Comparative genomic hybridizations reveal absence of large Streptomyces coelicolor genomic islands in Streptomyces lividans
1 Department of Chemical Engineering and Materials Science, University of Minnesota, 421 Washington Ave. SE., Minneapolis, MN 55455, USA
2 Life Sciences Institute, Departments of Medicinal Chemistry, Chemistry, Microbiology & Immunology, University of Michigan, 210 Washtenaw Ave., Ann Arbor, MI 48109, USA
3 Abbott Bioresearch Center, 100 Research Drive, Worcester, MA 01605, USA
4 Fonds National de la Recherche, 6 rue Antoine de Saint-Exupéry, L-1017 Kirchberg, Luxembourg
BMC Genomics 2007, 8:229 doi:10.1186/1471-2164-8-229Published: 10 July 2007
The genomes of Streptomyces coelicolor and Streptomyces lividans bear a considerable degree of synteny. While S. coelicolor is the model streptomycete for studying antibiotic synthesis and differentiation, S. lividans is almost exclusively considered as the preferred host, among actinomycetes, for cloning and expression of exogenous DNA. We used whole genome microarrays as a comparative genomics tool for identifying the subtle differences between these two chromosomes.
We identified five large S. coelicolor genomic islands (larger than 25 kb) and 18 smaller islets absent in S. lividans chromosome. Many of these regions show anomalous GC bias and codon usage patterns. Six of them are in close vicinity of tRNA genes while nine are flanked with near perfect repeat sequences indicating that these are probable recent evolutionary acquisitions into S. coelicolor. Embedded within these segments are at least four DNA methylases and two probable methyl-sensing restriction endonucleases. Comparison with S. coelicolor transcriptome and proteome data revealed that some of the missing genes are active during the course of growth and differentiation in S. coelicolor. In particular, a pair of methylmalonyl CoA mutase (mcm) genes involved in polyketide precursor biosynthesis, an acyl-CoA dehydrogenase implicated in timing of actinorhodin synthesis and bldB, a developmentally significant regulator whose mutation causes complete abrogation of antibiotic synthesis belong to this category.
Our findings provide tangible hints for elucidating the genetic basis of important phenotypic differences between these two streptomycetes. Importantly, absence of certain genes in S. lividans identified here could potentially explain the relative ease of DNA transformations and the conditional lack of actinorhodin synthesis in S. lividans.