Abstract

Mycobacterium abscessus is an opportunistic pathogen causing human diseases, especially in immunocompromised patients. M. abscessus strains with a rough morphotype are more virulent than those with a smooth morphotype. Morphotype switch may occur during a clinical infection. To investigate the genes involved in colony morphotype switching, we performed transposon mutagenesis in a rough clinical strain of M. abscessus. A morphotype switching mutant (smooth) named mab_3083c::Tn was obtained. This mutant was found to have a lower aggregative ability and a higher sliding motility than the wild type strain. However, its glycopeptidolipid (GPL) content remained the same as those of the wild type. Complementation of the mutant with a functional mab_3083c gene reverted its morphotype back to rough, indicating that mab_3083c is associated with colony morphology of M. abscessus. Bioinformatic analyses showed that mab_3083c has a 75.4% identity in amino acid sequence with the well-characterized ribonuclease J (RNase J) of M. smegmatis (RNase JMsmeg). Complementation of the mutant with the RNase J gene of M. smegmatis also switched its colony morphology from smooth back to rough. These results suggest that Mab_3083c is a homologue of RNase J and involved in regulating M. abscessus colony morphotype switching.

Highlights

  • Mycobacterium abscessus is a rapid-growing nontuberculous Mycobacterium (NTM) and is often present in soil and water [1,2]

  • We investigated the role of the mab_3083c gene, homologue of ribonuclease J (RNase J), in colony morphology switching and surface-associated properties of M. abscessus

  • M. smegmatis mc2 155 was purchased from the American Type Culture Collection (ATCC), and the clinical strain M. abscessus cs1c was obtained from the Veterans General

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Summary

Introduction

Mycobacterium abscessus is a rapid-growing nontuberculous Mycobacterium (NTM) and is often present in soil and water [1,2]. The prevalence of M. abscessus infection is increasing in hospitals in Taiwan [9,10]. Because M. abscessus is highly resistant to multiple antibiotics, treatment of M. abscessus infections is often difficult [11,12]. It has been shown that M. abscessus is resistant to first-line anti-tuberculosis agents such as rifampin and ethambutol [13,14]. Treatment for M. abscessus infection consists of intravenous amikacin combined with oral macrolide such as clarithromycin, as suggested by the American Thoracic Society and the Infectious Diseases Society of America [4]

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