Increased gene expression as a consequence of environmental stress is typically observed in mammalian cells upon exposure to ultraviolet (UV) radiation. In previous years the cis- and trans-acting genetic elements responsible for gene induction by short wavelength UVC (< 280nm) and intermediate wavelength UVB (280 - 320 nm) radiation have been well characterized. More recently, progress has also been made in understanding the mechanisms by which long wavelength UVA (320 - 400 nm) radiation induces transcriptional activation of human genes. From these studies it is now known that the photobiological as well as the molecular mechanisms involved in UVA radiation-induced gene expression differ from those previously identified for UVB- or UVC-induced gene expression. In particular, the reactive oxygen species singlet oxygen was found to serve as the primary effector in UVA radiation-induced gene expression by inducing a signal transduction cascade that depends on activation of transcription factor AP-2. These studies indicate a previously unrecognized role of AP-2 in the mammalian stress response.