Publication: Identification of Candidate Host Cell Factors Required for Actin-Based Motility of Burkholderia pseudomallei
Issued Date
2016-12-02
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ISSN
15353907
15353893
15353893
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2-s2.0-85000869992
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Mahidol University
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SCOPUS
Bibliographic Citation
Journal of Proteome Research. Vol.15, No.12 (2016), 4675-4685
Suggested Citation
Niramol Jitprasutwit, Nurhamimah Zainal-Abidin, Charles Vander Broek, Dominic Kurian, Sunee Korbsrisate, Mark P. Stevens, Joanne M. Stevens Identification of Candidate Host Cell Factors Required for Actin-Based Motility of Burkholderia pseudomallei. Journal of Proteome Research. Vol.15, No.12 (2016), 4675-4685. doi:10.1021/acs.jproteome.6b00760 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/42403
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Title
Identification of Candidate Host Cell Factors Required for Actin-Based Motility of Burkholderia pseudomallei
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Abstract
© 2016 American Chemical Society. Intracellular actin-based motility of the melioidosis pathogen Burkholderia pseudomallei requires the bacterial factor BimA. Located at one pole of the bacterium, BimA recruits and polymerizes cellular actin to promote bacterial motility within and between cells. Here, we describe an affinity approach coupled with mass spectrometry to identify cellular proteins recruited to BimA-expressing bacteria under conditions that promote actin polymerization. We identified a group of cellular proteins that are recruited to the B. pseudomallei surface in a BimA-dependent manner, a subset of which were independently validated with specific antisera including the ubiquitous scaffold protein Ras GTPase-activating-like protein (IQGAP1). IQGAP1 integrates several key cellular signaling pathways including those involved in actin dynamics and has been shown to be involved in the adhesion of attaching and effacing Escherichia coli to infected cells and invasion of host cells by Salmonella enterica serovar Typhimurium. Although a direct interaction between BimA and IQGAP1 could not be detected using either conventional pulldown or yeast two hybrid techniques, confocal microscopy revealed that IQGAP1 is recruited to B. pseudomallei actin tails in infected cells, and siRNA-mediated knockdown highlighted a role for this protein in controlling the length and actin density of B. pseudomallei actin tails.