| Literature DB >> 25149266 |
Clelia Peano1, Fabrizio Damiano2, Mattia Forcato3, Alessandro Pietrelli1, Carla Palumbo2, Giorgio Corti1, Luisa Siculella2, Fabio Fuligni1, Guidantonio Malagoli Tagliazucchi3, Giuseppe Egidio De Benedetto4, Silvio Bicciato3, Gianluca De Bellis1, Pietro Alifano5.
Abstract
Rifamycins are mainstay agents in treatment of many widespread diseases, but how an improved rifamycin producer can be created is still incompletely understood. Here, we describe a comparative genomic approach to investigate the mutational patterns introduced by the classical mutate-and-screen method in the genome of an improved rifamycin producer. Comparing the genome of the rifamycin B overproducer Amycolatopsis mediterranei HP-130 with those of the reference strains A. mediterranei S699 and U32, we identified 250 variations, affecting 227 coding sequences (CDS), 109 of which were HP-130-specific since they were absent in both S699 and U32. Mutational and transcriptional patterns indicated a series of genomic manipulations that not only proved the causative effect of mutB2 (coding for methylmalonyl-CoA mutase large subunit) and argS2 (coding for arginyl tRNA synthetase) mutations on the overproduction of rifamycin, but also constituted a rational strategy to genetically engineer a reference strain into an overproducer.Entities:
Keywords: Amycolatopsis mediterranei; Arginyl tRNA synthetase; Methylmalonyl-CoA mutase; Rifamycin; Strain improvement
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Year: 2014 PMID: 25149266 DOI: 10.1016/j.ymben.2014.08.001
Source DB: PubMed Journal: Metab Eng ISSN: 1096-7176 Impact factor: 9.783