UV-B-induced photomorphogenesis in Arabidopsis thaliana

Authors

  • Byung Chul Kim,

    1. Boyce Thompson Institute for Plant Research and Section of Genetics and Development, Tower Road, Ithaca, NY 14853, USA, and
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    • Present address: Hitachi Advanced Research Laboratory, Hatoyama, Saitama, 350–03, Japan.

  • Daniel J. Tennessen,

    1. Department of Floriculture and Ornamental Horticulture, Cornell University, Ithaca, NY 14853, USA
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    • Present address: Monsanto Company, Ag Sector, St. Louis, MO 63167, USA.

  • Robert L. Last

    1. Boyce Thompson Institute for Plant Research and Section of Genetics and Development, Tower Road, Ithaca, NY 14853, USA, and
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*For correspondence: Cereon Genomics LLP, One Kendall Square, Building 300, Cambridge, MA 02139, USA (e-mail rob.last@cereon.com).

Summary

Relatively little is known about the types of photomorphogenic responses and signal transduction pathways that plants employ in response to ultraviolet-B (UV-B, 290–320 nm) radiation. In wild-type Arabidopsis seedlings, hypocotyl growth inhibition and cotyledon expansion were both reproducibly promoted by continuous UV-B. The fluence rate response of hypocotyl elongation was examined and showed a biphasic response. Whereas photomorphogenic responses were observed at low doses, higher fluences resulted in damage symptoms. In support of our theory that photomorphogenesis, but not damage, occurs at low doses of UV-B, photomorphogenic responses of UV-B sensitive mutants were indistinguishable from wild-type plants at the low dose. This allowed us to examine UV-B-induced photomorphogenesis in photoreceptor deficient plants and constitutive photomorphogenic mutants. The cry1 cryptochrome structural gene mutant, and phytochrome deficient hy1, phyA and phyB mutant seedlings resembled wild-type seedlings, while phyA/phyB double mutants were less sensitive to the photomorphogenic effects of UV-B. These results suggest that either phyA or phyB is required for UV-B-induced photomorphogenesis. The constitutive photomorphogenic mutants cop1 and det1 did not show significant inhibition of hypocotyl growth in response to UV-B, while det2 was strongly affected by UV-B irradiation. This suggests that COP1 and DET1 work downstream of the UV-B signaling pathway.

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