The UV response involving the ras signaling pathway and AP-1 transcription factors is conserved between yeast and mammals

David Engelberg*, Charles Klein, Horacio Martinetto, Kevin Struhl, Michael Karin

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

207 Scopus citations


UV irradiation of mammalian cells activates AP-1 through a Ras-dependent pathway, independently of DNA damage. We show that the yeast S. cerevisiae has a remarkably similar UV response involving the AP-1 factor Gcn4, which is distinct from the DNA damage response. Transcriptional activation of HIS3 and HIS4 by Gcn4 is triggered by UV irradiation in a Ras-dependent fashion. Moreover, resistance of yeast to UV irradiation is correlated with the level of Ras activity and Gcn4 function. Like mammalian cells in which activated Ras leads to increased c-Jun synthesis and phosphorylation, the effects in yeast involve increased translation of GCN4 mRNA and a posttranslational event. However, this effect on GCN4 translation is different from the response to amino acid or purine starvation. Therefore, a UV signaling pathway involving Ras and AP-1 is an ancient and universal mechanism involved in protection against damage to cellular components other than DNA.

Original languageAmerican English
Pages (from-to)381-390
Number of pages10
Issue number3
StatePublished - 6 May 1994
Externally publishedYes

Bibliographical note

Funding Information:
Correspondence should be addressed to M. K. We thank Y. Devary for suggesting the UV experiment and the unknown reviewer for suggesting that we test the posttranslational control of Gcn4 activity. We also thank Drs. M. Wigler, K. Matsumoto, and A. Hinnebusch for yeast strains and plasmids. D. E. was supported by postdoctoral fellowships from the Human Frontier Science Program and the Israel Cancer Research Foundation. H. M. was supported by the Consejo National de lnvestigaciones Cientifcas y Tecnicas de la Republica Argentina and a Public Health Service Fogarty International Research Fellowship (#FO5 TWO4865-01). Supported by grants from the National Institutes of Health (CA50526, GM301 86) and Department of Energy (DE-FGOI-86ER80429).


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