Abstract
DPY19L3 has been identified as a C-mannosyltransferase for thrombospondin type-1 repeat domain-containing proteins. In this study, we focused on the role of DPY19L3 in the myogenic differentiation of C2C12 mouse myoblast cells. We carried out DPY19L3 gene depletion using the CRISPR/Cas9 system. The result showed that these DPY19L3-knockout cells could not be induced for differentiation. Moreover, the phosphorylation levels of MEK/ERK and p70S6K were suppressed in the DPY19L3-knockout cells compared with that of parent cells, suggesting that the protein(s) that is(are) DPY19L3-mediated C-mannosylated and regulate(s) MEK/ERK or p70S6K signaling is(are) required for the differentiation.
Highlights
Satellite cells, precursor of skeletal muscle cells, proliferate extensively and differentiate into myoblasts by muscle injury
Myogenic differentiation is an important event for the maintenance for muscle by turnover from old to new cells
It is suggested the possibility that DPY19L3-mediated C-mannosylation regulates these transcriptional factor activities
Summary
Precursor of skeletal muscle cells, proliferate extensively and differentiate into myoblasts by muscle injury. This involves the up-regulation of myogenic differentiation-related genes, such as MYOD, myogenin, and myosin heavy chain (MHC) [1,2,3]. C2C12 cells are usually used as a muscle regeneration model in vitro, because they have an ability to transition from proliferation into differentiation and form myofibers by adequate stimulus, similar with satellite cells [3]. We demonstrated that DPY19L3 is expressed during myogenic differentiation of C2C12 cells, and knockout of DPY19L3 gene inhibits the phosphorylation levels of MEK/ERK and p70S6K, and the differentiation. Molecules 2021, 26, 5685 from C2C12 cells every day after changing the medium to DM, and RT-PCR was performed.
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