Patterned CpG methylation of silenced B cell gene promoters in classical Hodgkin lymphoma-derived and primary effusion lymphoma cell lines

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Patterned CpG methylation of silenced B cell gene promoters in classical Hodgkin lymphoma-derived and primary effusion lymphoma cell lines. / Doerr, JR; Malone, CS; Fike, FM; Gordon, MS; Soghomonian, SV; Thomas, RK; Tao, Q; Murray, Paul; Diehl, V; Teitell, MA; Wall, R.

In: Journal of Molecular Biology, Vol. 350, 22.07.2005, p. 631-640.

Research output: Contribution to journalArticle

Harvard

Doerr, JR, Malone, CS, Fike, FM, Gordon, MS, Soghomonian, SV, Thomas, RK, Tao, Q, Murray, P, Diehl, V, Teitell, MA & Wall, R 2005, 'Patterned CpG methylation of silenced B cell gene promoters in classical Hodgkin lymphoma-derived and primary effusion lymphoma cell lines', Journal of Molecular Biology, vol. 350, pp. 631-640. https://doi.org/10.1016/j.jmb.2005.05.032

APA

Doerr, JR., Malone, CS., Fike, FM., Gordon, MS., Soghomonian, SV., Thomas, RK., Tao, Q., Murray, P., Diehl, V., Teitell, MA., & Wall, R. (2005). Patterned CpG methylation of silenced B cell gene promoters in classical Hodgkin lymphoma-derived and primary effusion lymphoma cell lines. Journal of Molecular Biology, 350, 631-640. https://doi.org/10.1016/j.jmb.2005.05.032

Vancouver

Author

Doerr, JR ; Malone, CS ; Fike, FM ; Gordon, MS ; Soghomonian, SV ; Thomas, RK ; Tao, Q ; Murray, Paul ; Diehl, V ; Teitell, MA ; Wall, R. / Patterned CpG methylation of silenced B cell gene promoters in classical Hodgkin lymphoma-derived and primary effusion lymphoma cell lines. In: Journal of Molecular Biology. 2005 ; Vol. 350. pp. 631-640.

Bibtex

@article{7949e11dc8354118a03aed4568f3e352,
title = "Patterned CpG methylation of silenced B cell gene promoters in classical Hodgkin lymphoma-derived and primary effusion lymphoma cell lines",
abstract = "Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL) and primary effusion lymphoma (PEL) are derived from germinal center (GC) and post-GC B cells, respectively. Neither express many of the B cell genes or surface markers typically expressed by other GC-derived B cell lymphomas or normal B cells. This loss of B cell gene expression is not due to a lack of essential transcription factors, as studies have shown that the ectopic expression of missing transcription factors failed to reactivate endogenous target genes. These results implicate epigenetic mechanisms extinguishing B cell gene expression. Silenced endogenous B cell genes representing a surface receptor, B29 (Igbeta, CD79b), a signaling molecule, TCL1, and a transcription factor, Bob1 (OCA-B, OBF-1), were reactivated by 5-aza-2'-deoxycytidine, indicating that gene silencing in HRS and PEL cells is due to DNA methylation. Genomic bisulfite sequencing corroborated this prediction and revealed three distinct patterns of methylation for the silenced B29 and TCL1 promoters. These distinct patterns consisted of 5' promoter CpG methylation alone, 5' and 3' promoter CpG methylation sparing sites in the central cores, and complete CpG methylation throughout the promoter regions. The silenced Bob1 promoter showed one pattern of dense CpG methylation at essentially all sites. These consistent patterns predict that, although gene silencing in many HRS and PEL cells mimics appropriate gene silencing, in some cases of complete CpG methylation throughout entire promoters both the activation and targeting of methylation is abnormal.",
keywords = "primary effusion lymphoma, gene reactivation, gene silencing, classical Hodgkin lymphoma, CpG DNA methylation",
author = "JR Doerr and CS Malone and FM Fike and MS Gordon and SV Soghomonian and RK Thomas and Q Tao and Paul Murray and V Diehl and MA Teitell and R Wall",
year = "2005",
month = jul,
day = "22",
doi = "10.1016/j.jmb.2005.05.032",
language = "English",
volume = "350",
pages = "631--640",
journal = "Journal of Molecular Biology",
issn = "0022-2836",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Patterned CpG methylation of silenced B cell gene promoters in classical Hodgkin lymphoma-derived and primary effusion lymphoma cell lines

AU - Doerr, JR

AU - Malone, CS

AU - Fike, FM

AU - Gordon, MS

AU - Soghomonian, SV

AU - Thomas, RK

AU - Tao, Q

AU - Murray, Paul

AU - Diehl, V

AU - Teitell, MA

AU - Wall, R

PY - 2005/7/22

Y1 - 2005/7/22

N2 - Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL) and primary effusion lymphoma (PEL) are derived from germinal center (GC) and post-GC B cells, respectively. Neither express many of the B cell genes or surface markers typically expressed by other GC-derived B cell lymphomas or normal B cells. This loss of B cell gene expression is not due to a lack of essential transcription factors, as studies have shown that the ectopic expression of missing transcription factors failed to reactivate endogenous target genes. These results implicate epigenetic mechanisms extinguishing B cell gene expression. Silenced endogenous B cell genes representing a surface receptor, B29 (Igbeta, CD79b), a signaling molecule, TCL1, and a transcription factor, Bob1 (OCA-B, OBF-1), were reactivated by 5-aza-2'-deoxycytidine, indicating that gene silencing in HRS and PEL cells is due to DNA methylation. Genomic bisulfite sequencing corroborated this prediction and revealed three distinct patterns of methylation for the silenced B29 and TCL1 promoters. These distinct patterns consisted of 5' promoter CpG methylation alone, 5' and 3' promoter CpG methylation sparing sites in the central cores, and complete CpG methylation throughout the promoter regions. The silenced Bob1 promoter showed one pattern of dense CpG methylation at essentially all sites. These consistent patterns predict that, although gene silencing in many HRS and PEL cells mimics appropriate gene silencing, in some cases of complete CpG methylation throughout entire promoters both the activation and targeting of methylation is abnormal.

AB - Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL) and primary effusion lymphoma (PEL) are derived from germinal center (GC) and post-GC B cells, respectively. Neither express many of the B cell genes or surface markers typically expressed by other GC-derived B cell lymphomas or normal B cells. This loss of B cell gene expression is not due to a lack of essential transcription factors, as studies have shown that the ectopic expression of missing transcription factors failed to reactivate endogenous target genes. These results implicate epigenetic mechanisms extinguishing B cell gene expression. Silenced endogenous B cell genes representing a surface receptor, B29 (Igbeta, CD79b), a signaling molecule, TCL1, and a transcription factor, Bob1 (OCA-B, OBF-1), were reactivated by 5-aza-2'-deoxycytidine, indicating that gene silencing in HRS and PEL cells is due to DNA methylation. Genomic bisulfite sequencing corroborated this prediction and revealed three distinct patterns of methylation for the silenced B29 and TCL1 promoters. These distinct patterns consisted of 5' promoter CpG methylation alone, 5' and 3' promoter CpG methylation sparing sites in the central cores, and complete CpG methylation throughout the promoter regions. The silenced Bob1 promoter showed one pattern of dense CpG methylation at essentially all sites. These consistent patterns predict that, although gene silencing in many HRS and PEL cells mimics appropriate gene silencing, in some cases of complete CpG methylation throughout entire promoters both the activation and targeting of methylation is abnormal.

KW - primary effusion lymphoma

KW - gene reactivation

KW - gene silencing

KW - classical Hodgkin lymphoma

KW - CpG DNA methylation

UR - http://www.scopus.com/inward/record.url?scp=20544472803&partnerID=8YFLogxK

U2 - 10.1016/j.jmb.2005.05.032

DO - 10.1016/j.jmb.2005.05.032

M3 - Article

C2 - 15967459

VL - 350

SP - 631

EP - 640

JO - Journal of Molecular Biology

JF - Journal of Molecular Biology

SN - 0022-2836

ER -