Developmental dynamics of miRNAs across chicken pectoral muscle and effect of gga-miRNA-454 on the differentiation of myoblasts
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ABSTRACT:
ORGANISM(S): Gallus gallus
PROVIDER: GSE139304 | GEO | 2020/06/17
REPOSITORIES: GEO
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Project description:Developmental dynamics of miRNAs across chicken pectoral muscle and effect of gga-miRNA-454 on the differentiation of myoblasts
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2020-12-18 | GSE152051 | GEO
Project description:Gene expression in satellite cell-derived primary myoblasts islolated from Gata4-loxP mice. Myoblasts were infected with nLacZ for control (Wt), Cre recombinase to knockout GATA4 (KO), or GATA4 expression vector to overexpress GATA4 (OE). Infected myoblasts were cultured in growth medium (day 0) then differentiated into myotubes in differentiation medium for 3 days (day 3). Total 18 samples. Three replicates in each myoblast; GATA4-Wt, -KO, and -OE myoblasts at day 0 and day 3.
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Project description:The gene expression pathways leading to muscle pathology in facioscapulohumeral dystrophy (FSHD) remain to be elucidated. This muscular dystrophy is caused by a contraction of an array of tandem 3.3-kb repeats (D4Z4) at 4q35.2. We compared expression of control and FSHD myoblasts and myotubes (three preparations each) on exon microarrays (Affymetrix Human Exon 1.0 ST) and validated FSHD-specific differences for representative genes by qRT-PCR on additional myoblast cell strains. The FSHD and control myoblasts used for these experiments were shown to grow and differentiate into myotubes equally efficiently as control myoblasts. There were no significant FSHD-control differences in RNA levels for MYOD1 and MYOG at the myoblast and myotube stages and for MYF5 and MYF6 at the myoblast stage. In contrast, 295 other genes were dysregulated at least 2-fold in FSHD vs. control myoblasts (p <0.01, adjusted for multiple comparisons). Remarkably, only 10% of the FSHD-associated gene dysregulation at the myoblast stage was downregulation. At the myotube stage, about ten times as many genes exhibited FSHD-associated downregulated as at the myoblast stage and twice as many genes displayed FSHD-associated upregulation. The FSHD-related changes in RNA levels appear to be due to posttranscriptional as well as transcriptional alterations. Among the prominently dysregulated pathways were signaling and oxidative stress pathways. By comparing expression profiles of control myoblasts and myotubes to each other and to 19 non-muscle cell types profiled identically, our study also revealed many new myogenesis associations for genes not previously annotated as muscle-specific. Keywords: Disease state analysis and time course for differentiation
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Project description:Controlled myogenic differentiation is integral to the development, maintenance and repair of skeletal muscle, necessitating precise regulation of myogenic progenitors and resident stem cells. The transformation of proliferative muscle progenitors into multinuclear syncytia involves intricate cellular processes driven by cytoskeletal reorganization. While actin and microtubles have been extensively studied, we illuminate the role of septins, an essential yet still often overlooked cytoskeletal component, in myoblast architecture. Notably, Septin9 emerges as a critical regulator of myoblast differentiation during the initial commitment phase. Knock-down of Septin9 in C2C12 cells and primary mouse myoblasts accelerates the transition from proliferation to committed progenitor transcriptional programs. Furthermore, we unveil significant reorganization and downregulation of Septin9 during myogenic differentiation. Collectively, we propose that filmamentous septin structures and their orchestrated reorganization in myoblasts are part of a temporal regulatory mechanism governing the differentiation of myogenic progenitors. This study sheds light on the dynamic interplay between cytoskeletal components underlying controlled myogenic differentiation.
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Project description:The goal of this study is to find skate pectoral fin motor neuron markers. Total RNA was extracted from manually sorted pectoral fin MNs, which were retrogradely labeled and tail spinal cord cells. By comparing RNA expression profiles of pectoral fin MNs and tail spinal cord neurons, we could identity general MN, MN columnar, and subset MN pool markers for fin MNs.
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Project description:Adult skeletal muscle is a plastic tissue that can adapt its size to workload and that can regenerate after demage. Here, we show that RhoA within primary myoblasts is needed for a correct muscle regeneration by controlling satellite cell fusion without affecting their proliferation or their differentiation. Moreover primary cultured myoblast loosing RhoA have no defects in cytoskeleton reorganization however their movement is altered compared to control cells. At the molecular level, we found that RhoA controls the expressions of different genes depending on step of differentiation process, not necessarly already described as implicated in fusion program. These findings unravel the implication of RhoA within satellite cells regulating myoblast fusion in response to demage in order to allow a correct regeneration process.
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