Expression data from wt, Lkb1 conditional knock out and LPS treated DC
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PROVIDER: PRJNA481663 | ENA |
REPOSITORIES: ENA
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Project description:To dissect the molecular mechanism by which Lkb1 controls DC function, we performed transcriptional profiling of DCs sorted from Lkb1f/f, LPS-treated mice and Cd11cCreLkb1f/f mice. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified
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Project description:We have shown that removal of Lkb1 in chondorcytes results in enchondroma-like structure in postnatal mouse long bones. To furhter understand the role of Lkb1 in this process, we performed microarrrays to compare the transcriptional profile between control and conditional Lkb1 mutant (Col2a1-Cre; Lkb1c/c) chondrocytes. Postnatal day 30 mouse growth plate chondorcytes from control and mutant mouse femurs and tibiae were isolated for RNA extraction and hybridization on Affymetrix microarrays.
2013-11-14 | E-GEOD-41898 | biostudies-arrayexpress
Project description:We have shown that removal of Lkb1 in chondorcytes results in enchondroma-like structure in postnatal mouse long bones. To furhter understand the role of Lkb1 in this process, we performed microarrrays to compare the transcriptional profile between control and conditional Lkb1 mutant (Col2a1-Cre; Lkb1c/c) chondrocytes.
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Project description:RNA-Seq was performed on pancreatic islets from four transgenic mouse strains affecting LKB1 and AMPK. A conditional LKB1 knockout strain was generated. Double conditional knockouts for AMPK alpha1 and AMPK alpha2 were also generated. These conditional strains were crossed with RIP-Cre (driven by rat insulin promoter) or Ins1-Cre mice to generate LKB1 knockout and AMPK double knockout strains.
2014-10-25 | E-MTAB-2791 | biostudies-arrayexpress
Project description:Transcriptional profiling of mouse comparing in vitro-derived DC progenitors from control and Gata2 conditional knockout mice. Two-condition experiment, Control DCs vs. G2 Knockout DCs. Biological replicates: 4 control, 3 Gata2 knockout, independently grown and harvested. One replicate per array. Dendritic cells (DCs) are critical immune response regulators; however, the mechanism of DC differentiation is not fully understood. Heterozygous germline GATA2 mutations induce GATA2 deficiency syndrome, characterized by monocytopenia, a predisposition to myelodysplasia/acute myeloid leukemia, and a profoundly reduced DC population, which is associated with increased susceptibility to viral infections, impaired phagocytosis, and decreased cytokine production. To define the role of GATA2 in DC differentiation and function, we studied Gata2 conditional knockout and haploinsufficient mice. Gata2 conditional deficiency significantly reduced the DC count, whereas Gata2 haploinsufficiency did not affect this population. GATA2 was required for the in vitro generation of DCs from Linâ??Sca-1+Kit+ cells, common myeloid-restricted progenitors, and common dendritic cell precursors, but not common lymphoid-restricted progenitors or granulocyte-macrophage progenitors, suggesting that GATA2 functions in the myeloid pathway of DC differentiation. Moreover, expression profiling demonstrated reduced expression of myeloid-related genes, including mafb, and increased expression of T-lymphocyte-related genes, including Gata3 and Tcf7, in Gata2-deficient DC progenitors. In addition, GATA2 was found to bind an enhancer element 190-kb downstream region of Gata3, and a reporter assay exhibited significantly reduced luciferase activity after adding this enhancer region to the Gata3 promoter, which was recovered by GATA sequence deletion within Gata3 +190. These results suggest that GATA2 plays an important role in cell fate specification toward the myeloid versus T lymphocyte lineage by regulating lineage-specific transcription factors in DC progenitors, thereby contributing to DC differentiation.
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Project description:We characterize the phenotype of mice in which the deletion of Lkb1 has been targeted in the liver. Lack of Lkb1 in the liver results in bile duct paucity leading to cholestasis. This phenotype is similar to that obtained upon inactivation of Notch signaling in the liver. We test the hypothesis of a functional overlap between the Lkb1 and Notch pathways by gene expression profiling of livers deficent in Lkb1 or in the Notch mediator RbpJκ. We used AlfpCre mice for liver-specific deletion of LKB1 that were crossed with a conditional knockout mouse model (LKB1 floxed mice). We used also AlfpCre mice for liver-specific inactivation of the Notch pathway. AlfpCre mice were crossed with the RbpJκ floxed mice. RNA was extracted from the liver of LKB1 KO mice (Lkb1Floxed, AlfpCre positive mice) and their wild-type counterpart (Lkb1Floxed, AlfpCre negative mice). RNA was also extracted from liver of RbpJK KO mice (RbpJK floxed, AlfpCre positive) and their wild type mice (RbpJK floxed, AlfpCe negative). 6 samples for the liver-specific deletion of LKB1 corresponding to 3 KO LKB1 (Cre positive) and 3 normal liver (Cre negative). 6 samples for the liver-specific inactivation of the Notch pathway corresponding to 3 KO RbpJk (Cre positive) and 3 normal liver (Cre negative).
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Project description:Liver Kinase B1 (LKB1) plays a key role in cellular metabolism by controlling AMPK activation. However, its function in dendritic cell (DC) biology has not been addressed. Here, we find that LKB1 functions as a critical brake on DC immunogenicity, and when lost, leads to reduced mitochondrial fitness and increased maturation, migration, and T cell priming of peripheral DCs. Concurrently, loss of LKB1 in DCs enhances their capacity to promote output of regulatory T cells (Tregs) from the thymus, which dominates the outcome of peripheral immune responses, as suggested by increased resistance to asthma and higher susceptibility to cancer in CD11cΔLKB1 mice. Mechanistically, we find that loss of LKB1 specifically primes thymic CD11b+ DCs to facilitate thymic Treg development and expansion, which is independent from AMPK signalling, but dependent on mTOR and enhanced phospholipase C β1-driven CD86 expression. Together, our results identify LKB1 as a critical regulator of DC-driven effector T cell and Treg responses both in the periphery and the thymus.
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