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dc.contributor.authorVitrinel, Burcu
dc.contributor.authorVogel, Christine
dc.contributor.authorChristiaen, Lionel
dc.date.accessioned2023-06-29T08:47:32Z
dc.date.available2023-06-29T08:47:32Z
dc.date.created2023-06-13T17:46:56Z
dc.date.issued2023-05-16
dc.identifier.issn1661-6596
dc.identifier.urihttps://hdl.handle.net/11250/3074297
dc.description.abstractDuring embryonic development, cell-fate specification gives rise to dedicated lineages that underlie tissue formation. In olfactores, which comprise tunicates and vertebrates, the cardiopharyngeal field is formed by multipotent progenitors of both cardiac and branchiomeric muscles. The ascidian Ciona is a powerful model to study cardiopharyngeal fate specification with cellular resolution, as only two bilateral pairs of multipotent cardiopharyngeal progenitors give rise to the heart and to the pharyngeal muscles (also known as atrial siphon muscles, ASM). These progenitors are multilineage primed, in as much as they express a combination of early ASM- and heart-specific transcripts that become restricted to their corresponding precursors, following oriented and asymmetric divisions. Here, we identify the primed gene ring finger 149 related (Rnf149-r), which later becomes restricted to the heart progenitors, but appears to regulate pharyngeal muscle fate specification in the cardiopharyngeal lineage. CRISPR/Cas9-mediated loss of Rnf149-r function impairs atrial siphon muscle morphogenesis, and downregulates Tbx1/10 and Ebf, two key determinants of pharyngeal muscle fate, while upregulating heart-specific gene expression. These phenotypes are reminiscent of the loss of FGF/MAPK signaling in the cardiopharyngeal lineage, and an integrated analysis of lineage-specific bulk RNA-seq profiling of loss-of-function perturbations has identified a significant overlap between candidate FGF/MAPK and Rnf149-r target genes. However, functional interaction assays suggest that Rnf149-r does not directly modulate the activity of the FGF/MAPK/Ets1/2 pathway. Instead, we propose that Rnf149-r acts both in parallel to the FGF/MAPK signaling on shared targets, as well as on FGF/MAPK-independent targets through (a) separate pathway(s).en_US
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleRing Finger 149-Related Is an FGF/MAPK-Independent Regulator of Pharyngeal Muscle Fate Specificationen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2023 the authorsen_US
dc.source.articlenumber8865en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.doi10.3390/ijms24108865
dc.identifier.cristin2154252
dc.source.journalInternational Journal of Molecular Sciencesen_US
dc.identifier.citationInternational Journal of Molecular Sciences. 2023, 24 (10), 8865.en_US
dc.source.volume24en_US
dc.source.issue10en_US


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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal