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Lamin B1 deletion in myeloid neoplasms alters hematopoietic cell fate and causes Pelger-Huët nuclear anomaly

ABSTRACT: Lamin B1 deletion in myeloid neoplasms alters hematopoietic cell fate and causes Pelger-Huët nuclear anomaly

PROVIDER: PRJNA730500 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14567235_1.fastq.gz	Fastqsanger.gz
	SRR14567235_2.fastq.gz	Fastqsanger.gz
	SRR14567236_1.fastq.gz	Fastqsanger.gz
	SRR14567236_2.fastq.gz	Fastqsanger.gz
	SRR14567237_1.fastq.gz	Fastqsanger.gz

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Lamin B1 deletion in myeloid neoplasms alters hematopoietic cell fate and causes Pelger-Huët nuclear anomaly

Project description:The most common cytogenetic abnormality found in complex karyotype high risk MDS/AML is del5q. Disease is often identified through visual inspection and recognition of abnormalities such as pseudo-Pelger-Huet anomaly (PPHA), which presents as deviations of normal neutrophil nuclear morphology. The link between PPHA and leukemia is unknown, but mutations in the lamin B1 receptor (LBR) have been identified as the cause of benign presence in otherwise normal individuals. Lamin B1 (LMNB1) is the ligand for LBR and is important for maintaining nuclear lamina integrity and influencing 3D gene structural changes that impact transcription; the LMNB1 gene locus is also contained with chromosome 5q, so we hypothesized that appearance of PPHA is potentially caused by del5q in MDS/AML containing the LMNB1. To help characterize the potential role of LMNB1 in normal hematopoietic stem and progenitor cells (HSPCs), we infected CD34+ cord blood HSPCs with lentiviruses expressing shRNAs targeting LMNB1 (LB1) and luciferase (C11) as a control and assessed changes in transcription due to LMNB1 disruption via RNSeq and 3D genome structural changes through HiC. Neutrophils were also differentiated from LMNB1 shRNA and control treated CD34+ cord blood HSPCs and transcriptional/structural changes identified via RNAseq and HiC. Additionally, to understand long-term in vivo effects of LMNB1 loss on self-renewal and lineage bias, we engrafted control and LMNB1 shRNA infected CD34+ HSPCs into NSG mice and harvest hCD34+ cells 12 weeks later for scRNAseq.

2022-03-11 | GSE174533 | GEO

Lamin B1 ChIPseq experiments from ER:RAS IMR90s

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Lamin B1 ChIPseq experiments from ER:RAS IMR90s

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Project description:Overexpression of Lamin B1 leads to the redistribution of H3K9me3 heterochromatin away from the nuclear periphery and into heterochromatic DNA foci within the nucleoplasm. These changes in chromatin organization correlate with misregulated gene expression (mRNA-sequencing), but do not correlate with altered H3K9me3 deposition across the genome (Cut&Run).

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Lamin B1 overexpression alters chromatin organization and gene expression (Cut&Run-seq)

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Lamin B1 regulates somatic mutations and progression of B cell malignancies

Project description:Somatic hypermutation (SHM) is a pivotal process in adaptive immunity that occurs in the germinal centre and allows B-cells to change their primary DNA sequence and diversify their antigen receptors. Here, we report that genome binding of Lamin B1, a component of the nuclear envelope involved in epigenetic chromatin regulation, is reduced during B cell activation and formation of lymphoid germinal centres. ChIP-Seq analysis showed that kappa and heavy variable immunoglobulin domains were released from the Lamin B1 suppressive environment when SHM was induced in B cells. RNAi-mediated reduction of Lamin B1 resulted in spontaneous SHM as well as kappa-light chain aberrant surface expression. Finally, Lamin B1 expression level was directly proportional to 5-year survival rate in chronic lymphocytic leukaemia, and was strongly involved in transformation of follicular lymphoma. In summary, here we report that Lamin B1 is a negative epigenetic regulator of SHM in normal B-cells and a "mutational gatekeeper", suppressing the aberrant mutations that drive lymphoid malignancy.

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Expression data from functional studies using RNAi on Lamin B1 in BL2 cells

Project description:Lamin B1 is a component of the nuclear envelope involved in epigenetic chromatin regulation and is reduced during B cell activation and formation of lymphoid germinal centres. RNAi-mediated reduction of Lamin B1 results in spontaneous SHM as well as kappa-light chain aberrant surface expression showing that Lamin B1 is a negative epigenetic regulator of SHM. We used Affymetrix Exon 1.0 ST microarrays to detail the global programme of gene expression underlying changes induced in siRNA-treated Lamin B1low BL2 cells. siRNA-mediated reduction of nuclear Lamin B1 incorporation resulted in a general upregulation of positive cell cycle regulatory genes which in turn occurred alongside an upregulation of genes responsible for cell cycle checkpoint execution or cell cycle arrest, and were specific for LMNB1 reduction.

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