The Effect of Jazf1 Overexpression in Zebrafish Cardiac Development

  • Shin, Mi-Jung (School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University) ;
  • Yuh, Hyung-Soo (School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University) ;
  • Seo, Byoung-Boo (Dept. of Animal Resources, College of Life & Environmental Science, Daegu University) ;
  • Park, Hum-Dai (Dept. of Biotechnology, College of Engineering, Daegu University) ;
  • Yoon, Du-Hak (School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University) ;
  • Ryoo, Zae-Young (School of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University)
  • 투고 : 2011.11.10
  • 심사 : 2011.11.20
  • 발행 : 2011.12.31

초록

JAZF1 (Juxtaposed with Another Zinc Finger gene 1) transcription factor are Zn-finger proteins that bind to the nuclear orphan receptor TAK/TR4 (Nakajima et al., 2004). The nuclear orphan receptor TAK1/TR4 functions as a positive as well as a negative regulator of transcription. It was recently reported that congenital cardiovascular malformations are significantly more frequent in Neurofibromatosis 1 (NF1) patients with microdeletion syndrome than in those with classical NF1. JAZF1 was expressed in adult heart of patients with microdeletion syndrome. JAZF1 is highly conserved among various species include zebrafish. We hypothesized that the expression of zebrafish Jazf1 may lead to severe forms of congenital heart disease that allow the survival of newborns and adults. In this study, we created Jazf1 transgenic zebrafish which over-express zebrafish Jazf1 cDNA under control of the CMV promoter. Our results suggested that Jazf1 expression may play an important role in zebrafish cardiac development.

키워드

참고문헌

  1. Bookout AL, Jeong Y, Downes M, Yu RT, Evans RM, Mangelsdorf DJ (2006): Anatomical profiling of nuclear receptor expression reveals a hierarchical transcriptional network. Cell 126:789-799. https://doi.org/10.1016/j.cell.2006.06.049
  2. Chen Z, Huang W, Dahme T, Rottbauer W, Ackerman MJ, Xu X (2008): Depletion of zebrafish essential and regulatory myosin light chains reduces cardiac function through distinct mechanisms. Cardiovasc Res 79:97-108. https://doi.org/10.1093/cvr/cvn073
  3. Clark KL, Yutzey KE, Benson DW (2006): Transcription factors and congenital heart defects. Annu Rev Physiol 68:97-121. https://doi.org/10.1146/annurev.physiol.68.040104.113828
  4. Dorschner MO, Sybert VP, Weaver M, Pletcher BA, Stephens K (2000): NF1 microdeletion breakpoints are clustered at flanking repetitive sequences. Hum Mol Genet 9:35-46. https://doi.org/10.1093/hmg/9.1.35
  5. Gelb BD (2001): Genetic basis of syndromes associated with congenital heart disease. Curr Opin Cardiol 16:188-194. https://doi.org/10.1097/00001573-200105000-00006
  6. Hoffman JI, Kaplan S (2002): The incidence of congenital heart disease. J Am Coll Cardiol 39:1890- 1900. https://doi.org/10.1016/S0735-1097(02)01886-7
  7. Hirose T, Fujimoto W, Tamaai T, Kim KH, Matsuura H, Jetten AM (1994): TAK1:molecular cloning and characterization of a new member of the nuclear receptor superfamily. Mol Endocrinol 8:1667- 1680. https://doi.org/10.1210/me.8.12.1667
  8. Jenne DE, Tinschert S, Reimann H, Lasinger W, Thiel G, Hameister H, Kehrer-Sawatzki H, 2001. Molecular characterization and gene content of breakpoint boundaries in patients with neurofibromatosis type 1 with 17q11.2 microdeletion. Am J Hum Genet 69:516-527. https://doi.org/10.1086/323043
  9. Lee HJ, Chang C (1995): Identification of human TR2 orphan receptor response element in the transcriptional initiation site of the simian virus 40 major late promoter. J Biol Chem 270:5434-5440. https://doi.org/10.1074/jbc.270.10.5434
  10. Lin AE, Birch PH, Korf BR, Tenconi R, Niimura M, Poyhonen M, Armfield Uhas K, Sigorini M, Virdis R, Romano C, Bonioli E, Wolkenstein P, Pivnick EK, Lawrence M, Friedman JM (2000): Cardiovascular malformations and other cardiovascular abnormalities in neurofibromatosis 1. Am J Med Genet 95:108-117. https://doi.org/10.1002/1096-8628(20001113)95:2<108::AID-AJMG4>3.0.CO;2-0
  11. Nakajima T, Fujino S, Nakanishi G, Kim YS, Jetten AM (2004): TIP27: A novel repressor of the nuclear orphan receptor TAK1/TR4. Nucleic Acids Res 32: 4194-4204. https://doi.org/10.1093/nar/gkh741
  12. Nemer M (2008): Genetic insights into normal and abnormal heart development. Cardiovasc Pathol 17: 48-54. https://doi.org/10.1016/j.carpath.2007.06.005
  13. Riva P, Corrado L, Natacci F, Castorina P, Wu BL, Schneider GH, Clementi M, Tenconi R, Korf BR, Larizza L (2000): NF1 microdeletion syndrome:refined FISH characterization of sporadic and familial deletions with locus-specific probes. Am J Hum Genet 66: 100-109. https://doi.org/10.1086/302709
  14. Srivastava D, Olson EN (2000): A genetic blueprint for cardiac development. Nature 407:221-226. https://doi.org/10.1038/35025190
  15. Svensson EC, Huggins GS, Dardik Fb, Polk CE, Leiden JM, 2000. Afunctionally conserved N-terminal domain of the friend of GATA-2 (FOG-2) protein represses GATA4-dependent transcription. J Biol Chem 275, 20762-20769. https://doi.org/10.1074/jbc.M001522200
  16. Tonsgard JH, Yelavarthi KK, Cushner S, Short MP, Lindgren V (1997): Do NF1 gene deletions result in a characteristic phenotype? Am J Med Genet 73:80- 86. https://doi.org/10.1002/(SICI)1096-8628(19971128)73:1<80::AID-AJMG16>3.0.CO;2-N
  17. van Schaick HS, Rosmalen JG, Lopes da Silva S, Chang C, Burbach JP (2000): Expression of the orphan receptor TR4 during brain development of the rat. Brain Res Mol Brain Res 77:104-110. https://doi.org/10.1016/S0169-328X(00)00046-2
  18. Venturin M, Guarnieri P, Natacci F, Stabile M, Tenconi R, Clementi M, Hernandez C, Thompson P, Upadhyaya M, Larizza L, Riva P (2004): Mental retardation and cardiovascular malformations in NF1 microdeleted patients point to candidate genes in 17 q11.2. J Med Genet 41:35-41. https://doi.org/10.1136/jmg.2003.014761
  19. Venturin M, Bentivegna A, Moroni R, Larizza L, Riva P (2005): Evidence by expression analysis of candidate genes for congenital heart defects in the NF1 microdeletion interval. Ann Hum Genet 69:508-516. https://doi.org/10.1111/j.1529-8817.2005.00203.x
  20. Whitley P, Gibbard AM, Koumanov F, Oldfield S, Kilgour EE, Prestwich GD, Holman GD, (2002): Identification of centaurinalpha2: A phosphatidylinositidebinding protein present in fat, heart and skeletal muscle. Eur J Cell Biol 81, 222-230. https://doi.org/10.1078/0171-9335-00242
  21. Yang X, Downes M, Yu RT, Bookout AL, He W, Straume M, Mangelsdorf DJ, Evans RM (2006): Nuclear receptor expression links the circadian clock to metabolism. Cell 126:801-810. https://doi.org/10.1016/j.cell.2006.06.050
  22. Young WJ, Smith SM, Chang C (1997): Induction of the intronic enhancer of the human ciliary neurotrophic factor receptor (CNTFRalpha) gene by the TR4 orphan receptor. A member of steroid receptor superfamily. J Biol Chem 272:3109-3116. https://doi.org/10.1074/jbc.272.5.3109