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Blood, 15 April 2005, Vol. 105, No. 8, pp. 3278-3285. Prepublished online as a Blood First Edition Paper on December 23, 2004; DOI 10.1182/blood-2004-08-3073. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 2004-08-3073v1 105/8/3278    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Langenau, D. M. Articles by Look, A. T. Search for Related Content PubMed PubMed Citation Articles by Langenau, D. M. Articles by Look, A. T. Related Collections Immunobiology Neoplasia Apoptosis Oncogenes and Tumor Suppressors Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Suppression of apoptosis by bcl-2 overexpression in lymphoid cells of transgenic zebrafish David M. Langenau, Cicely Jette, Stephane Berghmans, Teresa Palomero, John P. Kanki, Jeffery L. Kutok, and A. Thomas Look From the Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School; and the Department of Pathology, Brigham & Women's Hospital, Boston, MA. The zebrafish is an attractive vertebrate model for genetic studies of development, apoptosis, and cancer. Here we describe a transgenic zebrafish line in which T- and B-lymphoid cells express a fusion transgene that encodes the zebrafish bcl-2 protein fused to the enhanced green fluorescence protein (EGFP). Targeting EGFP-bcl-2 to the developing thymocytes of transgenic fish resulted in a 2.5-fold increase in thymocyte numbers and a 1.8-fold increase in GFP-labeled B cells in the kidney marrow. Fluorescent microscopic analysis of living rag2-EGFP-bcl-2 transgenic fish showed that their thymocytes were resistant to irradiation- and dexamethasone-induced apoptosis, when compared with control rag2-GFP transgenic zebrafish. To test the ability of bcl-2 to block irradiation-induced apoptosis in malignant cells, we compared the responsiveness of Myc-induced leukemias with and without EGFP-bcl-2 expression in living transgenic zebrafish. T-cell leukemias induced by the rag2-EGFP-Myc transgene were ablated by irradiation, whereas leukemias in double transgenic fish expressing both Myc and EGFP-bcl-2 were resistant to irradiation-induced apoptotic cell death. The forward genetic capacity of the zebrafish model system and the ability to monitor GFP-positive thymocytes in vivo make this an ideal transgenic line for modifier screens designed to identify genetic mutations or small molecules that modify bcl-2-mediated antiapoptotic pathways. (Blood. 2005;105:3278-3285) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Maurus and W. A. Harris Zic-associated holoprosencephaly: zebrafish Zic1 controls midline formation and forebrain patterning by regulating Nodal, Hedgehog, and retinoic acid signaling Genes & Dev., June 15, 2009; 23(12): 1461 - 1473. [Abstract] [Full Text] [PDF] H. Feitsma and E. Cuppen Zebrafish as a Cancer Model Mol. Cancer Res., May 1, 2008; 6(5): 685 - 694. [Abstract] [Full Text] [PDF] D. Carradice and G. J. Lieschke Zebrafish in hematology: sushi or science? Blood, April 1, 2008; 111(7): 3331 - 3342. [Abstract] [Full Text] [PDF] J. M. 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