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Dynamic integration and excision of filamentous phage XacF1 in Xanthomonas citri pv. citri, the causative agent of citrus canker disease
Inovirus XacF1 (7325 nucleotides) is integrated into the genome of Xanthomonas citri pv. citri (Xcc) strains at the host dif site (attB) by the host XerC/D recombination system. The XacF1 attP sequence is located within the coding region of ORF12, a possible phage regulator. After integration, this...
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Published in: | FEBS open bio 2017-11, Vol.7 (11), p.1715-1721 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Inovirus XacF1 (7325 nucleotides) is integrated into the genome of Xanthomonas citri pv. citri (Xcc) strains at the host dif site (attB) by the host XerC/D recombination system. The XacF1 attP sequence is located within the coding region of ORF12, a possible phage regulator. After integration, this open reading frame (ORF) is split into two pieces on the host genome. We examined dynamic integration/excision of XacF1 in Xcc strain MAFF 301080 and found that the integration started at 4 h postinfection (p.i.) and peaked at 12 h p.i. Thereafter, the ratio of integrated to free forms remained constant, suggesting equilibrium of integration and excision of XacF1 in the host genome. However, the integrated state became very unstable following a 5′‐deletion of ORF12 in XacF1, suggesting that ORF12 plays a key role in the integration cycle of XacF1 in Xcc strains.
Inovirus XacF1 integrates into Xanthomonas citri pv. citri by XerC/D‐mediated recombination between phage ORF12‐attP and attB (dif). After integration, ORF12 is split into two portions (ORF12′ and ORF12″) besides attL and attR. There is an equilibrium between integration and excision. The integrated state became very unstable following a 5′‐deletion of ORF12 in XacF1, suggesting that ORF12 plays a key role in the integration cycle. |
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ISSN: | 2211-5463 2211-5463 |
DOI: | 10.1002/2211-5463.12312 |