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Classically, hypercholesterolemia has been indicated as the driver of such metabolic alterations occurring in immune cells. ApoE KO or LDLR KO mice fed an atherogenic diet develop pronounced hypercholesterolemia and display an immune-activated phenotype characterized by increased T-effector memory cells, which mimics the profile observed in hypercolesterolemic patients17. In the same experimental settings, the overexpression of apolipoprotein A-I (apoA-I), which increases the ability to transport cholesterol back to the liver, results in a reduced cellular cholesterol accumulation and immune cell activation in lymph nodes18,19. These data point to a critical role for apolipoproteins, including apoA-I and apoE, in controlling cholesterol immunometabolism at both a systemic and cellular level.
Our data indicate that apoE controls DC function through a mechanism which appears to be restricted to MHC-II molecule compartmentalization on the cell surface. In B cells, antigen uptake was shown to be dependent on lipid raft-mediated endocytosis, and, more importantly, localization and internalization of MHC-I and MHC-II molecules in different membrane domains, with MHC-II molecules showing a strong co-clustering with lipid rafts65. Our observations expand these findings to DCs showing that accumulation of lipid rafts due to apoE deficiency leads to an increased EαGFP peptide uptake and processing through MHC-II molecules, which specifically elicits a CD4+ but not CD8+ T-cell activation. Consistently, apoE deficiency in DCs boosted CD4+ but not CD8+ T-cell proliferation, further confirming that the modulation of cellular cholesterol by apoE impacts mainly MHC-II function. Further, in vitro inhibition of cholesterol biosynthesis perturbed raft composition resulting in the alteration of antigen processing and presentation to CD4+ T cells66, which depends on MHC-II peptide complex clustering in DC lipid microdomains67.
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Elaeis guineensis as a tropical oil-crop is particularly sensitive to low temperature. Improvement of cold-tolerance may significantly increase the total cultivation area of this tropical oil-crop worldwide. We sequenced cold-treated and control (untreated) samples of Elaeis guineensis. De novo assembly generated 51,452 unigenes with an average length of 703 bp. Subsequently, these expressed sequences were functionally annotated. In the K category (transcription factors) of COG (Cluster of Orthologous Group) annotation, the largest proportion of genes induced and repressed at least two-fold under cold stress were from the AP2/ERE family, indicating that C-repeat binding factor, (CBFs, members of the AP2/ERE family) may play a central role in cold tolerance in Elaeis guineensis. Subsequently, the CBF-mediated signal transduction pathway was reconstructed based on transcriptome data and the gene expression profile involving the pathway was examined using real-time quantitative RT-PCR (qRT-PCR). CBFs reached maximum transcript level both at medium (4 h) and long period time points (7 days), contrary to the expression pattern of CBFs in Arabidopsis and rice. Moreover, the promoters of downstream Cold Responsive gene (CORs) regulated by CBFs were analyzed. Conservation, mutation and absence of the DRE core motif were detected in the promoters of six CORs. These mutations in DRE motifs suggest that CORs may not be induced via cold stress in Elaeis guineensis.
In Arabidopsis and rice, the CBF (C-repeat Binding Factor)-mediated signal transduction pathway has been proved to play a central role in cold tolerance. In Arabidopsis, the CBF/dehydration-responsive element-binding factor (DREB1) protein family contains three gene members: CBF1/DREB1B, CBF2/DREB1C and CBF3/DREB1A [13], [15]. Transgenic Arabidopsis plants constitutively expressing CBF1, CBF2 and CBF3 had increased cold tolerance [16], [17], [18]; while down-regulation of CBF expression by RNA interference and antisense RNA resulted in about a 25% to 50% decrease in freezing tolerance when plants were exposed to low temperatures [19]. The CBF protein can bind to cis-acting element DRE (dehydration-responsive element) or to CRT (C-repeat) so as to activate the expression of cold-responsive genes (CORs) which may encode enzymes involved in the biosynthesis of low-molecular-weight nitrogenous compounds, cryoprotectants such as sucrose, raffinose, proline, hydrophilic cryoprotective polypeptides etc [20].
ICE1 (inducer of CBF expression 1), a MYC-like basic helix-loop-helix transcription factor, is a major positive regulator of CBF genes. The constitutive expression of ICE1 will induce CBF3 expression without exposure to low temperature [21]. Miura et al. (2007) provide strong evidence that low temperature-induced sumoylation of ICE1 proteins mediated by SIZ1 proteins are required for activating the expression of CBF genes [22]. Meanwhile, ICE1 proteins can be inactivated due to ubiquitination and protein degradation mediated by HOS1 (High expression of Osmotically responsive genes1), a RING finger E3 ligase. At room temperature, the HOS1 gene is expressed in the cytoplasm. When Arabidopsis plants are exposed to cold environments, HOS1 gene expression is found in the nuclei [23], [24]. In Arabidopsis, low temperature seems to be able to initiate a cycle of activation and inactivation of ICE1 proteins based the SIZ1-HOS1 system, which contributes to accurately regulate the expression of CBF genes. Moreover, transgenic Arabidopsis constitutively expressing MYB15 will lead to a decrease in the expression of CBF genes and reduction of cold tolerance, indicating that MYB15 is a negative regulator of CBF gene expression. Meanwhile, the ice1 mutation in Arabidopsis shows a sustainable increased expression level of MYB15, indicating that ICE1 can negatively regulate the expression of the MYB15 gene [25], [26].
A BLAST analysis of the assembled transcripts against the KEGG database matched 22,687 transcripts with corresponding Enzyme Commission (EC) numbers and canonical KEGG reference pathways. 128 biosynthesis pathways were predicted. Differential expression analysis showed that some KEGG pathways were induced in response to cold stress (File S1). Of these cold-response pathways, some had been previously reported to be associated with cold-stress or environmental stress, such as Brassinosteroid biosynthesis, Zeatin biosynthesis, Benzoxazinoid biosynthesis, Flavoneand flavonol biosynthesis and plant-pathogen interactions (for which 33.33%, 31.58%, 26.92%, 21.35% and 18.84% of transcripts respectively were up-regulated at least two-fold). Pathways involving amino acid degradation or metabolism were also induced in response to cold stress, such as Tryptophan metabolism, Glutathione metabolism, Cysteine and methionine metabolism, Lysine degradation, Tyrosine metabolism and Phenylalanine metabolism (for which 25%, 21.99%, 21.43%, 20.78%, 19.23% and 18.59% of transcripts respectively were up-regulated at least two-fold). The involvement of these amino acid degradation and metabolism pathways may indicate that oil palm decreases some polypeptide synthesis to increase tolerance to cold stress. Moreover, mismatch repair, base excision repair and non-homologous end-joining (for which 24.24%, 21.51% and 20.45% of transcripts respectively were up-regulated at least two-fold), were also found to be induced in response to cold stress. These pathways may be involved in decreasing DNA damage when oil palm is suffering from cold stress. 2ff7e9595c
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