1887

Abstract

Chitin degradation and subsequent -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 strain A3(2), and we examined here the genetic setting of the erythromycin producer for GlcNAc and chitin utilization, as well as the transcriptional control thereof. efficiently utilize GlcNAc most likely via the phosphotransferase system (PTS); however, this strain is not able to grow when chitin or ,′-diacetylchitobiose [(GlcNAc)] is the sole nutrient source, despite a predicted extensive chitinolytic system ( genes). The inability of to utilize chitin and (GlcNAc) is probably because of the loss of genes encoding the DasABC transporter for (GlcNAc) import, and genes for intracellular degradation of (GlcNAc) by β--acetylglucosaminidases. Transcription analyses revealed that in all putative and GlcNAc utilization genes are repressed by DasR, whereas in DasR 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 activates gene expression, as opposed to the previously reported GlcNAc-mediated catabolite repression in . 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.

Funding
This study was supported by the:
  • National Natural Science Foundation of China (Award 21276079)
  • SRFDP (Award 20120074110009)
  • National Key Technologies R&D Programs (Award 2014AA021502 and 2007AA02Z331)
  • FRS-FNRS
  • Belgian Program of Interuniversity Attraction Poles
  • Federal Office for Scientific Technical and Cultural Affairs (Award P7/44)
  • University of Liège (Award R.CFRA.1237)
  • University of Queensland (Award 2010002194)
  • Mexican Council for Science and Technology
  • CONACYT
  • AIBN
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2014-09-01
2024-04-24
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