TY - EJOU AU - LI, WU AU - SI, JIANGZHE AU - QIU, SHUAI AU - LUO, JING AU - SUN, HUIQIONG AU - LI, XIAOQING AU - WAN, ZHIBIN AU - GAO, WEI AU - ZOU, HANLU AU - ZHANG, LEI AU - XIANG, XIAOHONG AU - LI, YANZHANG AU - TENG, TIESHAN TI - GP30 of the mycobacteriophage CASbig impairs mycobacterial adaptation during acidic stress and in macrophages T2 - BIOCELL PY - 2020 VL - 44 IS - 4 SN - 1667-5746 AB - The rapid emergence of multidrug-resistant and extensively drug-resistant Tuberculosis retrieved intense interest in phage-based therapy. This old approach, which was abandoned in the west in the 1940s but is generating renewed interest, has stimulated fresh research on mycobacteriophages and their lytic efficiency against their hosts. GP30 is a novel protein of the mycobacteriophage CASbig with undiscovered function. In this study, we analyzed the role of CASbig gp30 in the host Mycobacterium smegmatis. Overexpression of gp30 in the host led to reduced growth in acidic medium and attenuated the intracellular survival rate of M. smegmatis inside the THP-1 macrophages, which may be linked to the altered lipid profile of the recombinant bacterial cell wall. In a word, this study suggested that gp30, a novel gene from a mycobacteriophage, modulated lipid composition and content to hamper the survivability of bacteria under stress conditions. KW - Mycobacterium smegmatis KW - gp30 KW - CASbig KW - Acidic stress KW - Macrophage DO - 10.32604/biocell.2020.011941