Chromodomain helicase DNA‐binding 4 (CHD4) regulates early B cell identity and V(D)J recombination*

2021 ◽  
Author(s):  
James R. Hagman ◽  
Tessa Arends ◽  
Curtis Laborda ◽  
Jennifer R. Knapp ◽  
Laura Harmacek ◽  
...  
Keyword(s):  
Dna Binding ◽  
B Cell ◽  
Cell Identity

scholarly journals The influence of space and time on the establishment of B cell identity

2019 ◽  
Vol 42 (4) ◽  
pp. 209-217 ◽  
Author(s):  
Ramy Elsaid ◽  
Junjie Yang ◽  
Ana Cumano
Keyword(s):  
B Cell ◽  
Cell Identity ◽  
Space And Time

ERP, a new member of the ets transcription factor/oncoprotein family: cloning, characterization, and differential expression during B-lymphocyte development

1994 ◽  
Vol 14 (5) ◽  
pp. 3292-3309
Author(s):  
M Lopez ◽  
P Oettgen ◽  
Y Akbarali ◽  
U Dendorfer ◽  
T A Libermann
Keyword(s):  
Transcription Factor ◽  
Dna Binding ◽  
Gene Family ◽  
B Cell ◽  
Binding Sites ◽  
B Lymphocyte ◽  
Striking Similarity ◽  
Lymphocyte Development ◽  
B Lymphocyte Development ◽  
Ets Transcription Factor

The ets gene family encodes a group of proteins which function as transcription factors under physiological conditions and, if aberrantly expressed, can cause cellular transformation. We have recently identified two regulatory elements in the murine immunoglobulin heavy-chain (IgH) enhancer, pi and microB, which exhibit striking similarity to binding sites for ets-related proteins. To identify ets-related transcriptional regulators expressed in pre-B lymphocytes that may interact with either the pi or the microB site, we have used a PCR approach with degenerate oligonucleotides encoding conserved sequences in all members of the ets family. We have cloned the gene for a new ets-related transcription factor, ERP (ets-related protein), from the murine pre-B cell line BASC 6C2 and from mouse lung tissue. The ERP protein contains a region of high homology with the ETS DNA-binding domain common to all members of the ets transcription factor/oncoprotein family. Three additional smaller regions show homology to the ELK-1 and SAP-1 genes, a subgroup of the ets gene family that interacts with the serum response factor. Full-length ERP expresses only negligible DNA-binding activity by itself. Removal of the carboxy terminus enables ERP to interact with a variety of ets-binding sites including the E74 site, the IgH enhancer pi site, and the lck promoter ets site, suggesting a carboxy-terminal negative regulatory domain. At least three ERP-related transcripts are expressed in a variety of tissues. However, within the B-cell lineage, ERP is highly expressed primarily at early stages of B-lymphocyte development, and expression declines drastically upon B-cell maturation, correlating with the enhancer activity of the IgH pi site. These data suggest that ERP might play a role in B-cell development and in IgH gene regulation.

scholarly journals Mutant p63 affects epidermal cell identity through rewiring the enhancer landscape

2018 ◽  
Author(s):  
Jieqiong Qu ◽  
Sabine Tanis ◽  
Jos P.H. Smits ◽  
Evelyn N. Kouwenhoven ◽  
Martin Oti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Binding ◽  
Epidermal Cell ◽  
Developmental Disorders ◽  
Molecular Mechanisms ◽  
Epidermal Keratinocytes ◽  
Cell Identity ◽  
Keratinocyte Proliferation ◽  
Eec Syndrome ◽  
Proliferation And Differentiation

AbstractTranscription factor p63 is a key regulator of epidermal keratinocyte proliferation and differentiation. In humans mutations in p63 cause several developmental disorders with defects of ectoderm-derived structures including the epidermis. The underlying molecular mechanisms of these mutations however remain unclear. Here we characterized the transcriptome and epigenome from EEC syndrome patients carrying mutations in the p63 DNA-binding domain. The transcriptome of p63 mutant keratinocytes deviated from the normal epidermal cell identity. Epigenomic analyses showed that the deregulated gene expression in p63 mutant keratinocytes resulted from an altered enhancer landscape contributed by loss of p63-bound active enhancers and by unexpected gain of enhancers. The gained enhancers in mutant keratinocytes were frequently bound by deregulated transcription factors such as RUNX1. Reversing RUNX1 overexpression partially rescued deregulated gene expression as well as the enhancer distribution. Our findings support the pivotal role of p63 in controlling the enhancer landscape of epidermal keratinocytes and identify a novel mechanism whereby p63 DNA-binding mutations associated with EEC syndrome rewire the enhancer landscape and affect epidermal cell identity.

scholarly journals B-cell- and myocyte-specific E2-box-binding factors contain E12/E47-like subunits

1991 ◽  
Vol 11 (2) ◽  
pp. 1156-1160
Author(s):  
C Murre ◽  
A Voronova ◽  
D Baltimore
Keyword(s):  
Dna Binding ◽  
B Cell ◽  
Dna Sequence ◽  
Binding Proteins ◽  
Dna Binding Proteins ◽  
Dimerization Domain ◽  
Drosophila Development ◽  
Helix Loop Helix ◽  
Nuclear Factors ◽  
Biochemical Function

Recent studies have identified a family of DNA-binding proteins that share a common DNA-binding and dimerization domain with the potential to form a helix-loop-helix (HLH) structure. Various HLH proteins can form heterodimers that bind to a common DNA sequence, termed the E2-box. We demonstrate here that E2-box-binding B-cell- and myocyte-specific nuclear factors contain subunits which are identical or closely related to ubiquitously expressed (E12/E47) HLH proteins. These biochemical function for E12/E47-like molecules in mammalian differentiation, similar to the genetically defined function of daughterless in Drosophila development.

scholarly journals Repression of the B cell identity factor Pax5 is not required for plasma cell development

2020 ◽  
Vol 217 (11) ◽  
Author(s):  
Grace J. Liu ◽  
Markus Jaritz ◽  
Miriam Wöhner ◽  
Benedikt Agerer ◽  
Andreas Bergthaler ◽  
...  
Keyword(s):  
B Cell ◽  
Plasma Cell ◽  
Plasma Cells ◽  
Cell Development ◽  
Transcriptional Networks ◽  
Cell Fates ◽  
Cell Identity ◽  
Cell Expression ◽  
Expression Program ◽  
Antibody Secretion

B cell and plasma cell fates are controlled by different transcriptional networks, as exemplified by the mutually exclusive expression and cross-antagonism of the B cell identity factor Pax5 and the plasma cell regulator Blimp1. It has been postulated that repression of Pax5 by Blimp1 is essential for plasma cell development. Here, we challenged this hypothesis by analyzing the IghPax5/+ mouse, which expressed a Pax5 minigene from the immunoglobulin heavy-chain locus. Despite high Pax5 expression, plasma cells efficiently developed in young IghPax5/+ mice at steady state and upon immunization, while their number moderately declined in older mice. Although Pax5 significantly deregulated the plasma cell expression program, key plasma cell regulators were normally expressed in IghPax5/+ plasma cells. While IgM and IgA secretion by IghPax5/+ plasma cells was normal, IgG secretion was modestly decreased. Hence, Pax5 repression is not essential for robust plasma cell development and antibody secretion, although it is required for optimal IgG production and accumulation of long-lived plasma cells.

Abstract 1124: Transcriptional control of B cell identity restricts metabolic fitness in human leukemia

2015 ◽  
Author(s):  
Lai N. Chan ◽  
Daniel Braas ◽  
Christian Hurtz ◽  
Seyedmehdi Shojaee ◽  
Huimin Geng ◽  
...  
Keyword(s):  
B Cell ◽  
Transcriptional Control ◽  
Human Leukemia ◽  
Cell Identity ◽  
Metabolic Fitness

scholarly journals Analysis of FOXO1 mutations in diffuse large B-cell lymphoma

Blood ◽  
2013 ◽  
Vol 121 (18) ◽  
pp. 3666-3674 ◽  
Author(s):  
Diane L. Trinh ◽  
David W. Scott ◽  
Ryan D. Morin ◽  
Maria Mendez-Lago ◽  
Jianghong An ◽  
...  
Keyword(s):  
Dna Binding ◽  
B Cell ◽  
Cell Lymphoma ◽  
Phosphorylation Site ◽  
B Cell Lymphoma ◽  
Dna Binding Domain ◽  
Large B Cell Lymphoma ◽  
Key Points ◽  
Recurrent Mutations ◽  
Large B Cell

Key Points Recurrent mutations in FOXO1 affect the DNA binding domain and the T24 phosphorylation site, which disrupt interactions with 14-3-3. Presence of FOXO1 mutations is associated with decreased OS, particularly in DLBCL patients of the low-risk R-IPI categories.

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