Bit-1 is an essential regulator of myogenic differentiation

Journal of Cell Science
Genevieve S GriffithsMichelle L Matter

Abstract

Muscle differentiation requires a complex signaling cascade that leads to the production of multinucleated myofibers. Genes regulating the intrinsic mitochondrial apoptotic pathway also function in controlling cell differentiation. How such signaling pathways are regulated during differentiation is not fully understood. Bit-1 (also known as PTRH2) mutations in humans cause infantile-onset multisystem disease with muscle weakness. We demonstrate here that Bit-1 controls skeletal myogenesis through a caspase-mediated signaling pathway. Bit-1-null mice exhibit a myopathy with hypotrophic myofibers. Bit-1-null myoblasts prematurely express muscle-specific proteins. Similarly, knockdown of Bit-1 expression in C2C12 myoblasts promotes early differentiation, whereas overexpression delays differentiation. In wild-type mice, Bit-1 levels increase during differentiation. Bit-1-null myoblasts exhibited increased levels of caspase 9 and caspase 3 without increased apoptosis. Bit-1 re-expression partially rescued differentiation. In Bit-1-null muscle, Bcl-2 levels are reduced, suggesting that Bcl-2-mediated inhibition of caspase 9 and caspase 3 is decreased. Bcl-2 re-expression rescued Bit-1-mediated early differentiation in Bit-1-null myob...Continue Reading

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Citations

Apr 8, 2016·Skeletal Muscle·Ryan A V BellLynn A Megeney
May 6, 2020·Cell Death & Disease·Mahshid H DehkordiHoward O Fearnhead
Mar 23, 2017·American Journal of Medical Genetics. Part a·Rajech SharkiaMuhammad Mahajnah
Feb 9, 2017·Human Molecular Genetics·Jinger DoeMichelle L Matter
Dec 11, 2020·Cell Death Discovery·Austin D CorpuzMichelle L Matter
Apr 26, 2018·Biochimica Et Biophysica Acta. Molecular and Cell Biology of Lipids·Wenjia LouMiriam L Greenberg

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