Lineage specification and plasticity in CD19− early B cell precursors

Rumfelt, Lynn L.; Zhou, Yan; Rowley, Benjamin M.; Shinton, Susan A.; Hardy, Richard R.

doi:10.1084/jem.20052444

Cited by 172 publications

(198 citation statements)

References 59 publications

Supporting

Mentioning

180

Contrasting

Order By: Relevance

“…3 A). To investigate the consequence of this, we analyzed Hardy fractions in the bone marrow of WT miR-132 and WT MG mice (Rumfelt et al, 2006). We found that WT miR-132 mice had a comparable frequency of CLPs and an elevation in precursorprogenitor B (prepro-B) B cells (Hardy Fr.…”

Section: Enforced Expression Of Microrna-132 Inhibits B Cell Developmentmentioning

confidence: 99%

The microRNA-212/132 cluster regulates B cell development by targeting Sox4

Mehta¹,

Mann²,

Zhao³

et al. 2015

J Cell Biol

View full text Add to dashboard Cite

Section: Enforced Expression Of Microrna-132 Inhibits B Cell Developmentmentioning

confidence: 99%

The microRNA-212/132 cluster regulates B cell development by targeting Sox4

Mehta¹,

Mann²,

Zhao³

et al. 2015

J Cell Biol

View full text Add to dashboard Cite

“…Cells were spun at 2000 rpm for 5 min and then resuspended in 10 l 1X PCR buffer (Roche) with 0.1% Triton-X. Nested PCR to detect D H-JH rearrangement products were performed using primers as previously described (28).…”

Section: Dh-jh Rearrangementmentioning

confidence: 99%

Ebf1-mediated down-regulation of Id2 and Id3 is essential for specification of the B cell lineage

Thal

Carvalho

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

“…At an early stage in this process, B cell progenitors undergo a developmental transition that results in suppression of residual multi-lineage potentiality and commitment to a B cell fate. This transition coincides with dramatic changes in gene expression, resulting in the up-regulation of B cell-specific genes and the down-regulation of genes that promote alternative lineage fates (2)(3)(4)(5). In addition, B cell progenitors must express functional immunoglobulin heavy and light chain proteins to develop into mature B cells.…”

mentioning

confidence: 99%

The Developmental Regulator Protein Gon4l Associates with Protein YY1, Co-repressor Sin3a, and Histone Deacetylase 1 and Mediates Transcriptional Repression

Lü

Hankel

Hostager³

et al. 2011

Journal of Biological Chemistry

View full text Add to dashboard Cite

Genetic studies involving zebrafish and mice have demonstrated that the protein Gon4l (Gon4-like) is essential for hematopoiesis. These studies also suggested that Gon4l regulates gene expression during hematopoietic development, yet the biochemical function of Gon4l has not been defined. Here, we describe the identification of factors that interact with Gon4l and may cooperate with this protein to regulate gene expression. As predicted by polypeptide sequence conservation, Gon4l interacted and co-localized with the DNA-binding protein YY1 (Yin Yang 1). Density gradient sedimentation analysis of protein lysates from mouse M12 B cells showed that Gon4l and YY1 co-sediment with the transcriptional co-repressor Sin3a and its functional partner histone deacetylase (HDAC) 1. Consistent with these results, immunoprecipitation studies showed that Gon4l associates with Sin3a, HDAC1, and YY1 as a part of complexes that form in M12 cells. Sequential immunoprecipitation studies demonstrated that Gon4l, YY1, Sin3a, and HDAC1 could all associate as components of a single complex and that a conserved domain spanning the central portion of Gon4l was required for formation of this complex. When targeted to DNA, Gon4l repressed the activity of a nearby promoter, which correlated with the ability to interact with Sin3a and HDAC1. Our data suggest that Sin3a, HDAC1, and YY1 are co-factors for Gon4l and that Gon4l may function as a platform for the assembly of complexes that regulate gene expression.Antibody-secreting B cells are generated throughout life via a developmental pathway called B lymphopoiesis (1). At an early stage in this process, B cell progenitors undergo a developmental transition that results in suppression of residual multi-lineage potentiality and commitment to a B cell fate. This transition coincides with dramatic changes in gene expression, resulting in the up-regulation of B cell-specific genes and the down-regulation of genes that promote alternative lineage fates (2-5). In addition, B cell progenitors must express functional immunoglobulin heavy and light chain proteins to develop into mature B cells. Expression of these proteins requires rearrangement of the encoding loci as controlled by transcriptional and epigenetic mechanisms (6, 7). Thus, B lymphopoiesis relies on elaborate mechanisms of gene regulation to generate B cells that can respond to antigens and make antibodies.In our previous study (8), we described a novel mouse strain named Justy (for just T cells). This strain carries a chemically induced point mutation that, in the homozygous state, causes a profound arrest in B lymphopoiesis but does not affect other major aspects of mouse physiology. The identified developmental defect coincides with sustained expression of genes normally targeted for repression during the early stages of B lymphopoiesis. These data suggest that the mutation impairs mechanisms required for gene repression in developing B cells. The lesion responsible was shown to be a point mutation that disrupts splicing of RNA trans...

show abstract

Lineage specification and plasticity in CD19− early B cell precursors

Cited by 172 publications

References 59 publications

The microRNA-212/132 cluster regulates B cell development by targeting Sox4

The microRNA-212/132 cluster regulates B cell development by targeting Sox4

Ebf1-mediated down-regulation of Id2 and Id3 is essential for specification of the B cell lineage

The Developmental Regulator Protein Gon4l Associates with Protein YY1, Co-repressor Sin3a, and Histone Deacetylase 1 and Mediates Transcriptional Repression

Contact Info

Product

Resources

About