Transcriptomic analysis of endoplasmic reticulum stress (ERS) regulated genes in the liver of NFIL3 KO mice.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE122506 | GEO | 2020/04/29
REPOSITORIES: GEO
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Project description:Transcriptomic analysis of endoplasmic reticulum stress (ERS) regulated genes in the liver of NFIL3 KO mice.
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Project description:Tunicamycin inhibits the first step of protein N-glycosylation modification. However, the physiological, transcriptomic, and N-glycomic effects of tunicamycin on important marine diatom Phaeodactylum tricornutum are still unknown. In this study, comprehensive approaches were used to study the effects. The results showed that cell growth and photosynthesis were significantly inhibited in P. tricornutum under the tunicamycin stress. The soluble protein content was significantly decreased, while the soluble sugar and neutral lipid were dramatically increased to orchestrate the balance of carbon and nitrogen metabolism. 0.3 μg m-1 tunicamycin could not complete inhibited the N-glycosylation of protein, but it resulted in the differentially expression of ERQC and ERAD related genes. The upregulation of genes involved in ERQC and the activation of anti-oxidases were speculated to alleviate the tunicamycin stress. The differentially expression of genes related to ERAD was suggested to degrade the unfolded and/or incorrect N-glycoproteins induced by tunicamycin. The identification of mannose-type and complex-type N-glycan structures enriched the N-glycan database of diatom P. tricornutum and provided important information for studying the function of N-glycosylation modification on proteins. All in all, the proposed working models of ERQC and ERAD will provide a solid foundation for further in-depth study the related mechanism and the diatom expression system.
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Project description:Nfil3 has multiple functions during conventional NK cell and thymic NK cell development. Nfil3 controls NK cell development from the earliest committed NK cell progenitor stage. Nfil3-/- prepro NK cells retained T-cell potential due to the failure to repress T cell specific genes. At later stages of NK cell development, Nfil3 regulates the formation of mature NK cells by promoting directly or indirectly the expression of transcription factor Eomes. We also demonstrate that Nfil3 is important for thymic NK cell development whereas Trail+ immature NK cells generated in the bone marrow of neonates and in the adult liver develop independent of Nfil3 function. We used microarrays to analyse the changes in gene expression due to the presence or absence of Nfil3, both in prepro NK cells and ALP cells (all lymphoid progenitors)
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Project description:Natural killer (NK) cells can be grouped into distinct subsets that are localized to different organs and exhibit different capacity to secrete cytokines and mediate cytotoxicity. Despite these hallmarks that reflect tissue-specific specialization in NK cells, little is known about the factors that control the development of these distinct subsets. The basic leucine zipper transcription factor nuclear factor interleukin 3 (Nfil3; E4bp4) is essential for bone marrow-derived NK cell development but it is not clear whether Nfil3 is equally important for all NK cell subsets nor how it induces NK lineage commitment. Here we show that Nfil3 is required for the formation of Eomesodermin (Eomes)-expressing NK cells, including conventional medullary and thymic NK cells, whereas TRAIL+ Eomes- NK cells develop independent of Nfil3. Loss of Nfil3 during the development of bone marrow-derived NK cells resulted in reduced expression of Eomes and, conversely, restoration of Eomes expression in Nfil3-/- progenitors rescued NK cell development and maturation. Collectively, these findings demonstrate that Nfil3 drives the formation of mature NK cell by inducing Eomes expression and reveal the differential requirements of NK cell subsets for Nfil3.
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Project description:Nfil3 has multiple functions during conventional NK cell and thymic NK cell development. Nfil3 controls NK cell development from the earliest committed NK cell progenitor stage. Nfil3-/- prepro NK cells retained T-cell potential due to the failure to repress T cell specific genes. At later stages of NK cell development, Nfil3 regulates the formation of mature NK cells by promoting directly or indirectly the expression of transcription factor Eomes. We also demonstrate that Nfil3 is important for thymic NK cell development whereas Trail+ immature NK cells generated in the bone marrow of neonates and in the adult liver develop independent of Nfil3 function. We used microarrays to analyse the changes in gene expression due to the presence or absence of Nfil3, both in prepro NK cells and ALP cells (all lymphoid progenitors) Samples were obtained on two experimentation dates. Replicate 1 was processed in April 2012, replicate 2 was processed in May 2012.
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Project description:Chronic endoplasmic reticulum (ER) stress results in toxicity that contributes to multiple human disorders. We report a stress resolution pathway initiated by the nuclear receptor LRH-1 that is independent of known unfolded protein response (UPR) pathways. Like mice lacking primary UPR components, hepatic Lrh-1-null mice cannot resolve ER stress, despite a functional UPR. In response to ER stress, LRH-1 induces expression of the kinase Plk3, which phosphorylates and activates the transcription factor ATF2. Plk3-null mice also cannot resolve ER stress, and restoring Plk3 expression in Lrh-1-null cells rescues ER stress resolution. Reduced or heightened ATF2 activity also sensitizes or desensitizes cells to ER stress, respectively. LRH-1 agonist treatment increases ER stress resistance and decreases cell death. We conclude that LRH-1 initiates a novel pathway of ER stress resolution that is independent of the UPR, yet equivalently required. Targeting LRH-1 may be beneficial in human disorders associated with chronic ER stress. 24 total samples. One sample represents one mouse. Three samples were analyzed from the following groups: Lrh-1 f/f (control littermates) treated with vehicle, Lrh-1 f/f treated with tunicamycin (TM; 1mg/kg BW for 24h), Lrh-1 f/f treated with tunicamycin and DLPC (100mg/kg BW 4x), Lrh-1 f/f treated with tunicamycin and vehicle for DLPC, Lrh-1 liver-specific KO mice (LKO) treated with vehicle, Lrh-1 LKO treated with tunicamycin, and Lrh-1 LKO treated with tunicamycin and DLPC, Lrh-1 LKO treated with tunicamycin and vehicle for DLPC
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Project description:Natural killer (NK) cells can be grouped into distinct subsets that are localized to different organs and exhibit different capacity to secrete cytokines and mediate cytotoxicity. Despite these hallmarks that reflect tissue-specific specialization in NK cells, little is known about the factors that control the development of these distinct subsets. The basic leucine zipper transcription factor nuclear factor interleukin 3 (Nfil3; E4bp4) is essential for bone marrow-derived NK cell development but it is not clear whether Nfil3 is equally important for all NK cell subsets nor how it induces NK lineage commitment. Here we show that Nfil3 is required for the formation of Eomesodermin (Eomes)-expressing NK cells, including conventional medullary and thymic NK cells, whereas TRAIL+ Eomes- NK cells develop independent of Nfil3. Loss of Nfil3 during the development of bone marrow-derived NK cells resulted in reduced expression of Eomes and, conversely, restoration of Eomes expression in Nfil3-/- progenitors rescued NK cell development and maturation. Collectively, these findings demonstrate that Nfil3 drives the formation of mature NK cell by inducing Eomes expression and reveal the differential requirements of NK cell subsets for Nfil3. RNA-sequencing of natural killer (NK) cell subsets
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