Crosstalk between integrin/FAK and Crk/Vps25 governs invasion of bovine mammary epithelial cells by S. agalactiae

Zhixin Guo; Yuze Ma; Zhibo Jia; Liping Wang; Xinyue Lu; Yuhao Chen; Yanfeng Wang; Huifang Hao; Shuixing Yu; Zhigang Wang

doi:10.1016/j.isci.2023.107884

Crosstalk between integrin/FAK and Crk/Vps25 governs invasion of bovine mammary epithelial cells by S. agalactiae

iScience. 2023 Sep 9;26(10):107884. doi: 10.1016/j.isci.2023.107884. eCollection 2023 Oct 20.

Authors

Zhixin Guo^{1

2}, Yuze Ma¹, Zhibo Jia¹, Liping Wang¹, Xinyue Lu¹, Yuhao Chen^{1

3}, Yanfeng Wang¹, Huifang Hao¹, Shuixing Yu¹, Zhigang Wang¹

Affiliations

¹ State Key Laboratory of Reproductive Regulation & Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot 010021, China.
² School of Fisheries and Life Science, Dalian Ocean University, Dalian 116023, China.
³ School of Life Sciences, Jining Normal University, Jining 012000, China.

Abstract

Streptococcus agalactiae (S. agalactiae) is a contagious obligate parasite of the udder in dairy cows. Here, we examined S. agalactiae-host interactions in bovine mammary epithelial cells (BMECs) in vitro. We found that S. agalactiae infected BMECs through laminin β2 and integrin. Crk, Vps25, and RhoA were differentially expressed in S. agalactiae-infected cells. S. agalactiae infection activated FAK and Crk. FAK deficiency decreased the number of intracellular S. agalactiae and Crk activation. Knockdown of Crk or Vps25 increased the level of intracellular S. agalactiae, whereas its overexpression had the opposite effect. RhoA expression and actin cytoskeleton were altered in S. agalactiae-infected BMECs. Crk and Vps25 interact in cells, and invaded S. agalactiae also activates Crk, allowing it to cooperate with Vps25 to defend against intracellular infection by S. agalactiae. This study provides insights into the mechanism by which intracellular infection by S. agalactiae is regulated in BMECs.

Keywords: Bacteriology; Cell biology; Genetics.