Transcription of the unrearranged mouse Cκ locus: Sequence of the initiation region and comparison of activity with a rearranged Vκ-Cκ gene

Ness, Brian G. Van; Weigert, Martin; Coleclough, Christopher; Mather, Elizabeth L.; Kelley, Dawn E.; Perry, Robert P.

doi:10.1016/0092-8674(81)90401-3

Cited by 183 publications

(116 citation statements)

References 26 publications

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“…To confirm this result, real-time PCR was performed to quantitate levels of Ig germline transcripts. 0 transcripts initiate at a site 5Ј to the germline J 1 gene (47,48). We found that 0 transcript levels were decreased by 2.9-fold in PU.1 Ϫ/Ϫ Spi-B Ϫ/Ϫ pro-B cells relative to wild-type cells (Fig.…”

Section: Pu1 ϫ/ϫ Spi-b ϫ/ϫ Cell Lines Have Decreased Levels Of Ig Trmentioning

confidence: 67%

Analysis of Gene Expression and Ig Transcription in PU.1/Spi-B-Deficient Progenitor B Cell Lines

Schweitzer

DeKoter

2004

The Journal of Immunology

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A number of presumptive target genes for the Ets-family transcription factor PU.1 have been identified in the B cell lineage. However, the precise function of PU.1 in B cells has not been studied because targeted null mutation of the PU.1 gene results in a block to lymphomyeloid development at an early developmental stage. In this study, we take advantage of recently developed PU.1−/−Spi-B−/− IL-7 and stromal cell-dependent progenitor B (pro-B) cell lines to analyze the function of PU.1 and Spi-B in B cell development. We show that contrary to previously published expectations, PU.1 and/or Spi-B are not required for Ig H chain (IgH) gene transcription in pro-B cells. In fact, PU.1−/−Spi-B−/− pro-B cells have increased levels of IgH transcription compared with wild-type pro-B cells. In addition, high levels of Igκ transcription are induced after IL-7 withdrawal of wild-type or PU.1−/−Spi-B−/− pro-B cells. In contrast, we found that Igλ transcription is reduced in PU.1−/−Spi-B−/− pro-B cells relative to wild-type pro-B cells after IL-7 withdrawal. These results suggest that Igλ, but not IgH or Igκ, transcription, is dependent on PU.1 and/or Spi-B. The PU.1−/−Spi-B−/− pro-B cells have other phenotypic changes relative to wild-type pro-B cells including increased proliferation, increased CD25 expression, decreased c-Kit expression, and decreased RAG-1 expression. Taken together, our observations suggest that reduction of PU.1 and/or Spi-B activity in pro-B cells promotes their differentiation to a stage intermediate between late pro-B cells and large pre-B cells.

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Section: Pu1 ϫ/ϫ Spi-b ϫ/ϫ Cell Lines Have Decreased Levels Of Ig Trmentioning

confidence: 67%

Analysis of Gene Expression and Ig Transcription in PU.1/Spi-B-Deficient Progenitor B Cell Lines

Schweitzer

DeKoter

2004

The Journal of Immunology

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“…We have uncovered no evidence that the octanucleotide sequences are systematically associated with the 5' ends of genes encoding nonimmunoglobulin proteins (37), although the sequence A-T-T-T-G-C-A-T occurs at an intriguingly similar location in the heavy chain gene of HLA-DR (38), a protein evolutionarily related to the immunoglobulins. The organization of the pseudogene promoter of the unrearranged CK locus differs in several respects from the consensus V gene structure and includes no detectable homology to the octanucleotide block (39).…”

Section: Resultsmentioning

confidence: 99%

Structure of the 5' ends of immunoglobulin genes: a novel conserved sequence.

Parslow¹,

Blair²,

Murphy³

et al. 1984

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

504

232

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“…Moreover, a truncated immunoglobulin (Ig) mRNA encoding a surface protein was identi®ed in pre B cells (Reth and Alt, 1984;Tsubata et al, 1991). This lead to the assumption that germline transcription of the Ig superfamily may have functions which are not associated with the activity of the recombinase machinery (Van Ness et al, 1981). The regulatory mechanisms that control the usage of intronic sequences in TCR mRNAs that may encode putative alternative versions of the protein, have been widely studied (Qian et al, 1993;Sutton et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

The mesenchyme expresses T cell receptor mRNAs: relevance to cell growth control

et al. 2002

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The mesenchyme plays a crucial regulatory role in organ formation and maintenance. However, comprehensive molecular characterization of these cells is lacking. We found unexpectedly that primary mesenchyme, as well as mesenchymal cell clones, express T cell receptor (TCR)ab mRNAs, lacking the variable region. Immunological and genetic evidence support the expression of a corresponding TCRb protein. Additionally, mRNAs encoding TCR complex components including CD3 and z chain are present. A relatively higher expression of the mesenchymal TCRb mRNA by cultured mesenchymal cell clones correlates with fast growth, whereas poorly expressing cells are slow growers and are contact inhibited. The clones that express relatively higher amount of the TCR mRNA exhibit an increased capacity to form tumors in nude mice. However, the expression of this mRNA in the mesenchyme is not per se leading to tumorigenesis, as demonstrated by primary mesenchyme that does not form tumors in mice while expressing moderate amounts of the TCR transcripts. The expression of mesencymal TCRb was con®ned to the G2/M phases of the cell cycle in the MBA-13 mesenchymal cell line. This cell cycle dependent expression, considered together with the correlation between growth properties and the level of TCR expression by cell clones, implies association of mesenchymal TCR with cell growth control.

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Transcription of the unrearranged mouse Cκ locus: Sequence of the initiation region and comparison of activity with a rearranged Vκ-Cκ gene

Cited by 183 publications

References 26 publications

Analysis of Gene Expression and Ig Transcription in PU.1/Spi-B-Deficient Progenitor B Cell Lines

Analysis of Gene Expression and Ig Transcription in PU.1/Spi-B-Deficient Progenitor B Cell Lines

Structure of the 5' ends of immunoglobulin genes: a novel conserved sequence.

The mesenchyme expresses T cell receptor mRNAs: relevance to cell growth control

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