Isolation of bacteria degrading poly(butylene succinate- co-butylene adipate) and their lip A gene
Two bacteria, Burkholderia cepacia PBSA-1 and Pseudomonas aeruginosa PBSA-2, capable of degrading poly(butylene succinate- co-butylene adipate) (PBSA) were isolated from activated sludge soil and cultivating soil in Korea by using the enrichment culture and the clear zone test at 27 °C and 37 °C. In...
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Veröffentlicht in: | International biodeterioration & biodegradation 2010-06, Vol.64 (3), p.184-190 |
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Sprache: | eng |
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Zusammenfassung: | Two bacteria,
Burkholderia cepacia PBSA-1 and
Pseudomonas aeruginosa PBSA-2, capable of degrading poly(butylene succinate-
co-butylene adipate) (PBSA) were isolated from activated sludge soil and cultivating soil in Korea by using the enrichment culture and the clear zone test at 27 °C and 37 °C. In this study, two bacteria showed a very high activity for PBSA degradation so that 78% of PBSA with an initial concentration of 0.01% was mineralized into CO
2 during 40 days of the modified Sturm test. To analyze the PBSA-degrading enzyme encoding gene,
lip A, PCR, cloning and sequencing were performed on the PBSA-degrading strains. The
lip A appeared at about 1.5 kb. The amino acid sequences possessed the lipase box, Gly-His-Ser-Gln-Gly and sequences of the two strains received their accession number of EF189714 and EF189715, respectively, from GenBank. The
lip A showed 87.9% homology between those of
B. cepacia PBSA-1 and
P. aeruginosa PBSA-2. Also they showed 83.2–86.9% and 85.9–89.7% homology compared with the
Pseudomonas lipase subfamily, respectively. However, the genes of
B. cepacia PBSA-1 and
P. aeruginosa PBSA-2 exhibited no more than 22.9–26.9% and 21.3–23.5% of homology, respectively, when compared with the previously reported bioplastics-degrading enzyme encoding genes. Consequently, the PBSA-degrading enzyme lipase gene,
lip A, was presumed to be a characteristic gene distinct from other bioplastics-degrading enzyme encoding genes. |
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ISSN: | 0964-8305 1879-0208 |
DOI: | 10.1016/j.ibiod.2010.01.002 |