Gene profiling of embryonic skeletal muscle lacking type I ryanodine receptor Ca(2+) release channel

Scientific Reports
Dilyana FilipovaSymeon Papadopoulos

Abstract

In mature skeletal muscle, the intracellular Ca(2+) concentration rises dramatically upon membrane depolarization, constituting the link between excitation and contraction. This process requires Ca(2+) release from the sarcoplasmic reticulum via the type 1 ryanodine receptor (RYR1). However, RYR1's potential roles in muscle development remain obscure. We used an established RyR1- null mouse model, dyspedic, to investigate the effects of the absence of a functional RYR1 and, consequently, the lack of RyR1-mediated Ca(2+) signaling, during embryogenesis. Homozygous dyspedic mice die after birth and display small limbs and abnormal skeletal muscle organization. Skeletal muscles from front and hind limbs of dyspedic fetuses (day E18.5) were subjected to microarray analyses, revealing 318 differentially expressed genes. We observed altered expression of multiple transcription factors and members of key signaling pathways. Differential regulation was also observed for genes encoding contractile as well as muscle-specific structural proteins. Additional qRT-PCR analysis revealed altered mRNA levels of the canonical muscle regulatory factors Six1, Six4, Pax7, MyoD, MyoG and MRF4 in mutant muscle, which is in line with the severe develo...Continue Reading

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Citations

Nov 9, 2018·Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics·Tokunbor A LawalKatherine G Meilleur
Dec 26, 2019·Disease Models & Mechanisms·Aurora FustoElena Pegoraro
Jul 4, 2020·Biochimica Et Biophysica Acta. Molecular Cell Research·Yi-Zhong WangHui Wang

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Datasets Mentioned

BETA
E-MTAB-3608

Methods Mentioned

BETA
PCA
PCR
in-vitro transcription
chips

Software Mentioned

LIMMA
DAVID
MGI GO
package
Affymetrix GCOS
Enrichr
prcomp
Panther
MGI
Panther GO

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