A phosphatidylinositol 4,5-bisphosphate redistribution-based sensing mechanism initiates a phagocytosis programing

Libing Mu, Zhongyuan Tu, Lin Miao, Hefei Ruan, Ning Kang, Yongzhen Hei, Jiahuan Chen, Wei Wei, Fangling Gong, Bingjie Wang, Yanan Du, Guanghui Ma, Matthias W. Amerein, Tie Xia () and Yan Shi ()
Additional contact information
Libing Mu: Tsinghua University
Zhongyuan Tu: University of Calgary
Lin Miao: Tsinghua University
Hefei Ruan: Tsinghua University
Ning Kang: Tsinghua University
Yongzhen Hei: Tsinghua University
Jiahuan Chen: Tsinghua University
Wei Wei: Chinese Academy of Sciences
Fangling Gong: Chinese Academy of Sciences
Bingjie Wang: Tsinghua University
Yanan Du: Tsinghua University
Guanghui Ma: Chinese Academy of Sciences
Matthias W. Amerein: University of Calgary
Tie Xia: Tsinghua University
Yan Shi: Tsinghua University

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract Phagocytosis is one of the earliest cellular functions, developing approximately 2 billion years ago. Although FcR-based phagocytic signaling is well-studied, how it originated from ancient phagocytosis is unknown. Lipid redistribution upregulates a phagocytic program recapitulating FcR-based phagocytosis with complete dependence on Src family kinases, Syk, and phosphoinositide 3-kinases (PI3K). Here we show that in phagocytes, an atypical ITAM sequence in the ancient membrane anchor protein Moesin transduces signal without receptor activation. Plasma membrane deformation created by solid structure binding generates phosphatidylinositol 4,5-bisphosphate (PIP2) accumulation at the contact site, which binds the Moesin FERM domain and relocalizes Syk to the membrane via the ITAM motif. Phylogenic analysis traces this signaling using PI3K and Syk to 0.8 billion years ago, earlier than immune receptor signaling. The proposed general model of solid structure phagocytosis implies a preexisting lipid redistribution-based activation platform collecting intracellular signaling components for the emergence of immune receptors.

Date: 2018
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DOI: 10.1038/s41467-018-06744-7

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