@Article{biocell.2020.011941,
AUTHOR = {WU LI, JIANGZHE SI, SHUAI QIU, JING LUO, HUIQIONG SUN, XIAOQING LI, ZHIBIN WAN, WEI GAO, HANLU ZOU, LEI ZHANG, XIAOHONG XIANG, YANZHANG LI, TIESHAN TENG},
TITLE = {GP30 of the mycobacteriophage CASbig impairs mycobacterial adaptation during acidic stress and in macrophages},
JOURNAL = {BIOCELL},
VOLUME = {44},
YEAR = {2020},
NUMBER = {4},
PAGES = {695--701},
URL = {http://www.techscience.com/biocell/v44n4/41001},
ISSN = {1667-5746},
ABSTRACT = {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 <i>Mycobacterium smegmatis</i>. Overexpression of gp30 in the host led to reduced growth
in acidic medium and attenuated the intracellular survival rate of <i>M. smegmatis</i> 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.},
DOI = {10.32604/biocell.2020.011941}
}