Open AccessDeletion of phosphatidylserine flippase β-subunit <i>Tmem30a</i> in satellite cells leads to delayed skeletal muscle regeneration
Author(s) -
Kuanxiang Sun,
Xiaoyan Jiang,
Xiao Li,
Yu-Jing Su,
Ju-Lin Wang,
Lin Zhang,
Yeming Yang,
Xuejun Zhu
Publication year - 2021
Publication title -
zoological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 19
ISSN - 2095-8137
DOI - 10.24272/j.issn.2095-8137.2021.195
Subject(s) - skeletal muscle , microbiology and biotechnology , phosphatidylserine , regeneration (biology) , biology , myod , myocyte , conditional gene knockout , chemistry , biochemistry , anatomy , myogenesis , phenotype , membrane , phospholipid , gene
Phosphatidylserine (PS) is distributed asymmetrically in the plasma membrane of eukaryotic cells. Phosphatidylserine flippase (P4-ATPase) transports PS from the outer leaflet of the lipid bilayer to the inner leaflet of the membrane to maintain PS asymmetry. The β subunit TMEM30A is indispensable for transport and proper function of P4-ATPase. Previous studies have shown that the ATP11A and TMEM30A complex is the molecular switch for myotube formation. However, the role of Tmem30a in skeletal muscle regeneration remains elusive. In the current study, Tmem30a was highly expressed in the tibialis anterior (TA) muscles of dystrophin-null ( mdx ) mice and BaCl 2 -induced muscle injury model mice. We generated a satellite cell (SC)-specific Tmem30a conditional knockout (cKO) mouse model to investigate the role of Tmem30a in skeletal muscle regeneration. The regenerative ability of cKO mice was evaluated by analyzing the number and diameter of regenerated SCs after the TA muscles were injured by BaCl 2 -injection. Compared to the control mice, the cKO mice showed decreased Pax7 + and MYH3 + SCs, indicating diminished SC proliferation, and decreased expression of muscular regulatory factors (MYOD and MYOG), suggesting impaired myoblast proliferation in skeletal muscle regeneration. Taken together, these results demonstrate the essential role of Tmem30a in skeletal muscle regeneration.