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SIX1 and SIX4 homeoproteins regulate PAX7+ progenitor cell properties during fetal epaxial myogenesis

ABSTRACT: SIX1 and SIX4 homeoproteins regulate PAX7+ progenitor cell properties during fetal epaxial myogenesis

PROVIDER: PRJNA667661 | ENA |

REPOSITORIES: ENA

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SIX1 and SIX4 homeoproteins regulate PAX7+ progenitor cell properties during fetal epaxial myogenesis

Project description:Identification of the gene targets of the SIX transcription factors in myogenic stem cells and in whole back muscles during murine fetal development Pax7 expression marks stem cells in developing skeletal muscles and adult satellite cells during homeostasis and muscle regeneration. The genetic determinants that control the entrance into the myogenic program and the appearance of PAX7+ cells during embryogenesis are poorly understood. SIX homeoproteins are encoded by the Sine oculis homeobox related Six1-Six6 genes in vertebrates. Six1, Six2, Six4 and Six5 are expressed in the muscle lineage. Here we tested the hypothesis that Six1 and Six4 could participate in the genesis of myogenic stem cells. We show that fewer PAX7+ cells occupy a satellite cell position between the myofiber and its associated basal lamina in Six1 and Six4 (s1s4KO) at E18. However, PAX7+ cells are detected in remaining muscle masses present in the epaxial region of the double mutant embryos and are able to divide and contribute to muscle growth. To further characterize the properties of s1s4KO PAX7+ cells, we analyzed their transcriptome and tested their properties after transplantation in adult regenerating tibialis anterior (TA) muscle. Mutant stem cells form hypotrophic myofibers that are not innervated but retain the ability to self-renew.

2020-10-07 | GSE159079 | GEO

Gene Expression Profiling of siRNA Knock-Down of Six1, Six4 and Myogenin in C2C12

Project description:Six1, Six4 and Myogenin are transcription factors that are known to be required for skeletal myogenesis. Currently, very little is known about the genes targeted by Six1 and Six4. Gene expression profiling when one or both transcription factors were knock-down by siRNA was performed to identify genes affected by their absence. We also hypothesized that Six1 and Six4 can work in cooperation with the myogenic regulatory factor (MRFs) family of transcription factors, such as Myogenin. Therefore, we performed the same type of experiment where the myogenin was knocked-down by siRNA to identify genes that are possibly regulated by the Six1 or Six4 in conjunction with Myogenin. C2C12 Myoblasts were transfected with siRNA against Six1, Six4, Six1 with Six4, Myogenin, or control 24h before start of differentiation. The cells were allowed to differentiate in differentiation medium for 24h and were harvested for gene expression profiling. Four replicates per siRNA were performed.

2010-07-30 | E-GEOD-19967 | biostudies-arrayexpress

Gene Expression Profiling of siRNA Knock-Down of Six1, Six4 and Myogenin in C2C12

2010-07-05 | GSE19967 | GEO

Six1 and Six4 function in myoblast differentiation

Project description:Six1 and Six4 function in myoblast differentiation

| PRJNA120151 | ENA

Genomic mapping of Six1 binding sites during skeletal myoblast differentiation

2010-07-05 | GSE20150 | GEO

Transcriptional Dominance of Pax7 in Adult Myogenesis Is Due to High-Affinity Recognition of Homeodomain Motifs

Project description:This SuperSeries is composed of the following subset Series: GSE25064: ChIP-Seq of Pax7 and Pax3 in myoblasts GSE32266: Mouse Myoblast Pax3, Pax7 overexpression and control Refer to individual Series

2012-05-22 | E-GEOD-25092 | biostudies-arrayexpress

Transcription profiling of mouse back muscle from Six1-/-Six4-/- and control embryos in order to identify genes under the control of Six proteins at E18.5. E18.5

Project description:The aim of the experiment was to compare the transcriptome of Six1-/-Six4-/- and control embryos in order to identify genes under the control of Six proteins at E18.5. E18.5 RNAs from back muscles of three SixdKO and two control embryos were hybridized on Affymetrix mouse genome 430A2.0 arrays (Affymetrix, Strasbourg - France).

2009-10-08 | E-MEXP-1848 | biostudies-arrayexpress

Loss of CRY2 promotes regenerative myogenesis by enhancing PAX7 expression and satellite cell proliferation

Project description:Loss of CRY2 promotes regenerative myogenesis by enhancing PAX7 expression and satellite cell proliferation

| PRJNA720410 | ENA

Genomic mapping of Six1 binding sites during skeletal myoblast differentiation

Project description:In this study, the C2C12 cell line, a model used to study myogenesis and regeneration, was allowed to differentiate from myoblast precursor cells to myotubes. Cells were harvested at 3 different timepoints to perform ChIP-on-Chip of Six1, which is a key muscle regulator. We identified global loci bound by Six1 during skeletal myoblast differentiation. C2C12 Myoblasts were allowed to differentiate into myotubes. Cells at three timepoints were harvested for ChIP-on-Chip, including myoblasts stage, 24h after differentiation and myotubes (96h after differentiation). Myotubes were detached from the undifferentiated myoblast reserve cells using diluted trypsin. 3 independent biological replicates were used for each time point experiment. A microarray set counts 3 arrays (Custom Arrays A, B and C) for a total of approximately 2.9 million probes.

2010-07-05 | E-GEOD-20150 | biostudies-arrayexpress

Divergent transcriptional and transforming properties of PAX3-FOXO1 and PAX7-FOXO1 paralogs

Project description:Hallmarks of the alveolar subclass of Rhabdomyosarcoma are chromosomal translocations that generate PAX3-FOXO1 or PAX7-FOXO1 chimeric transcription factors. Both PAX-FOXO1s drive related cell transformation in animal models, yet the two mutations are associated with distinct pathological manifestations in patients. To evaluate the mechanisms underlying these differences, we generated isogenic fibroblast lines expressing either PAX-FOXO1 paralog. Mapping their genome recruitment using CUT&Tag revealed that the two chimeric proteins have distinct DNA binding preferences. Furthermore, PAX7-FOXO1 causes stronger de novo transactivation of its bound regions than PAX3-FOXO1, resulting in greater transcriptomic dynamics involving genes regulating cell shape and cycle. Consistently, PAX3-FOXO1 accentuates fibroblast cellular traits associated with contractility and surface adhesion and limits entry to M phase. Instead, PAX7-FOXO1 pushes cells to adopt an amoeboid-like shape, reduce S phase entry and provokes more genome instabilities. Altogether, our results demonstrate that PAX7-FOXO1 has a greater chromatin remodelling and transactivating abilities and is more deleterious to cells than PAX3-FOXO1. Altogether our results argue that the diversity in rhabdomyosarcoma manifestation stems, in part, from the diverging transcriptional activity of PAX3-FOXO1 and PAX7-FOXO1. Furthermore, PAX7-FOXO1 pronounced deleterious effects provides an explanation for the low frequency of the translocation generating this factor in Rhabdomyosarcoma patients.

2021-08-15 | GSE180919 | GEO

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