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