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ORIGINAL RESEARCH article

Front. Microbiol.
Sec. Infectious Agents and Disease
Volume 15 - 2024 | doi: 10.3389/fmicb.2024.1533640

Anaplasma phagocytophilum AFAP targets host nucleolus and inhibits induced apoptosis

Provisionally accepted
Daxiu Zhang Daxiu Zhang Lifeng Yu Lifeng Yu Hui Tang Hui Tang Hua Niu Hua Niu *
  • Affiliated Hospital of Guilin Medical University, Guilin, China

The final, formatted version of the article will be published soon.

    Anaplasma phagocytophilum, the aetiologic agent of human granulocytic anaplasmosis (HGA) is an obligate intracellular Gram-negative bacterium. During infection, A. phagocytophilum transfers its type IV secretion system (T4SS) effector proteins into host cells to manipulate cellular processes.AFAP (an actin filament-associated Anaplasma phagocytophilum protein), was identified as a T4SS effector protein and found interacting with host nucleolin in previous study. Here proteomic analysis was performed to extensively identify AFAP-interacting proteins in host cells, and analyze the potential role of AFAP in modulating host cellular processes. 586 host proteins were identified interacting with AFAP by data-independent acquisition mass spectrometry, and annotated to 501 Gene Ontology (GO) terms, with the significantly over-represented ones related to ribosomes, nucleolus, DNA binding, rRNA metabolic process. Given the role of nucleolus in cellular stress response, the targeting of AFAP to nucleolus, and the identification of dozens of AFAP-interacting proteins which were annotated to the GO term (GO:0072331, signal transduction by p53 class mediator), the role of AFAP in modulating host apoptosis was determined. AFAP was found capable to inhibit induced apoptosis. Thus, the proteomic analysis of AFAP-interacting proteins and determination of AFAP with anti-apoptotic activity may help elucidate the role of this T4SS effector protein in HGA pathogenesis.

    Keywords: Anaplasma phagocytophilum 1, type IV secretion system 2, proteomic analysis 3, apoptosis 4, nucleolus 5

    Received: 24 Nov 2024; Accepted: 19 Dec 2024.

    Copyright: © 2024 Zhang, Yu, Tang and Niu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Hua Niu, Affiliated Hospital of Guilin Medical University, Guilin, China

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