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Vol. 16, Issue 6, 2934-2946, June 2005

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Drosophila Activating Transcription Factor-2 Is Involved in Stress Response via Activation by p38, but Not c-Jun NH₂-Terminal Kinase

Yuji Sano ^* , Hiroshi Akimaru ^* , Tomoo Okamura ^* , Tomoko Nagao ^*, Masahiro Okada ^*, and Shunsuke Ishii ^* 

^* Laboratory of Molecular Genetics, RIKEN Tsukuba Institute, Tsukuba, Ibaraki 305-0074, Japan; Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan

Submitted November 17, 2004; Revised January 25, 2005; Accepted March 5, 2005
Monitoring Editor: Carl-Henrik Heldin

Activating transcription factor (ATF)-2 is a member of the ATF/cAMP response element-binding protein family of transcription factors, and its trans-activating capacity is enhanced by stress-activated protein kinases such as c-Jun NH₂-terminal kinase (JNK) and p38. However, little is known about the in vivo roles played by ATF-2. Here, we identified the Drosophila homologue of ATF-2 (dATF-2) consisting of 381 amino acids. In response to UV irradiation and osmotic stress, Drosophila p38 (dp38), but not JNK, phosphorylates dATF-2 and enhances dATF-2-dependent transcription. Consistent with this, injection of dATF-2 double-stranded RNA (dsRNA) into embryos did not induce the dorsal closure defects that are commonly observed in the Drosophila JNK mutant. Furthermore, expression of the dominant-negative dp38 enhanced the aberrant wing phenotype caused by expression of a dominant-negative dATF-2. Similar genetic interactions between dATF-2 and the dMEKK1-dp38 signaling pathway also were observed in the osmotic stress-induced lethality of embryos. Loss of dATF-2 in Drosophila S2 cells by using dsRNA abrogated the induction of 40% of the osmotic stress-induced genes, including multiple immune response-related genes. This indicates that dATF-2 is a major transcriptional factor in stress-induced transcription. Thus, dATF-2 is critical for the p38-mediated stress response.

Abbreviations used: dATF-2, Drosophila ATF-2; dp38, Drosophila p38; dsRNA, double-stranded RNA; JNK, Jun NH₂-terminal protein kinase; MAPK, mitogen-activated protein kinase; SAPKs, stress-activated protein kinases.

These authors contributed equally to the experimental work.

Address correspondence to: Shunsuke Ishii (sishii{at}rtc.riken.jp).

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