This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Takatsu, Y.
Right arrow Articles by Ueno, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takatsu, Y.
Right arrow Articles by Ueno, N.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, May 2000, p. 3015-3026, Vol. 20, No. 9
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

TAK1 Participates in c-Jun N-Terminal Kinase Signaling during Drosophila Development

Yoshihiro Takatsu,1,2 Makoto Nakamura,1,* Mark Stapleton,3 Maria C. Danos,3 Kunihiro Matsumoto,4 Michael B. O'Connor,3 Hiroshi Shibuya,1,5 and Naoto Ueno1,6

Division of Morphogenesis, Department of Developmental Biology, National Institute for Basic Biology,1 and Department of Molecular Biomechanics, School of Life Science, The Graduate University for Advanced Studies,6 Okazaki 444-8585, Department of Molecular Biology, Faculty of Pharmaceutical Science, Hokkaido University, Sapporo 060,2 Department of Molecular Biology, Faculty of Science, Nagoya University, Nagoya 464-01,4 and Precursory Research for Embryonic Science and Technology, Japan Science and Technology Corporation, Kyoto 619-02,5 Japan, and Howard Hughes Medical Institute, Department of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, Minnesota 554553

Received 17 May 1999/Returned for modification 30 June 1999/Accepted 27 January 2000

Transforming growth factor beta  (TGF-beta )-activated kinase 1 (TAK1) is a member of the MAPKKK superfamily and has been characterized as a component of the TGF-beta /bone morphogenetic protein signaling pathway. TAK1 function has been extensively studied in cultured cells, but its in vivo function is not fully understood. In this study, we isolated a Drosophila homolog of TAK1 (dTAK1) which contains an extensively conserved NH2-terminal kinase domain and a partially conserved COOH-terminal domain. To learn about possible endogenous roles of TAK1 during animal development, we generated transgenic flies which express dTAK1 or the mouse TAK1 (mTAK1) gene in the fly visual system. Ectopic activation of TAK1 signaling leads to a small eye phenotype, and genetic analysis reveals that this phenotype is a result of ectopically induced apoptosis. Genetic and biochemical analyses also indicate that the c-Jun amino-terminal kinase (JNK) signaling pathway is specifically activated by TAK1 signaling. Expression of a dominant negative form of dTAK during embryonic development resulted in various embryonic cuticle defects including dorsal open phenotypes. Our results strongly suggest that in Drosophila melanogaster, TAK1 functions as a MAPKKK in the JNK signaling pathway and participates in such diverse roles as control of cell shape and regulation of apoptosis.

* Corresponding author. Mailing address: Division of Morphogenesis, Department of Developmental Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan. Phone: (81)-564-55-7574. Fax: (81)-564-55-7571. E-mail: mack{at}nibb.ac.jp.

Molecular and Cellular Biology, May 2000, p. 3015-3026, Vol. 20, No. 9
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Mallik, M., Lakhotia, S. C. (2009). The Developmentally Active and Stress-Inducible Noncoding hsr{omega} Gene Is a Novel Regulator of Apoptosis in Drosophila. Genetics 183: 831-852 [Abstract] [Full Text]  
  • Hilgenfeldt, S., Erisken, S., Carthew, R. W. (2008). Physical modeling of cell geometric order in an epithelial tissue. Proc. Natl. Acad. Sci. USA 105: 907-911 [Abstract] [Full Text]  
  • Huh, J. R., Foe, I., Muro, I., Chen, C. H., Seol, J. H., Yoo, S. J., Guo, M., Park, J. M., Hay, B. A. (2007). The Drosophila Inhibitor of Apoptosis (IAP) DIAP2 Is Dispensable for Cell Survival, Required for the Innate Immune Response to Gram-negative Bacterial Infection, and Can Be Negatively Regulated by the Reaper/Hid/Grim Family of IAP-binding Apoptosis Inducers. J. Biol. Chem. 282: 2056-2068 [Abstract] [Full Text]  
  • Kaur, S., Wang, F., Venkatraman, M., Arsura, M. (2005). X-linked Inhibitor of Apoptosis (XIAP) Inhibits c-Jun N-terminal Kinase 1 (JNK1) Activation by Transforming Growth Factor {beta}1 (TGF-{beta}1) through Ubiquitin-mediated Proteosomal Degradation of the TGF-{beta}1-activated Kinase 1 (TAK1). J. Biol. Chem. 280: 38599-38608 [Abstract] [Full Text]  
  • Hocevar, B. A., Prunier, C., Howe, P. H. (2005). Disabled-2 (Dab2) Mediates Transforming Growth Factor {beta} (TGF{beta})-stimulated Fibronectin Synthesis through TGF{beta}-activated Kinase 1 and Activation of the JNK Pathway. J. Biol. Chem. 280: 25920-25927 [Abstract] [Full Text]  
  • Prime, S.S., Pring, M., Davies, M., Paterson, I.C. (2004). TGF-{beta} SIGNAL TRANSDUCTION IN ORO-FACIAL HEALTH AND NON-MALIGNANT DISEASE (PART I). CROBM 15: 324-336 [Abstract] [Full Text]  
  • Cha, G.-H., Cho, K. S., Lee, J. H., Kim, M., Kim, E., Park, J., Lee, S. B., Chung, J. (2003). Discrete Functions of TRAF1 and TRAF2 in Drosophila melanogaster Mediated by c-Jun N-Terminal Kinase and NF-{kappa}B-Dependent Signaling Pathways. Mol. Cell. Biol. 23: 7982-7991 [Abstract] [Full Text]  
  • Edlund, S., Bu, S., Schuster, N., Aspenstrom, P., Heuchel, R., Heldin, N.-E., ten Dijke, P., Heldin, C.-H., Landstrom, M. (2003). Transforming Growth Factor-beta 1 (TGF-beta )-induced Apoptosis of Prostate Cancer Cells Involves Smad7-dependent Activation of p38 by TGF-beta -activated Kinase 1 and Mitogen-activated Protein Kinase Kinase 3. Mol. Biol. Cell 14: 529-544 [Abstract] [Full Text]  
  • Itoh, S., Thorikay, M., Kowanetz, M., Moustakas, A., Itoh, F., Heldin, C.-H., ten Dijke, P. (2003). Elucidation of Smad Requirement in Transforming Growth Factor-beta Type I Receptor-induced Responses. J. Biol. Chem. 278: 3751-3761 [Abstract] [Full Text]  
  • Chen, W., White, M. A., Cobb, M. H. (2002). Stimulus-specific Requirements for MAP3 Kinases in Activating the JNK Pathway. J. Biol. Chem. 277: 49105-49110 [Abstract] [Full Text]  
  • Sem, K. P., Zahedi, B., Tan, I., Deak, M., Lim, L., Harden, N. (2002). ACK Family Tyrosine Kinase Activity Is a Component of Dcdc42 Signaling during Dorsal Closure in Drosophila melanogaster. Mol. Cell. Biol. 22: 3685-3697 [Abstract] [Full Text]  
  • Stronach, B., Perrimon, N. (2002). Activation of the JNK pathway during dorsal closure in Drosophila requires the mixed lineage kinase, slipper. Genes Dev. 16: 377-387 [Abstract] [Full Text]  
  • Parkinson, D. B., Dong, Z., Bunting, H., Whitfield, J., Meier, C., Marie, H., Mirsky, R., Jessen, K. R. (2001). Transforming Growth Factor beta (TGFbeta ) Mediates Schwann Cell Death In Vitro and In Vivo: Examination of c-Jun Activation, Interactions with Survival Signals, and the Relationship of TGFbeta -Mediated Death to Schwann Cell Differentiation. J. Neurosci. 21: 8572-8585 [Abstract] [Full Text]  
  • Vidal, S., Khush, R. S., Leulier, F., Tzou, P., Nakamura, M., Lemaitre, B. (2001). Mutations in the Drosophila dTAK1 gene reveal a conserved function for MAPKKKs in the control of rel/NF-{kappa}B-dependent innate immune responses. Genes Dev. 15: 1900-1912 [Abstract] [Full Text]  
  • Raymond, K., Bergeret, E., Dagher, M.-C., Breton, R., Griffin-Shea, R., Fauvarque, M.-O. (2001). The Rac GTPase-activating Protein RotundRacGAP Interferes with Drac1 and Dcdc42 Signalling in Drosophila melanogaster. J. Biol. Chem. 276: 35909-35916 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»