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Molecular and Cellular Biology, January 1999, p. 751-763, Vol. 19, No. 1
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Withdrawal of Survival Factors Results in Activation of the JNK Pathway in Neuronal Cells Leading to Fas Ligand Induction and Cell Death

Helen Le-Niculescu,1,2 Emanuela Bonfoco,3 Yoshitoshi Kasuya,1 Francois-Xavier Claret,1 Douglas R. Green,3 and Michael Karin1,*

Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology,1 and Program in Molecular Pathology,2 University of California at San Diego, La Jolla, California 92093, and Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, California 921213

Received 16 July 1998/Returned for modification 19 August 1998/Accepted 5 October 1998

The JNK pathway modulates AP-1 activity. While in some cells it may have proliferative and protective roles, in neuronal cells it is involved in apoptosis in response to stress or withdrawal of survival signals. To understand how JNK activation leads to apoptosis, we used PC12 cells and primary neuronal cultures. In PC12 cells, deliberate JNK activation is followed by induction of Fas ligand (FasL) expression and apoptosis. JNK activation detected by c-Jun phosphorylation and FasL induction are also observed after removal of either nerve growth factor from differentiated PC12 cells or KCl from primary cerebellar granule neurons (CGCs). Sequestation of FasL by incubation with a Fas-Fc decoy inhibits apoptosis in all three cases. CGCs derived from gld mice (defective in FasL) are less sensitive to apoptosis caused by KCl removal than wild-type neurons. In PC12 cells, protection is also conferred by a c-Jun mutant lacking JNK phosphoacceptor sites and a small molecule inhibitor of p38 mitogen-activated protein kinase and JNK, which inhibits FasL induction. Hence, the JNK-to-c-Jun-to-FasL pathway is an important mediator of stress-induced neuronal apoptosis.

* Corresponding author. Mailing address: Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, University of California at San Diego, 9500 Gilman Dr., La Jolla, CA 92093. Phone: (619) 534-1361. Fax: (619) 534-8158. E-mail: Karinoffice{at}ucsd.edu.

Molecular and Cellular Biology, January 1999, p. 751-763, Vol. 19, No. 1
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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