English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/210602
logo share SHARE   Add this article to your Mendeley library MendeleyBASE
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE
Exportar a otros formatos:


New roles of MYF5 in dorsal somitic progenitors

AuthorsLópez-Mayorga, Macarena ; Moncaut, Natalia; Vicente García, Cristina; Teboul, Lydia; Rigby, Peter W. J.; Carvajal, Jaime J.
Issue Date23-Oct-2019
CitationEuropean Developmental Biology Congress (2019)
AbstractSkeletal muscles originate from different mesoderms: presomitic (limb and trunk muscles), head (extraocular muscles) and pharyngeal mesoderm (facial muscles). Independently from their origin, all muscles develop under the control of the four Myogenic Regulatory Factors: Myf5, Mrf4, MyoD and MyoG. Myf5 is the first to be expressed, and controls myogenic specification. MyoD function overlaps with that of Myf5, and rescues the Myf5-KO phenotype. Myf5/MyoD double mutants have a general lack of skeletal muscles as myogenic precursors are not specified. MyoG drives terminal differentiation and in its absence adult muscles are not formed. Mrf4 plays roles in specification and differentiation, although its function remains poorly understood. The Early Epaxial Enhancer (EEE) directs the earliest Myf5 expression, starting in the somitic dorsomedial lip. We have generated a new mouse allele in which the EEE has been removed. This new mutant only loses Myf5 expression in the dorsal part of the first 5-6 somites. RNA-seq reveals differences in myogenic, innervation and limb, neurogenesis and chondrogenesis gene-networks. We have now validated several of the identified genes by qPCR and/or ISH. Because EEE-KO animals lack an overt phenotype, we generated EEE/MyoD double mutants, thus abolishing MyoD rescue in dorsal somitic progenitors. In these animals, we observe severe defects in diaphragm, ribcage and posture (kyphosis), which lead us to study the epaxial musculature more in detail to see if there is a particular group of muscles affected. Also, we are trying to elucidate how absence of Myf5 impacts upon Pax1 expression, presumably causing the ribcage defects.
DescriptionResumen del trabajo presentado en el European Developmental Biology Congress, celebrado en Alicante (España), del 23 al 26 de octubre de 2019
Appears in Collections:(CABD) Comunicaciones congresos
Files in This Item:
File Description SizeFormat 
NEW ROLES OF MYF5.pdf82,64 kBAdobe PDFThumbnail
Show full item record
Review this work

WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.