Control of chitin and N-acetylglucosamine utilization in Saccharopolyspora erythraea

Chitin degradation and subsequentN-acetylglucosamine (GlcNAc) catabolism is thought to be a common trait of a large majority of actinomycetes. Utilization of aminosugars had been poorly investigated outside the model strainStreptomyces coelicolorA3(2), and we examined here the genetic setting of the erythromycin producerSaccharopolyspora erythraeafor GlcNAc and chitin utilization, as well as the transcriptional control thereof.Sacch. erythraeaefficiently utilize GlcNAc most likely via the phosphotransferase system (PTSGlcNAc); however, this strain is not able to grow when chitin orN,N′-diacetylchitobiose [(GlcNAc)2] is the sole nutrient source, despite a predicted extensive chitinolytic system (chigenes). The inability ofSacch. erythraeato utilize chitin and (GlcNAc)2is probably because of the loss of genes encoding the DasABC transporter for (GlcNAc)2import, and genes for intracellular degradation of (GlcNAc)2by β-N-acetylglucosaminidases. Transcription analyses revealed that inSacch. erythraeaall putativechiand GlcNAc utilization genes are repressed by DasR, whereas inStrep. coelicolorDasR displayed either activating or repressing functions whether it targets genes involved in the polymer degradation or genes for GlcNAc dimer and monomer utilization, respectively. A transcriptomic analysis further showed that GlcNAc not only activates the transcription of GlcNAc catabolism genes but also activateschigene expression, as opposed to the previously reported GlcNAc-mediated catabolite repression inStrep. coelicolor. Finally, synteny exploration revealed an identical genetic background for chitin utilization in other rare actinomycetes, which suggests that screening procedures that used only the chitin-based protocol for selective isolation of antibiotic-producing actinomycetes could have missed the isolation of many industrially promising strains.