All sun-exposed organisms have to encounter ultraviolet-B (UV-B, 280-320 nm), an integral part of solar radiation. Depending on its energy levels, UV-B can be harmful or beneficial to biological organisms. High- level UV-B causes direct harms including DNA damage, eye cataracts, skin cancer, and immune system suppression in animals, as well as retarded growth and depressed photosynthesis in plants. On the other hand, low-level UV-B can provide beneficial effects including serving as developmental signals in plants and aiding vitamin D synthesis in human. Opposing effects of UV-B on human cancers have also been reported. While UV-B is a known carcinogen that causes skin cancer, it can help suppress prostate cancer development. The damaging effects of high-level UV-B have been intensively studied in many organisms, but little is known about the molecular mechanism of how cells sense low-level UV-B and transduce its specific signals. Low-level UV-B perception and signaling are well-documented physiological phenomena in plants, but the molecular nature of the involved UV-B-specific receptor(s) remains elusive. Understanding the molecular mechanism of how cells sense and respond to UV-B at all levels is fundamentally important to both agriculture and human health. It has been difficult to genetically pin down a specific pathway that is activated by low-level UV-B because of the lack of unambiguous screenable phenotypes specifically associated with low-level UV-B. We have identified an Arabidopsis mutant, rus1 that is specifically hypersensitive to low- level UV-B. The striking phenotypes and extreme UV-B sensitivities of rus1 provide a feasible platform to identify genetic components that can be good candidates for UV-B specific receptors and signaling components. Our long-term goal is to delineate the molecular mechanism of low-level UV-B signaling in Arabidopsis. Our objective in this application is to characterize signaling components that genetically and biochemically interact with RUS1. Our central hypothesis is that RUS1 and its partners function as key players in low-level UV-B perception. We propose the following two specific aims:
Aim 1 : Characterize specific UV-B signaling components by mapping and cloning extragenic rus1 suppressor genes;
Aim 2 : Investigate functional roles of RUS1-interacting proteins in UV-B signaling. These studies are innovative in that the dissection of the UV-B signaling pathway would provide vital information of how cells sense and respond to low-level UV-B. At the completion of these studies we expect to know the molecular mechanism of how RUS1 works with other components to respond to environmental low-level UV-B. The successful completion of these studies will help bring a more profound understanding of how cells sense and respond to UV-B at different levels and what is learned can be ultimately used to develop enhanced agricultural practices and better health recommendations for both animals and human.
Ultraviolet-B, an unavoidable environmental factor, can be either harmful as a human carcinogen or beneficial as a prostate cancer suppressor. While much is known about the damaging effect of high-level UV-B, little is known about the molecular mechanism of how cells can be benefited by perceiving low-level UV-B. Our contribution here is to be a detailed molecular understanding of how Arabidopsis cells sense and respond to low-level UV-B. This contribution can be ultimately used to develop better health recommendations and enhanced agricultural practices.
|Leasure, Colin D; Chen, Yi-Pei; He, Zheng-Hui (2013) Enhancement of indole-3-acetic acid photodegradation by vitamin B6. Mol Plant 6:1992-5|
|Zhang, Zhisheng; Lu, Yusheng; Zhai, Liguang et al. (2012) Glycolate oxidase isozymes are coordinately controlled by GLO1 and GLO4 in rice. PLoS One 7:e39658|
|Leasure, Colin D; He, Zheng-Hui (2012) CLE and RGF family peptide hormone signaling in plant development. Mol Plant 5:1173-5|
|Leasure, Colin D; Tong, Hong-Yun; Hou, Xue-Wen et al. (2011) root uv-b sensitive mutants are suppressed by specific mutations in ASPARTATE AMINOTRANSFERASE2 and by exogenous vitamin B6. Mol Plant 4:759-70|