DNA photolyase from Antarctic marine bacterium Rhodococcus sp. NJ-530 can repair DNA damage caused by ultraviolet
Marine bacterium Rhodococcus sp. NJ-530 has developed several ultraviolet (UV) adaptive characteristics for survival and growth in extreme Antarctic environment. Rhodococcus sp. NJ-530 DNA photolyase encoded by a 1146 bp photolyase-homologous region (phr) was identified in genome. Quantitative real-...
Published in: | 3 Biotech |
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Main Authors: | , , , |
Format: | Text |
Language: | English |
Published: |
Springer International Publishing
2021
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Subjects: | |
Online Access: | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7846625/ http://www.ncbi.nlm.nih.gov/pubmed/33552830 https://doi.org/10.1007/s13205-021-02660-8 |
Summary: | Marine bacterium Rhodococcus sp. NJ-530 has developed several ultraviolet (UV) adaptive characteristics for survival and growth in extreme Antarctic environment. Rhodococcus sp. NJ-530 DNA photolyase encoded by a 1146 bp photolyase-homologous region (phr) was identified in genome. Quantitative real-time PCR demonstrated that transcriptional levels of phr were highly up-regulated by ultraviolet-B (UV-B) radiation (90 μW·cm(−2)) and increased to a maximum of 149.17-fold after exposure for 20 min. According to the results of SDS-PAGE and western blot, PHR was effectively induced by isopropyl-β-d-1-thiogalactopyranoside (IPTG) at the genetically engineered BL21(DE3)-pET-32a( +)-phr construct under the condition of 15 °C for 16 h and 37 °C for 4 h. In terms of in vivo activity, compared with a phr-defective E. coli strain, phr-transformed E. coli exhibited higher survival rate under high UV-B intensity of 90 μW·cm(−2). Meanwhile, the purified PHR, with blue light, presented obvious photorepair activity toward UV-induced DNA damage in vitro assays. To sum up, studying the mechanisms of Rhodococcus sp. NJ-530 photolyase is of great interest to understand the adaptation of polar bacteria to high UV radiation, and such data present important therapeutic value for further UV-induced human skin and genetic damage diseases. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-021-02660-8. |
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