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MBC in Press, published online ahead of print March 23, 2005
Mol. Biol. Cell 10.1091/mbc.E04-11-1008

A more recent version of this article appeared on June 1, 2005
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Submitted on November 17, 2004
Revised on January 25, 2005
Accepted on March 5, 2005

Drosophila ATF-2 Is Involved in Stress Response via Activation by p38, but not JNK

Yuji Sano,*{dagger} Hiroshi Akimaru,*{dagger} Tomoo Okamura,*{ddagger} Tomoko Nagao,* Masahiro Okada,* and Shunsuke Ishii*{ddagger}

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

Monitoring Editor: Carl-Henrik Heldin

ATF-2 is a member of the ATF/CREB family of transcription factors, and its trans-activating capacity is enhanced by stress-activated protein kinases such as 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 osomotic 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 was also 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.

{dagger}These authors contributed equally to the experimental work.

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




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