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 Adachi-Yamada, T.
Right arrow Articles by Matsumoto, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Adachi-Yamada, T.
Right arrow Articles by Matsumoto, K.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, March 1999, p. 2322-2329, Vol. 19, No. 3
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

p38 Mitogen-Activated Protein Kinase Can Be Involved in Transforming Growth Factor beta  Superfamily Signal Transduction in Drosophila Wing Morphogenesis

Takashi Adachi-Yamada,1,* Makoto Nakamura,2 Kenji Irie,1 Yoshinori Tomoyasu,2 Yorikata Sano,1 Eiji Mori,1 Satoshi Goto,3 Naoto Ueno,2 Yasuyoshi Nishida,1 and Kunihiro Matsumoto1

Division of Biological Science, Graduate School of Science, Nagoya University, and CREST, Japan Science and Technology Corporation, Chikusa-ku, Nagoya 464-8602,1 Division of Morphogenesis, Department of Developmental Biology, National Institute for Basic Biology, Myodaiji, Okazaki 444-8585,2 and Invertebrate Genetics Laboratory, Genetics Strains Research Center, National Institute of Genetics, Yata, Mishima 411-8540,3 Japan

Received 3 September 1998/Returned for modification 22 October 1998/Accepted 3 December 1998

p38 mitogen-activated protein kinase (p38) has been extensively studied as a stress-responsive kinase, but its role in development remains unknown. The fruit fly, Drosophila melanogaster, has two p38 genes, D-p38a and D-p38b. To elucidate the developmental function of the Drosophila p38's, we used various genetic and pharmacological manipulations to interfere with their functions: expression of a dominant-negative form of D-p38b, expression of antisense D-p38b RNA, reduction of the D-p38 gene dosage, and treatment with the p38 inhibitor SB203580. Expression of a dominant-negative D-p38b in the wing imaginal disc caused a decapentaplegic (dpp)-like phenotype and enhanced the phenotype of a dpp mutant. Dpp is a secretory ligand belonging to the transforming growth factor beta  superfamily which triggers various morphogenetic processes through interaction with the receptor Thick veins (Tkv). Inhibition of D-p38b function also caused the suppression of the wing phenotype induced by constitutively active Tkv (TkvCA). Mosaic analysis revealed that D-p38b regulates the Tkv-dependent transcription of the optomotor-blind (omb) gene in non-Dpp-producing cells, indicating that the site of D-p38b action is downstream of Tkv. Furthermore, forced expression of TkvCA induced an increase in the phosphorylated active form(s) of D-p38(s). These results demonstrate that p38, in addition to its role as a transducer of emergency stress signaling, may function to modulate Dpp signaling.

* Corresponding author. Mailing address: Laboratory of Developmental Biology, Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan. Phone: 81-52-789-5039. Fax: 81-52-789-2511. E-mail: adachi{at}bio.nagoya-u.ac.jp.

Molecular and Cellular Biology, March 1999, p. 2322-2329, Vol. 19, No. 3
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Machado, R. D., Eickelberg, O., Elliott, C. G., Geraci, M. W., Hanaoka, M., Loyd, J. E., Newman, J. H., Phillips, J. A. III, Soubrier, F., Trembath, R. C., Chung, W. K. (2009). Genetics and genomics of pulmonary arterial hypertension.. J Am Coll Cardiol 54: S32-S42 [Abstract] [Full Text]  
  • Jaramillo, M. S., Lovato, C. V., Baca, E. M., Cripps, R. M. (2009). Crossveinless and the TGF{beta} pathway regulate fiber number in the Drosophila adult jump muscle. Development 136: 1105-1113 [Abstract] [Full Text]  
  • Shimizu, H., Shimoda, M., Yamaguchi, T., Seong, K.-H., Okamura, T., Ishii, S. (2008). Drosophila ATF-2 Regulates Sleep and Locomotor Activity in Pacemaker Neurons. Mol. Cell. Biol. 28: 6278-6289 [Abstract] [Full Text]  
  • Babcock, D. T., Brock, A. R., Fish, G. S., Wang, Y., Perrin, L., Krasnow, M. A., Galko, M. J. (2008). Circulating blood cells function as a surveillance system for damaged tissue in Drosophila larvae. Proc. Natl. Acad. Sci. USA 105: 10017-10022 [Abstract] [Full Text]  
  • Balakireva, M., Rosse, C., Langevin, J., Chien, Y.-c., Gho, M., Gonzy-Treboul, G., Voegeling-Lemaire, S., Aresta, S., Lepesant, J.-A., Bellaiche, Y., White, M., Camonis, J. (2006). The Ral/Exocyst Effector Complex Counters c-Jun N-Terminal Kinase-Dependent Apoptosis in Drosophila melanogaster. Mol. Cell. Biol. 26: 8953-8963 [Abstract] [Full Text]  
  • Janody, F., Treisman, J. E. (2006). Actin capping protein {alpha} maintains vestigial-expressing cells within the Drosophila wing disc epithelium. Development 133: 3349-3357 [Abstract] [Full Text]  
  • Sano, Y., Akimaru, H., Okamura, T., Nagao, T., Okada, M., Ishii, S. (2005). Drosophila Activating Transcription Factor-2 Is Involved in Stress Response via Activation by p38, but Not c-Jun NH2-Terminal Kinase. Mol. Biol. Cell 16: 2934-2946 [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]  
  • Bakin, A. V., Rinehart, C., Tomlinson, A. K., Arteaga, C. L. (2002). p38 mitogen-activated protein kinase is required for TGF{beta}-mediated fibroblastic transdifferentiation and cell migration. J. Cell Sci. 115: 3193-3206 [Abstract] [Full Text]  
  • Ferguson, C. M., Schwarz, E. M., Reynolds, P. R., Puzas, J. E., Rosier, R. N., O'Keefe, R. J. (2000). Smad2 and 3 Mediate Transforming Growth Factor-{beta}1-Induced Inhibition of Chondrocyte Maturation. Endocrinology 141: 4728-4735 [Abstract] [Full Text]  
  • Fahmi, H., Cochet, C., Hmama, Z., Opolon, P., Joab, I. (2000). Transforming Growth Factor Beta 1 Stimulates Expression of the Epstein-Barr Virus BZLF1 Immediate-Early Gene Product ZEBRA by an Indirect Mechanism Which Requires the MAPK Kinase Pathway. J. Virol. 74: 5810-5818 [Abstract] [Full Text]  
  • Takatsu, Y., Nakamura, M., Stapleton, M., Danos, M. C., Matsumoto, K., O'Connor, M. B., Shibuya, H., Ueno, N. (2000). TAK1 Participates in c-Jun N-Terminal Kinase Signaling during Drosophila Development. Mol. Cell. Biol. 20: 3015-3026 [Abstract] [Full Text]  
  • Massagué, J., Chen, Y.-G. (2000). Controlling TGF-beta signaling. Genes Dev. 14: 627-644 [Full Text]  
  • Miyazono, K (2000). Positive and negative regulation of TGF-beta signaling. J. Cell Sci. 113: 1101-1109 [Abstract]  
  • Hanafusa, H., Ninomiya-Tsuji, J., Masuyama, N., Nishita, M., Fujisawa, J.-i., Shibuya, H., Matsumoto, K., Nishida, E. (1999). Involvement of the p38 Mitogen-activated Protein Kinase Pathway in Transforming Growth Factor-beta -induced Gene Expression. J. Biol. Chem. 274: 27161-27167 [Abstract] [Full Text]  
  • Ashburner, M., Misra, S., Roote, J., Lewis, S. E., Blazej, R., Davis, T., Doyle, C., Galle, R., George, R., Harris, N., Hartzell, G., Harvey, D., Hong, L., Houston, K., Hoskins, R., Johnson, G., Martin, C., Moshrefi, A., Palazzolo, M., Reese, M. G., Spradling, A., Tsang, G., Wan, K., Whitelaw, K., Kimmel, B., Celniker, S., Rubin, G. M. (1999). An Exploration of the Sequence of a 2.9-Mb Region of the Genome of Drosophila melanogaster: The Adh Region. Genetics 153: 179-219 [Abstract] [Full Text]  
  • Peron, P., Rahmani, M., Zagar, Y., Durand-Schneider, A.-M., Lardeux, B., Bernuau, D. (2001). Potentiation of Smad Transactivation by Jun Proteins during a Combined Treatment with Epidermal Growth Factor and Transforming Growth Factor-beta in Rat Hepatocytes. ROLE OF PHOSPHATIDYLINOSITOL 3-KINASE-INDUCED AP-1 ACTIVATION. J. Biol. Chem. 276: 10524-10531 [Abstract] [Full Text]  
  • Sasaki, A., Masuda, Y., Ohta, Y., Ikeda, K., Watanabe, K. (2001). Filamin Associates with Smads and Regulates Transforming Growth Factor-beta Signaling. J. Biol. Chem. 276: 17871-17877 [Abstract] [Full Text]  
  • Chipuk, J. E., Bhat, M., Hsing, A. Y., Ma, J., Danielpour, D. (2001). Bcl-xL Blocks Transforming Growth Factor-beta 1-induced Apoptosis by Inhibiting Cytochrome c Release and Not by Directly Antagonizing Apaf-1-dependent Caspase Activation in Prostate Epithelial Cells. J. Biol. Chem. 276: 26614-26621 [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»