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Deletion of the AMPylase mFICD alters cytokine secretion and affects cognitive plasticity in vivo

McCaul, N.; Porter, C. M.; Becker, A.; Tang, C.-H. A.; Wijne, C.; Chatterjee, B. K.; Bousbaine, D.; Bilate, A. M.; Hu, C.-C. A.; Ploegh, H. L.; Truttmann, M. C.

2021-04-17 molecular biology
10.1101/2021.04.16.440208 bioRxiv
Show abstract

Fic domain-containing AMP transferases (fic AMPylases) are conserved enzymes that catalyze the covalent transfer of AMP to proteins. This post-translational modification regulates the function of several proteins, including the ER-resident chaperone Grp78/BiP. Here we introduce a mFICD AMPylase knock-out mouse model to study fic AMPylase function in vertebrates. We find that mFICD deficiency is well-tolerated in unstressed mice. We show that mFICD-deficient mouse embryonic fibroblasts are depleted of AMPylated proteins. mFICD deletion alters protein synthesis and secretion in splenocytes, including that of IgM and IL-1{beta}, without affecting the unfolded protein response. Finally, we demonstrate that older mFICD-/- mice show improved cognitive plasticity. Together, our results suggest a role for mFICD in adaptive immunity and neuronal plasticity in vivo.

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