scholarly journals Dynein light chain regulates adaptive and innate B cell development by distinctive genetic mechanisms

PLoS Genetics ◽  
2017 ◽  
Vol 13 (9) ◽  
pp. e1007010 ◽  
Author(s):  
Ashleigh King ◽  
Lingli Li ◽  
David M. Wong ◽  
Rui Liu ◽  
Rebecca Bamford ◽  
...  
Keyword(s):  
B Cell ◽  
Light Chain ◽  
Cell Development ◽  
B Cell Development ◽  
Dynein Light Chain ◽  
Genetic Mechanisms

Human Peripheral B Cell Development sIgM?IgD+CD38+Hypermutated Germinal Center Centroblasts Preferentially Express Ig? Light Chain and Have Undergone ?-to-? Switch

1997 ◽  
Vol 815 (1 B-Lymphocytes) ◽  
pp. 193-196 ◽  
Author(s):  
CHRISTOPHE ARPIN ◽  
ODETTE de BOUTEILLER ◽  
DIANE RAZANAJAONA ◽  
FRANCINE BRIÈRE ◽  
JACQUES BANCHEREAU ◽  
...  
Keyword(s):  
B Cell ◽  
Light Chain ◽  
Germinal Center ◽  
Cell Development ◽  
B Cell Development

scholarly journals Changes in Locus-specific V(D)J Recombinase Activity Induced by Immunoglobulin Gene Products during B Cell Development

1997 ◽  
Vol 185 (4) ◽  
pp. 609-620 ◽  
Author(s):  
Andrei Constantinescu ◽  
Mark S. Schlissel
Keyword(s):  
B Cells ◽  
B Cell ◽  
Heavy Chain ◽  
Light Chain ◽  
Immunoglobulin Heavy Chain ◽  
Cell Development ◽  
B Cell Development ◽  
Allelic Exclusion ◽  
Chain Locus ◽  
Heavy Chain Locus

The process of V(D)J recombination is crucial for regulating the development of B cells and for determining their eventual antigen specificity. Here we assess the developmental regulation of the V(D)J recombinase directly, by monitoring the double-stranded DNA breaks produced in the process of V(D)J recombination. This analysis provides a measure of recombinase activity at immunoglobulin heavy and light chain loci across defined developmental stages spanning the process of B cell development. We find that expression of a complete immunoglobulin heavy chain protein is accompanied by a drastic change in the targeting of V(D)J recombinase activity, from being predominantly active at the heavy chain locus in pro-B cells to being exclusively restricted to the light chain loci in pre-B cells. This switch in locus-specific recombinase activity results in allelic exclusion at the immunoglobulin heavy chain locus. Allelic exclusion is maintained by a different mechanism at the light chain locus. We find that immature, but not mature, B cells that already express a functional light chain protein can undergo continued light chain gene rearrangement, by replacement of the original rearrangement on the same allele. Finally, we find that the developmentally regulated targeting of V(D)J recombination is unaffected by enforced rapid transit through the cell cycle induced by an Eμ-myc transgene.

scholarly journals The Identification of a Nonclassical Cadherin Expressed during B Cell Development and Its Interaction with Surrogate Light Chain

2000 ◽  
Vol 275 (40) ◽  
pp. 31134-31144 ◽  
Author(s):  
Kazuo Ohnishi ◽  
Takeyuki Shimizu ◽  
Hajime Karasuyama ◽  
Fritz Melchers
Keyword(s):  
B Cell ◽  
Light Chain ◽  
Cell Development ◽  
B Cell Development ◽  
Surrogate Light Chain

scholarly journals PU.1 Regulates Ig Light Chain Transcription and Rearrangement in Pre-B Cells during B Cell Development

2017 ◽  
Vol 198 (4) ◽  
pp. 1565-1574 ◽  
Author(s):  
Carolina R. Batista ◽  
Stephen K. H. Li ◽  
Li S. Xu ◽  
Lauren A. Solomon ◽  
Rodney P. DeKoter
Keyword(s):  
B Cells ◽  
B Cell ◽  
Light Chain ◽  
Cell Development ◽  
B Cell Development

The surrogate light chain in B-cell development

1993 ◽  
Vol 14 (2) ◽  
pp. 60-68 ◽  
Author(s):  
Fritz Melchers ◽  
Hajime Karasuyama ◽  
Dirk Haasner ◽  
Steven Bauer ◽  
Akira Kudo ◽  
...  
Keyword(s):  
B Cell ◽  
Light Chain ◽  
Cell Development ◽  
B Cell Development ◽  
Surrogate Light Chain

Enforced BCL6 Expression Inhibits B Cell Development in Vivo.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1535-1535
Author(s):  
Davide F. Robbiani ◽  
Kaity Colon ◽  
Kruti Naik ◽  
Helen Nickerson ◽  
Maurizio Affer ◽  
...  
Keyword(s):  
B Cells ◽  
Transgenic Mice ◽  
B Cell ◽  
Light Chain ◽  
Germinal Center ◽  
Regulatory Elements ◽  
Cell Development ◽  
B Cell Development ◽  
Kappa Light Chain

Abstract The B-Cell Lymphoma 6 (BCL6) gene encodes for a zinc finger motifs containing transcriptional repressor that is frequently dysregulated by chromosomal translocations in germinal center lymphomas. A putative protooncogene, its transforming ability in vivo was reported in I-mu-HA-BCL6 knock-in mice by Cattoretti et al last year. We also tested this assumption in transgenic mice expressing BCL6 in B cells under the control of kappa light chain regulatory elements. We replaced the murine C-kappa locus with the 16kb human BCL6 genomic locus in a construct containing the murine kappa light chain regulatory elements (Vk, EiK, 3′RR). While control transgenics were readily obtained (5/32 founders), only 3/68 founders were positive for the BCL6 transgene, of which only one (bearing a single copy of the transgene) was able to transmit the transgene to its progeny, thus suggesting embryonal toxicity of exogenous BCL6. In the bone marrow, flow cytometry revealed a nearly complete block of B cell development at the pro-B to pre-B transition. This was also the stage at which we first detected expression of EGFP in control reporter mice that were generated in parallel. Spleens of transgenic mice weighed about 50% of control spleens and less than 5% of splenocytes were CD19+ B cells. These were IgM high, IgD intermediate, corresponding to an immature B cell phenotype. Lymph nodes were smaller and B cells barely detected. Peyers’ patches were not visible. Combined, our analysis of 6–8 weeks old VkHABCL6 transgenic mice reveals that enforced expression of BCL6 early in development results in a profound block of B lymphocyte differentiation. How transgenic BCL6 modulates this effect at the transcriptional level remains to be investigated. To test the oncogenic potential of BCL6 in B cells, it will be interesting to precisely turn on this gene in the germinal center.

scholarly journals The Zinc-finger protein ASCIZ regulates B cell development via DYNLL1 and Bim

2012 ◽  
Vol 209 (9) ◽  
pp. 1629-1639 ◽  
Author(s):  
Sabine Jurado ◽  
Kimberly Gleeson ◽  
Kristy O’Donnell ◽  
David J. Izon ◽  
Carl R. Walkley ◽  
...  
Keyword(s):  
Dna Damage ◽  
B Cell ◽  
Zinc Finger Protein ◽  
Cell Loss ◽  
Cell Development ◽  
B Cell Development ◽  
Dynein Light Chain ◽  
Ataxia Telangiectasia Mutated ◽  
Finger Protein ◽  
B Cell Precursors

Developing B lymphocytes expressing defective or autoreactive pre-B or B cell receptors (BCRs) are eliminated by programmed cell death, but how the balance between death and survival signals is regulated to prevent immunodeficiency and autoimmunity remains incompletely understood. In this study, we show that absence of the essential ATM (ataxia telangiectasia mutated) substrate Chk2-interacting Zn2+-finger protein (ASCIZ; also known as ATMIN/ZNF822), a protein with dual functions in the DNA damage response and as a transcription factor, leads to progressive cell loss from the pre-B stage onwards and severely diminished splenic B cell numbers in mice. This lymphopenia cannot be suppressed by deletion of p53 or complementation with a prearranged BCR, indicating that it is not caused by impaired DNA damage responses or defective V(D)J recombination. Instead, ASCIZ-deficient B cell precursors contain highly reduced levels of DYNLL1 (dynein light chain 1; LC8), a recently identified transcriptional target of ASCIZ, and normal B cell development can be restored by ectopic Dynll1 expression. Remarkably, the B cell lymphopenia in the absence of ASCIZ can also be fully suppressed by deletion of the proapoptotic DYNLL1 target Bim. Our findings demonstrate a key role for ASCIZ in regulating the survival of developing B cells by activating DYNLL1 expression, which may then modulate Bim-dependent apoptosis.

The murine VpreB1 and VpreB2 genes both encode a protein of the surrogate light chain and are co-expressed during B cell development

1996 ◽  
Vol 26 (4) ◽  
pp. 906-913 ◽  
Author(s):  
Jeanne L. Dul ◽  
Yair Argon ◽  
Thomas Winkler ◽  
Edwin ten Boekel ◽  
Fritz Melchers ◽  
...  
Keyword(s):  
B Cell ◽  
Light Chain ◽  
Cell Development ◽  
B Cell Development ◽  
Surrogate Light Chain
Sign in / Sign up

Export Citation Format

Share Document