in Schizosaccharomyces pombe

Project description:The sre1 pathway senses molecular oxygen in the fission yeast, Schizosaccharomyces pombe. When oxygen becomes limiting, Sre1 is trafficked from the ER to the Golgi where it is cleaved through the actions of the 5-member Dsc E3 ligase complex. The released N-terminus then upregulates genes required for adaptation to hypoxia. Although the sre1 pathway is responsible for regulating a majority of the genes required for hypoxic growth, it is evident that other regulatory genes are involved in this response. To identify novel regulators of adaptation to hypoxia, we screened the S. pombe nonessential haploid deletion collection. This genome wide screen identified nine genes required for production of the membrane-bound transcription factor Sre1N. The characterization of one of these, the S. pombe transcriptional activator mga2, is presented. mga2 is the homolog of SPT23 and MGA2 in S. cerevisiae. In S. cerevisiae SPT23 and MGA2 regulate the transcription of genes involved in lipid metabolism, including the delta-9 fatty acid desaturase, OLE1. We show S. pombe mga2 also regulates lipid metabolism, and that in the absence of mga2, the lipidome is disrupted. Supplementation with unsaturated fatty acids rescued Sre1 cleavage in mga2Δ cells. However, mga2 is not simply required for activation of Sre1 as mga2Δ cells have a normoxia growth defect that is unrelated to Srel activity. Loss of mga2 results in aberrant Dsc1 glycosylation, suggesting that the Dsc complex is not properly localized to the Golgi. These results establish unsaturated fatty acids as a regulator of the SREBP pathway in fission yeast.

2016-04-06 | GSE60544 | GEO

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