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Mus musculus

ABSTRACT: LIM domain binding protein 1 regulates a transcriptional program essential for hematopoietic stem cell maintenance

PROVIDER: PRJNA135497 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR087804.fastq.gz	Fastqsanger.gz
	SRR087805.fastq.gz	Fastqsanger.gz
	SRR087806.fastq.gz	Fastqsanger.gz
	SRR087807.fastq.gz	Fastqsanger.gz
	SRR087808.fastq.gz	Fastqsanger.gz

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Project description:A LIM domain binding protein 2, LDB2, is important for HF-SC maintenance and epidermal homeostasis

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LIM domain binding protein 1 regulates a transcriptional program essential for hematopoietic stem cell maintenance

Project description:We used ChIP-Seq to map Ldb1, Scl and Gata2 binding sites in mouse hematopoietic progenitor cells (HPCs). Together with functional studies using conventional and conditional Ldb1 deficient mouse models and bioinformatics analysis, we systematically determined a transcriptional program controlled by Ldb1 complexes in HSC maintenance. To evaluate the role of Ldb1 in hematopoietic stem cell maintenance.

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Cofactors of LIM domain (CLIM) proteins modulate Wnt signaling and regulate corneal epithelial stem cell maintenance

Project description:Cofactors of LIM domain proteins (CLIM1 and CLIM2) are widely expressed transcriptional cofactors that are recruited to gene regulatory regions by DNA-binding proteins, including LIM domain transcription factors. In the cornea, epithelial specific expression of a dominant negative (DN) CLIM under the Keratin 14 (K14) promoter causes blistering, inflammation, epithelial hyperplasia and neovascularization, followed by epithelial thinning and subsequent epidermal-like differentiation of the cornea epithelium. This phenotype resembles aspects of limbal stem cell deficiency, suggesting that CLIM proteins may be involved in regulating cornea stem cell maintenance. Consistent with this notion, the K14-DN-Clim cornea epithelium has fewer progenitor cells, and altered proliferation dynamics during epithelial development. Differentially regulated genes in DN-CLIM corneas include those in pathways crucial for stem cell maintenance and regulation of proliferation. In vivo ChIP-Seq experiments in the cornea epithelium show that CLIM associates with DNA regulatory elements containing binding sites for HLH and other non-LIM homeodomain factors, and that many genes that are highly expressed in the limbal epithelium, as well as genes with known roles in stem cell maintenance, are directly regulated by CLIM cofactors. DN-CLIM decreases the expression of Wnt inhibitors, including the direct target Wnt5a, causing increased Wnt signaling in the limbal region of DN-CLIM corneas. Together our results indicate that CLIMs regulate cornea stem cell maintenance by controlling Wnt activity and suggest the possibility that this pathway may be altered in limbal stem cell deficiency.

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Depletion of ZNF185 causes delay of keratinocyte differentiation

Project description:Development of epidermis includes a complicated program of keratinocyte differentiation. Here we study a new membrane LIM-domain containing Zn-finger protein ZNF185 which is expressed in upper layers of human skin and is up-regulated during keratinocyte differentiation in vitro. Interestingly, depletion of ZNF185 causes delay of keratinocyte differentiation with decreased levels of FLG, LOR, LCEs expression.

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Project description:FoxM1 is essential for quiescence and maintenance of hematopoietic stem cell

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Project description:RNA binding protein SYNCRIP regulates the leukemia stem cell program

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LIM domain binding protein 1 regulates a transcriptional program essential for hematopoietic stem cell maintenance

2011-01-04 | GSE26031 | GEO

Enhancer looping protein LDB1 affects T-ALL cell proliferation by cooperating with master transcription factors [RNA-Seq]

Project description:LIM domain-binding protein 1 (LDB1) is a highly conserved and widely expressed chromatin looping protein that connects enhancer-promoter genes through LIM and LIM homologous domains in various cell types. LDB1 has been confirmed to play a crucial role in various physiological and pathological processes. In our study, we aim to investigate the function and mechanisms of LDB1 in the context of T-cell acute lymphoblastic leukemia (T-ALL). RNA-seq was conducted and the differently expressed genes were revealed in the LDB1-knockdown 6T-CEM and J.gamma1 cells in comparison to control group. Cleavage Under Targets and Tagmentation (CUT&Tag) showed the co-localization of LDB1 with several master transcription factors on chromatin in 6T-CEM cells.

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Enhancer looping protein LDB1 affects T-ALL cell proliferation by cooperating with master transcription factors [CUT&Tag]

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Exome sequencing

Project description:Human telomere biology disorders (TBD), a heterogeneous group of disorders characterized by telomere attrition and premature aging phenotypes, are caused by inherited loss-of-function mutations in telomere-associated genes. Here, we identify three germline heterozygous missense variants in RPA1 gene in four unrelated probands presenting with short telomeres and varying clinical features of TBD including bone marrow failure, myelodysplastic syndrome, T- and B-cell lymphopenia, pulmonary fibrosis, and skin manifestations. All variants cluster to DNA binding domain A of RPA1 protein. RPA1 is an essential single-strand DNA-binding protein essential for DNA replication and repair. RPA1 has been implicated in telomere maintenance but the mechanism remains elusive. Thus far, no genetic disorder had been linked to RPA1. Using FRET assays, we showed that RPA1E240K and RPA1V227A exhibit increased binding to single-strand and telomeric DNA, implying a gain in DNA-binding function while RPA1T270A has binding properties similar to wild type. To study the mutational effect, RPA1E240K, with the highest binding capacity, was knocked-in iPSCs using CRISPR/Cas9, which showed severe telomere shortening and impaired hematopoietic differentiation. Furthermore, in the RPA1E240K patient, stable blood counts over two decades due coincided with clonal rescue hematopoiesis with an RNA-degrading truncating RPA1 mutation and a uniparental isodisomy 17p with loss of RPA1E240K allele. Using single cell DNA sequencing, the two somatic genetic rescue events were proven to be independently acquired in hematopoietic stem cells. In summary, we describe the first human disease caused by germline RPA1 variants in individuals with TBD.

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