Mus musculus strain:C57BL/6J
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA998173 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25658936_1.fastq.gz | Fastqsanger.gz | |||
| SRR25658936_2.fastq.gz | Fastqsanger.gz | |||
| SRR25658937_1.fastq.gz | Fastqsanger.gz | |||
| SRR25658937_2.fastq.gz | Fastqsanger.gz | |||
| SRR25658938_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 36 |
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Project description:Epithelial regeneration is critical for barrier maintenance and organ function after intestinal injury. Here, we found that Bach2 deficiency promotes the intestinal epithelial cell proliferation during homeostasis and facilitates the crypt regeneration after irradiation, resulting in a reduction of mortality. RNA-seq analysis of isolated crypts revealed that Bach2 deficiency altered expression of numerous genes including those regulating DSBs repair. Crypts were isolated from the small intestines of Bach2 KO and control mice (n=3, respectively) 10 days after tamoxifen administration. Total RNA was extracted for sequencing using RNA-Seq.
2021-01-12 | E-MTAB-9865 | biostudies-arrayexpress
Project description:The differentiation and homeostasis of Foxp3+ regulatory T (Treg) cells is strictly controlled by T cell receptor (TCR) signals; however, the molecular regulators of these processes are incompletely known. Here we found that Bach2 was a key regulator of Treg cell differentiation and homeostasis downstream of TCR signalling. Bach2 prevented premature differentiation of fully suppressive effector (e)Treg cells, limited IL-10 production and was required for the development of peripherally induced (p)Treg cells in the gastrointestinal tract. We found that Bach2 attenuated TCR signalling-induced and IRF4-dependent Treg cell differentiation programs. Deletion of IRF4 promoted inducible Treg cell differentiation and rescued pTreg cell differentiation in the absence of Bach2. In turn, loss of Bach2 normalised eTreg cell differentiation of IRF4-deficient Treg cells. Mechanistically, Bach2 counteracted DNA-binding activity of IRF4 and limited chromatin accessibility, thereby attenuating IRF4-dependent transcriptional programs. Thus, Bach2 balanced TCR signalling induced transcriptional activity of IRF4 to maintain Treg cell homeostasis.
2019-11-07 | GSE137246 | GEO
Project description:The differentiation and homeostasis of Foxp3+ regulatory T (Treg) cells is strictly controlled by T cell receptor (TCR) signals; however, the molecular regulators of these processes are incompletely known. Here we found that Bach2 was a key regulator of Treg cell differentiation and homeostasis downstream of TCR signalling. Bach2 prevented premature differentiation of fully suppressive effector (e)Treg cells, limited IL-10 production and was required for the development of peripherally induced (p)Treg cells in the gastrointestinal tract. We found that Bach2 attenuated TCR signalling-induced and IRF4-dependent Treg cell differentiation programs. Deletion of IRF4 promoted inducible Treg cell differentiation and rescued pTreg cell differentiation in the absence of Bach2. In turn, loss of Bach2 normalised eTreg cell differentiation of IRF4-deficient Treg cells. Mechanistically, Bach2 counteracted DNA-binding activity of IRF4 and limited chromatin accessibility, thereby attenuating IRF4-dependent transcriptional programs. Thus, Bach2 balanced TCR signalling induced transcriptional activity of IRF4 to maintain Treg cell homeostasis.
2019-11-07 | GSE126810 | GEO
Project description:The differentiation and homeostasis of Foxp3+ regulatory T (Treg) cells is strictly controlled by T cell receptor (TCR) signals; however, the molecular regulators of these processes are incompletely known. Here we found that Bach2 was a key regulator of Treg cell differentiation and homeostasis downstream of TCR signalling. Bach2 prevented premature differentiation of fully suppressive effector (e)Treg cells, limited IL-10 production and was required for the development of peripherally induced (p)Treg cells in the gastrointestinal tract. We found that Bach2 attenuated TCR signalling-induced and IRF4-dependent Treg cell differentiation programs. Deletion of IRF4 promoted inducible Treg cell differentiation and rescued pTreg cell differentiation in the absence of Bach2. In turn, loss of Bach2 normalised eTreg cell differentiation of IRF4-deficient Treg cells. Mechanistically, Bach2 counteracted DNA-binding activity of IRF4 and limited chromatin accessibility, thereby attenuating IRF4-dependent transcriptional programs. Thus, Bach2 balanced TCR signalling induced transcriptional activity of IRF4 to maintain Treg cell homeostasis.
2019-11-07 | GSE126806 | GEO
Project description:The differentiation and homeostasis of Foxp3+ regulatory T (Treg) cells is strictly controlled by T cell receptor (TCR) signals; however, the molecular regulators of these processes are incompletely known. Here we found that Bach2 was a key regulator of Treg cell differentiation and homeostasis downstream of TCR signalling. Bach2 prevented premature differentiation of fully suppressive effector (e)Treg cells, limited IL-10 production and was required for the development of peripherally induced (p)Treg cells in the gastrointestinal tract. We found that Bach2 attenuated TCR signalling-induced and IRF4-dependent Treg cell differentiation programs. Deletion of IRF4 promoted inducible Treg cell differentiation and rescued pTreg cell differentiation in the absence of Bach2. In turn, loss of Bach2 normalised eTreg cell differentiation of IRF4-deficient Treg cells. Mechanistically, Bach2 counteracted DNA-binding activity of IRF4 and limited chromatin accessibility, thereby attenuating IRF4-dependent transcriptional programs. Thus, Bach2 balanced TCR signalling induced transcriptional activity of IRF4 to maintain Treg cell homeostasis.
2019-11-07 | GSE126800 | GEO
Project description:The differentiation and homeostasis of Foxp3+ regulatory T (Treg) cells is strictly controlled by T cell receptor (TCR) signals; however, the molecular regulators of these processes are incompletely known. Here we found that Bach2 was a key regulator of Treg cell differentiation and homeostasis downstream of TCR signalling. Bach2 prevented premature differentiation of fully suppressive effector (e)Treg cells, limited IL-10 production and was required for the development of peripherally induced (p)Treg cells in the gastrointestinal tract. We found that Bach2 attenuated TCR signalling-induced and IRF4-dependent Treg cell differentiation programs. Deletion of IRF4 promoted inducible Treg cell differentiation and rescued pTreg cell differentiation in the absence of Bach2. In turn, loss of Bach2 normalised eTreg cell differentiation of IRF4-deficient Treg cells. Mechanistically, Bach2 counteracted DNA-binding activity of IRF4 and limited chromatin accessibility, thereby attenuating IRF4-dependent transcriptional programs. Thus, Bach2 balanced TCR signalling induced transcriptional activity of IRF4 to maintain Treg cell homeostasis.
2019-11-07 | GSE137243 | GEO
Project description:The transcriptional repressors BCL6 and BACH2 are crucial regulators of germinal center (GC) B-cell fate, and are known to interact and repress transcription of PRDM1, a key driver of plasma cell differentiation. How these factors cooperate is not fully understood. Herein we show that while GC formation is only minimally impaired in Bcl6+/- or Bach2+/- mice, double heterozygous Bcl6+/-Bach2+/- mice exhibit profound reduction in GC formation. Splenic B-cells from Bcl6+/- Bach2+/- mice display accelerated plasmacytic differentiation and high expression of key plasma cell genes such as Prdm1, Xbp1 and CD138. ChIP-seq revealed that in B-cells BACH2 is mostly bound to genes together with its heterodimer partner MAFK. The BACH2-MAFK complex binds to sets of genes known to be involved in the GC response, 60% of which are also targets of BCL6. Approximately 30% of BACH2 peaks overlap with BCL6 including cis-regulatory sequences of the PRDM1 gene. BCL6 also modulates BACH2 protein stability and their protein levels are positively correlated in GC B-cells. Therefore, BCL6 and BACH2 cooperate to orchestrate gene expression patterning in GC B cells through both transcriptional and biochemical mechanisms, which collectively determine the proper initiation and timing of terminal differentiation. ChIP-seq using P18 antibodies in OCI-Ly7 cells
2013-11-17 | E-GEOD-47784 | biostudies-arrayexpress
Project description:Pulmonary alveolar proteinosis (PAP) results from a dysfunction of alveolar macrophages (AMs), chiefly due to disruptions in the signaling of granulocyte macrophage colony-stimulating factor (GM-CSF). We found that mice deficient for the B lymphoid transcription repressor BTB and CNC homology 2 (Bach2) developed PAP-like accumulation of surfactant proteins in the lungs. Bach2 was expressed in AMs, and Bach2-deficient AMs showed alterations in lipid handling in comparison with wild-type (WT) cells. Although Bach2-deficient AMs showed a normal expression of the genes involved in the GM-CSF signaling, they showed an altered expression of the genes involved in chemotaxis, lipid metabolism, and alternative M2 macrophage activation with increased expression of Ym1 and arginase-1, and the M2 regulator Irf4. Peritoneal Bach2-deficient macrophages showed increased Ym1 expression when stimulated with interleukin-4. More eosinophils were present in the lung and peritoneal cavity of Bach2-deficient mice compared with WT mice. The PAP-like lesions in Bach2-deficient mice were relieved by WT bone marrow transplantation even after their development, confirming the hematopoietic origin of the lesions. These results indicate that Bach2 is required for the functional maturation of AMs and pulmonary homeostasis, independently of the GM-CSF signaling. WT (n=8) and Bach2KO (n=3) AMs. One expreriment was performed.
2014-01-15 | E-GEOD-54050 | biostudies-arrayexpress
Project description:The molecular circuits that direct early T-dependent B cell responses and alternative cell-fate decisions remain poorly understood. Here, we show that either B cell receptor (BCR) or CD40 signals promoted mTORC1-dependent translation of the transcription factor Bach2. Transient up-regulation of Bach2 protein restrained activated B cell expansion and differentiation into plasma cell while promoting the germinal center (GC) and memory B cell fates at the pre-GC stage. However, enforced Bach2 expression facilitated memory B cell generation versus other cell fates. Mechanistically, Bach2 limited access of AP-1 factors and formed a reciprocal repression loop with IRF4. BCR and CD40 signals also down-regulated Bach2 transcript in antigen-activated B cells, and diversified its abundance in various effector populations, predisposing Bach2 protein expression and subsequent cell-fate choices during memory recall and GC reaction. Thus signaling-induced differential dynamics of Bach2 protein and mRNA in activated B cell control their cell-fate outcomes and imprint the fate of their descendant effector cells.
2022-06-08 | GSE180460 | GEO
Project description:The molecular circuits that direct early T-dependent B cell responses and alternative cell-fate decisions remain poorly understood. Here, we show that either B cell receptor (BCR) or CD40 signals promoted mTORC1-dependent translation of the transcription factor Bach2. Transient up-regulation of Bach2 protein restrained activated B cell expansion and differentiation into plasma cell while promoting the germinal center (GC) and memory B cell fates at the pre-GC stage. However, enforced Bach2 expression facilitated memory B cell generation versus other cell fates. Mechanistically, Bach2 limited access of AP-1 factors and formed a reciprocal repression loop with IRF4. BCR and CD40 signals also down-regulated Bach2 transcript in antigen-activated B cells, and diversified its abundance in various effector populations, predisposing Bach2 protein expression and subsequent cell-fate choices during memory recall and GC reaction. Thus signaling-induced differential dynamics of Bach2 protein and mRNA in activated B cell control their cell-fate outcomes and imprint the fate of their descendant effector cells.
2021-07-18 | GSE180277 | GEO