Preliminary Study On The Interactions Of M-cadherin With MyoD And MyoG In Regulation Of Myoblast Fusion Process

Cell-cell fusion is a crucial and highly regulated event, cadherins and MRFs can be adjustedfor this process. Many research reports focus on the regulation of M-cadherin, MyoD and MyoGduring myoblast fusion process. M-cadherin is a member of cadherins, which is one of fivecategories adhesion molecules, mediated adhesion between the same types of cells. M-cadherinis the only member of the cadherin superfamily whose expression is restricted in the developingskeletal muscle and correlated with differentiation of myogenic cells. In the study reported thatM-cadherin Related to the establishment of adhesion sites during myoblast fusion process,M-cadherin mutual adhesion between myoblasts as well as mutual fusion between myoblasts hasan important role in the process of forming the muscle fibers. MRFs mainly consists of fourmembers: MyoG, MyoD, Myf5, and MRF4. MyoG and MyoD are the regulation factor aboutmyoblast fusion. MyoD can make the skeletal muscle satellite cells transformed into myoblasts,and also can make Fibroblast and Fat cells transformed into myoblasts. MyoD also can makeMyoblast fuse to muscle fibers. MyoG, also known as myogenin, can control the initiation fusionof Myoblast and promote mononuclear myoblasts fusing to form multinucleated muscle fibers.MyoG played a leading role in the MRFs family.Although many researches about the regulation of M-cadherin, MyoD and MyoG during themyoblast fusion have been reported, But for adhesion molecules and myogenic regulatory factoris how the interaction of muscle fusion of the regulation of this process has rarely been reported.Many issues are worth doing further research. Therefore, in my study, choosing C2C12skeletalmuscle satellite cells of mouse in the differentiation model at6time point to researchM-cadherin, MyoD, and Myog expression of the gene transcriptional regulationin the myoblastfusion process From the above results, the Real-time results of molecular are compared. At thetime point T1, MyoD expression level is the highest, compared with the MyoG and M-cadherinexpression level. At the time point T2, MyoD expression level is still the highest, whileM-cadherin expression level reaches the highest value. This is consistent with the literature, thatMyoD can act on the promoter of M-cadherin to control M-cadherin expression. The MyoDrelatively high expression promotes M-cadherin expression. This indicates that MyoD cancontrol M-cadherin expression. The highest expression level of Myog is at the time point T3.This may be due to the high expression of M-cadherin establishing a stable adhesion betweenmyoblasts at T2. The signal of this stable adhesion is transduced into cells, which promotesmyog to achieve high expression at T3. According to the above results, when the interference isused to get rid of the M-cadherin, the MyoG expression is indeed affected. Analyzed andcompared the SIM-cadherin experimental group with the control group from the whole point-in-time, the fusion of Myoblast is inhibited; almost no integration happens. These resultsinitially validate our inference about the muscle fusion molecules adjustment mechanism: MyoDactivated the expression of M-cadherin, to induce the expression of MyoG. This article hopes tolay the theoretical foundation for the muscle fusion of the molecular mechanism.