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<i>Mycobacterium abscessus</i> is an opportunistic pathogen causing human diseases, especially in immunocompromised patients. <i>M. abscessus</i> 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 <i>M. abscessus</i>. A morphotype switching mutant (smooth) named <i>mab_3083c</i>::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 <i>mab_3083c</i> gene reverted its morphotype back to rough, indicating that <i>mab_3083c</i> is associated with colony morphology of <i>M. abscessus</i>. Bioinformatic analyses showed that <i>mab_3083c</i> has a 75.4% identity in amino acid sequence with the well-characterized ribonuclease J (RNase J) of <i>M. smegmatis</i> (RNase J_Msmeg). Complementation of the mutant with the RNase J gene of <i>M. smegmatis</i> 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 <i>M. abscessus</i> colony morphotype switching.