Open Access

ARTICLE

GP30 of the mycobacteriophage CASbig impairs mycobacterial adaptation during acidic stress and in macrophages

WU LI¹, JIANGZHE SI², SHUAI QIU², JING LUO¹, HUIQIONG SUN¹, XIAOQING LI¹, ZHIBIN WAN¹, WEI GAO¹, HANLU ZOU¹, LEI ZHANG², XIAOHONG XIANG³, YANZHANG LI², TIESHAN TENG^2,*

1 Key Laboratory of Regional Characteristic Agricultural Resources, College of Life Sciences, Neijiang Normal University, Neijiang, 641100, China
2 School of Medical Sciences, College of Medicine, Henan University, Kaifeng, 475004, China
3 School of Pharmacy, Chongqing Medical and Pharmaceutical College, Chongqing, 401331, China

* Address correspondence to: Tieshan Teng,

BIOCELL 2020, 44(4), 695-701. https://doi.org/10.32604/biocell.2020.011941

Received 06 June 2020; Accepted 12 August 2020; Issue published 24 December 2020

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 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.

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Keywords

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