Low threshold levels of ultraviolet‐B in a background of photosynthetically active radiation trigger rapid degradation of the D2 protein of photosystem‐II

Jansen, Marcel A. K.; Gaba, Victor; Greenberg, Bruce M.; Mattoo, Autar K.; Edelman, Marvin

doi:10.1046/j.1365-313x.1996.9050693.x

Cited by 102 publications

(60 citation statements)

References 48 publications

(56 reference statements)

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“…The UV-B-induced photoinhibition we observed following broadband UV-B stress is presumably due to UV-B-induced PSII damage that exceeds the rate of repair (Takahashi et al, 2010;Takahashi and Badger, 2011). PSII subunit D1 in particular is a well known photosynthetic target of UV-B damage (Jansen et al, 1996;Takahashi et al, 2010), and photoinhibition has long been associated with a decrease in D1 and, albeit to a lesser extent, D2 protein level (Schuster et al, 1988). In agreement, we observed decreases in D1 and D2 protein levels in UV-B-exposed Chlamydomonas that correlated well with the extent of UV-B-induced photoinhibition.…”

Section: Uv-b Acclimation and Tolerance In Chlamydomonasmentioning

confidence: 84%

UV-B Perception and Acclimation in Chlamydomonas reinhardtii

et al. 2016

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Plants perceive UV-B, an intrinsic component of sunlight, via a signaling pathway that is mediated by the photoreceptor UV RESISTANCE LOCUS8 (UVR8) and induces UV-B acclimation. To test whether similar UV-B perception mechanisms exist in the evolutionarily distant green alga Chlamydomonas reinhardtii, we identified Chlamydomonas orthologs of UVR8 and the key signaling factor CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1). Cr-UVR8 shares sequence and structural similarity to Arabidopsis thaliana UVR8, has conserved tryptophan residues for UV-B photoreception, monomerizes upon UV-B exposure, and interacts with Cr-COP1 in a UV-B-dependent manner. Moreover, Cr-UVR8 can interact with At-COP1 and complement the Arabidopsis uvr8 mutant, demonstrating that it is a functional UV-B photoreceptor. Chlamydomonas shows apparent UV-B acclimation in colony survival and photosynthetic efficiency assays. UV-B exposure, at low levels that induce acclimation, led to broad changes in the Chlamydomonas transcriptome, including in genes related to photosynthesis. Impaired UV-B-induced activation in the Cr-COP1 mutant hit1 indicates that UVR8-COP1 signaling induces transcriptome changes in response to UV-B. Also, hit1 mutants are impaired in UV-B acclimation. Chlamydomonas UV-B acclimation preserved the photosystem II core proteins D1 and D2 under UV-B stress, which mitigated UV-B-induced photoinhibition. These findings highlight the early evolution of UVR8 photoreceptor signaling in the green lineage to induce UV-B acclimation and protection.

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Section: Uv-b Acclimation and Tolerance In Chlamydomonasmentioning

confidence: 84%

UV-B Perception and Acclimation in Chlamydomonas reinhardtii

et al. 2016

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“…At that time, levels of UV-B would have exceeded those presently on earth because the ozone layer was not fully developed (Rozema et al, 1997). UV-B penetrates into water and would have been potentially damaging to photosynthetic algae; photosystem II is particularly susceptible to damage by UV-B (Jansen et al, 1996;Takahashi et al, 2010). Thus, UVR8 may have evolved to stimulate UV-protective mechanisms in early photosynthetic plants.…”

Section: Evolutionary Conservationmentioning

confidence: 99%

The UV-B Photoreceptor UVR8: From Structure to Physiology

2014

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Low doses of UV-B light (280 to 315 nm) elicit photomorphogenic responses in plants that modify biochemical composition, photosynthetic competence, morphogenesis, and defense. UV RESISTANCE LOCUS8 (UVR8) mediates photomorphogenic responses to UV-B by regulating transcription of a set of target genes. UVR8 differs from other known photoreceptors in that it uses specific Trp amino acids instead of a prosthetic chromophore for light absorption during UV-B photoreception. Absorption of UV-B dissociates the UVR8 dimer into monomers, initiating signal transduction through interaction with CONSTITUTIVELY PHOTOMORPHOGENIC1. However, much remains to be learned about the physiological role of UVR8 and its interaction with other signaling pathways, the molecular mechanism of UVR8 photoreception, how the UVR8 protein initiates signaling, how it is regulated, and how UVR8 regulates transcription of its target genes.

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“…This in turn could give rise to a population of cells with damaged DNA but low apoptotic capabilities thus enabling malignantly transformed cells to persist. It should be noted, however, that while DNA damage in the skin is commonly described in association with UV-B irradiation [31] the direct degradation of proteins following exposure to UV-B light is far less frequently observed [32].…”

Section: Discussionmentioning

confidence: 99%