|Title||Role of a Microcin-C-like biosynthetic gene cluster in allelopathic interactions in marine Synechococcus|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Paz-Yepes J., Brahamsha B, Palenik B|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|Type of Article||Article|
|Keywords||adaptation; allelopathy; antibiotics; cyanobacteria; diversity; escherichia-coli; genomics; horizontal gene transfer; north-atlantic; plasmid genes; Secondary metabolites; transfer-rna synthetase|
Competition between phytoplankton species for nutrients and light has been studied for many years, but allelopathic interactions between them have been more difficult to characterize. We used liquid and plate assays to determine whether these interactions occur between marine unicellular cyanobacteria of the genus Synechococcus. We have found a clear growth impairment of Synechococcus sp. CC9311 and Synechococcus sp. WH8102 when they are cultured in the presence of Synechococcus sp. CC9605. The genome of CC9605 contains a region showing homology to genes of the Escherichia coli Microcin C (McC) biosynthetic pathway. McC is a ribosome-synthesized peptide that inhibits translation in susceptible strains. We show that the CC9605 McC gene cluster is expressed and that three genes (mccD, mccA, and mccB) are further induced by coculture with CC9311. CC9605 was resistant to McC purified from E. coli, whereas strains CC9311 and WH8102 were sensitive. Cloning the CC9605 McC biosynthetic gene cluster into sensitive CC9311 led this strain to become resistant to both purified E. coli McC and Synechococcus sp. CC9605. A CC9605 mutant lacking mccA1, mccA2, and the N-terminal domain of mccB did not inhibit CC9311 growth, whereas the inhibition of WH8102 was reduced. Our results suggest that an McC-like molecule is involved in the allelopathic interactions with CC9605.