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TMEM55a localizes to macrophage phagosomes to downregulate phagocytosis

Morioka, Shin, Nigorikawa, Kiyomi, Okada, Eri, Tanaka, Yoshimasa, Kasuu, Yoshihiro, Yamada, Miho, Kofuji, Satoshi, Takasuga, Shunsuke, Nakanishi, Hiroki, Sasaki, Takehiko, Hazeki, Kaoru·2018·Journal of Cell Science
DOI 10.1242/jcs.213272
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Abstract

TMEM55a (also known as PIP4P2) is an enzyme that dephosphorylates the phosphatidylinositol (PtdIns) PtdIns(4,5)P2 to form PtdIns(5)P in vitro. However, the in vivo conversion of the polyphosphoinositide into PtdIns(5)P by the phosphatase has not yet been demonstrated, and the role of TMEM55a remains poorly understood. Here, we found that mouse macrophages (Raw264.7) deficient in TMEM55a showed an increased engulfment of large particles without affecting the phagocytosis of Escherichia coli. Transfection of a bacterial phosphatase with similar substrate specificity to TMEM55a, namely IpgD, into Raw264.7 cells inhibited the engulfment of IgG-erythrocytes in a manner dependent on its phosphatase activity. In contrast, cells transfected with PIP4K2a, which catalyzes PtdIns(4,5)P2 production from PtdIns(5)P, increased phagocytosis. Fluorescent TMEM55a transfected into Raw264.7 cells was found to mostly localize to the phagosome. The accumulation of PtdIns(4,5)P2, PtdIns(3,4,5)P3 and F-actin on the phagocytic cup was increased in TMEM55a-deficient cells, as monitored by live-cell imaging. Phagosomal PtdIns(5)P was decreased in the knockdown cells, but the augmentation of phagocytosis in these cells was unaffected by the exogenous addition of PtdIns(5)P. Taken together, these results suggest that TMEM55a negatively regulates the phagocytosis of large particles by reducing phagosomal PtdIns(4,5)P2 accumulation during cup formation.

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Research works printed but not linked: 31

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Metadata

Authors
Morioka, S., Nigorikawa, K., Okada, E., Tanaka, Y., Kasuu, Y., Yamada, M., Kofuji, S., Takasuga, S., Nakanishi, H., Sasaki, T., & Hazeki, K.
Affiliations
  • Graduate School of Biomedical & Health Sciences, Hiroshima University 1 , Hiroshima 734-8553 , Japan
  • Akita University School of Medicine 2 Department of Pathology and Immunology , , Akita 010-8543 , Japan
  • Research Center for Biosignal, Akita University School of Medicine 3 , Akita 010-8543 , Japan
ORCID
Venue
Journal of Cell Science
Publisher
The Company of Biologists
Published
2018-03-01
Volume
131
Issue
5
ISSN
  • 1477-9137
  • 0021-9533
DOI
10.1242/jcs.213272
Cited by
18
References
3
Language
en
Licence
www.biologists.com/user-licence-1-1/ (vor, 184 d)
Funders
Home for Innovative Researchers and Academic Knowledge Users

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