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Molecular and Cellular Biology, August 2008, p. 4883-4895, Vol. 28, No. 15
0270-7306/08/$08.00+0     doi:10.1128/MCB.02074-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

A Member of the p38 Mitogen-Activated Protein Kinase Family Is Responsible for Transcriptional Induction of Dopa decarboxylase in the Epidermis of Drosophila melanogaster during the Innate Immune Response{triangledown} ,{dagger}

Monica M. Davis,1 David A. Primrose,2 and Ross B. Hodgetts1*

Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2E9, Canada,1 Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta T6G 2H7, Canada2

Received 19 November 2007/ Returned for modification 2 January 2008/ Accepted 22 May 2008

Drosophila innate immunity is controlled primarily by the activation of IMD (immune deficiency) or Toll signaling leading to the production of antimicrobial peptides (AMPs). IMD signaling also activates the JUN N-terminal kinase (JNK) cascade, which is responsible for immune induction of non-antimicrobial peptide immune gene transcription though the transcription factor AP-1. Transcription of the Dopa decarboxylase (Ddc) gene is induced in response to gram-negative and gram-positive septic injury, but not aseptic wounding. Transcription is induced throughout the epidermis and not specifically at the site of infection. Ddc transcripts are detectible within 2 h and remain high for several hours following infection with either gram-negative or gram-positive bacteria. Using Ddc-green fluorescent protein (GFP) reporter gene constructs, we show that a conserved consensus AP-1 binding site upstream of the Ddc transcription start site is required for induction. However, neither the Toll, IMD, nor JNK pathway is involved. Rather, Ddc transcription depends on a previously uncharacterized member of the p38 mitogen-activated protein kinase family, p38c. We propose that the involvement of DDC in a new pathway involved in Drosophila immunity increases the levels of dopamine, which is metabolized to produce reactive quinones that exert an antimicrobial effect on invading bacteria.

* Corresponding author. Mailing address: Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2E9, Canada. Phone: (780) 492-5379. Fax: (780) 492-9234. E-mail: ross.hodgetts{at}ualberta.ca

{triangledown} Published ahead of print on 2 June 2008.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, August 2008, p. 4883-4895, Vol. 28, No. 15
0270-7306/08/$08.00+0     doi:10.1128/MCB.02074-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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