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Multiple self-splicing introns in bacteriophage T4: evidence from autocatalytic GTP labeling of RNA in vitro
Authors:J M Gott  D A Shub  M Belfort
Institution:2. Wadsworth Center for Laboratories and Research New York State Department of Health Albany, New York 12201 USA;1. State Key Laboratory of Engines, Tianjin University, Tianjin 300072, PR China;2. Centre for Advanced Powertrain and Fuels, Brunel University, London, UK;1. School of Chemical Engineering and Environment, North University of China, Taiyuan 030051, People’s Republic of China;2. Research Institute of Gan Su Yin Guang Chemical Industry Group, Baiyin 730900, People’s Republic of China;1. School of Materials Science and Engineering, Yunnan University, 650091 Kunming, People''s Republic of China;2. Key Lab of Quantum Information of Yunnan Province, Yunnan University, 650091 Kunming, People''s Republic of China;3. Department of Physics, Yunnan University, 650091 Kunming, People''s Republic of China;1. School of Civil Engineering, Hefei University of Technology, Hefei 230009, China;2. Anhui International Joint Research Center on Hydrogen Safety, Hefei 230009, China;1. Turkish Land Forces NCO Vocational College, Automotive Sciences Department, 10110 Balikesir, Turkey;2. Balikesir University, Department of Mechanical Engineering, 10145 Balikesir, Turkey
Abstract:RNA from T4-infected cells yielded multiple end-labeled species when incubated with alpha-32P-GTP under self-splicing conditions. One of these corresponds to the previously identified intron from the td gene of T4, while others appear to represent additional group I introns in T4. Two loci distinct from the td gene were found to hybridize to a mixed alpha-32P-GTP-labeled T4 RNA probe. These mapped in or near the unlinked genes nrdB and nrdC. A fragment from the nrdB region that contains the intron has been cloned and shown to generate characteristic group I splice products with RNA synthesized in vivo and in vitro. Multiple introns, and the prospect that these occur within several genes in the same metabolic pathway, suggest a possible regulatory role for splicing in T4.
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