Skip to main content

Thank you for visiting You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Disruption of B-myb in DT40 cells reveals novel function for B-Myb in the response to DNA-damage


B-Myb is a highly conserved vertebrate member of the Myb transcription factor family, which is expressed in virtually all proliferating cells. A large body of evidence suggests that B-Myb plays an important role in cell cycle regulation; however, the exact nature of its function has not yet been clarified. We have used gene targeting in chicken DT40 cells, a cell line exhibiting very high rates of homologous recombination, to create cells expressing endogenous B-myb in a doxycyclin-dependent manner. We find that the cells proliferate well in the absence of B-Myb, suggesting that B-Myb is not essential for cell proliferation per se. However, cells lacking B-Myb are more sensitive to DNA-damage induced by UV-irradiation and alkylation. Our work provides the first direct evidence for a novel function of B-Myb in the response to DNA-damage. The cells described here should be a useful model to characterize this function in more detail.

This is a preview of subscription content, access via your institution

Relevant articles

Open Access articles citing this article.

Access options

Buy article

Get time limited or full article access on ReadCube.


All prices are NET prices.

Figure 1
Figure 2
Figure 3
Figure 4
Figure 5


  • Appl H and Klempnauer K-H . (2002). Oncogene, 21, 3076–3081.

  • Beall EL, Manak JR, Zhou S, Bell M, Lipsick JS and Botchan MR . (2002). Nature, 420, 833–837.

  • Buerstedde JM and Takeda S . (1991). Cell, 67, 179–188.

  • Cervellera M, Raschella G, Santilli G, Tanno B, Ventura A, Mancini C, Sevignani C, Calabretta B and Sala A . (2000). J. Biol. Chem., 275, 21055–21060.

  • Cervellera MN and Sala A . (2000). J. Biol. Chem., 275, 10692–10696.

  • Davidson C, Tirouvanziam R, Herzenberg L and Lipsick J . (2004). Genetics, 169, 215–229.

  • Fitzpatrick CA, Sharkov NV, Ramsay G and Katzen AL . (2002). Development, 129, 4497–4507.

  • Foos G, Grimm S and Klempnauer K-H . (1992). EMBO J., 11, 4619–4629.

  • Foos G, Grimm S and Klempnauer K-H . (1994). Oncogene, 9, 2481–2488.

  • Grassilli E, Salomoni P, Perrotti D, Franceschi C and Calabretta B . (1999). Cancer Res., 59, 2451–2456.

  • Huber A, Bai P, de Murcia JM and de Murcia G . (2004). DNA Repair, 3, 1103–1108.

  • Joaquin M, Bessa M, Saville MK and Watson RJ . (2002). Oncogene, 21, 7923–7932.

  • Joaquin M and Watson RJ . (2003). Cell Mol. Life Sci., 60, 2389–2401.

  • Kamano H, Burk B, Noben-Trauth K and Klempnauer K-H . (1995). Oncogene, 11, 2575–2582.

  • Katzen AL, Jackson J, Harmon BP, Fung SM, Ramsay G and Bishop JM . (1998). Genes Dev., 12, 831–843.

  • Klempnauer K-H and Bishop JM . (1983). J. Virol., 4, 565–572.

  • Lam EW-F and Watson RJ . (1993). EMBO J., 12, 2705–2713.

  • Lane S, Farlie P and Watson R . (1997). Oncogene, 14, 2445–2453.

  • Lang D, Dohle F, Terstesse M, Bangen P, August C, Pauels HG and Heidenreich S . (2002). J. Immunol., 168, 6152–6158.

  • Lang G, Gombert WM and Gould HJ . (2005). Immunology, 114, 25–36.

  • Manak JR, Mitiku N and Lipsick JS . (2002). Proc. Natl. Acad. Sci. USA, 99, 7438–7443.

  • Mucenski ML, McLain K, Kier AB, Swerdlow SH, Schreiner CM, Miller TA, Pietryga DW, Scott Jr WJ and Potter SS . (1991). Cell, 65, 677–689.

  • Neiman PE, Ruddell A, Jasoni C, Loring G, Thomas SJ, Brandvold KA, Lee R, Burnside J and Delrow J . (2001). Proc. Natl. Acad. Sci. USA, 98, 6378–6383.

  • Nyberg KA, Michelson RJ, Putnam CW and Weinert TA . (2002). Annu. Rev. Genet., 36, 617–656.

  • Sitzmann J, Noben-Trauth K, Kamano H and Klempnauer K-H . (1996). Oncogene, 12, 1889–1894.

  • Tanaka Y, Patestos NP, Maekawa T and Ishii S . (1999). J. Biol. Chem., 274, 28067–28070.

  • Toscani A, Mettus RV, Coupland R, Simpkins H, Litvin J, Orth J, Hatton KS and Reddy EP . (1997). Nature, 386, 713–717.

  • Zhu W, Giangrande PH and Nevins JR . (2004). EMBO J., 23, 4615–4626.

  • Ziebold U, Bartsch O, Marais R, Ferrari S and Klempnauer K-H . (1997). Curr. Biol., 7, 253–260.

Download references


We thank D Wenning for excellent technical assistance and J Delrow and the staff of the microarray facility of the Fred Hutchinson Cancer Research Center for performing the microarray experiments. This work was supported by the DFG (KL461/9-2).

Author information

Authors and Affiliations


Corresponding author

Correspondence to Karl-Heinz Klempnauer.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Ahlbory, D., Appl, H., Lang, D. et al. Disruption of B-myb in DT40 cells reveals novel function for B-Myb in the response to DNA-damage. Oncogene 24, 7127–7134 (2005).

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI:


  • B-myb
  • DT40
  • homologous recombination
  • DNA-damage

This article is cited by


Quick links