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Ciglar, L., Girardot, C., Wilczyński, B., Braun, M., Furlong, E.E. (2014). Coordinated repression and activation of two transcriptional programs stabilizes cell fate during myogenesis.  Development 141(13): 2633--2643.
FlyBase ID
FBrf0225471
Publication Type
Research paper
Abstract
Molecular models of cell fate specification typically focus on the activation of specific lineage programs. However, the concurrent repression of unwanted transcriptional networks is also essential to stabilize certain cellular identities, as shown in a number of diverse systems and phyla. Here, we demonstrate that this dual requirement also holds true in the context of Drosophila myogenesis. By integrating genetics and genomics, we identified a new role for the pleiotropic transcriptional repressor Tramtrack69 in myoblast specification. Drosophila muscles are formed through the fusion of two discrete cell types: founder cells (FCs) and fusion-competent myoblasts (FCMs). When tramtrack69 is removed, FCMs appear to adopt an alternative muscle FC-like fate. Conversely, ectopic expression of this repressor phenocopies muscle defects seen in loss-of-function lame duck mutants, a transcription factor specific to FCMs. This occurs through Tramtrack69-mediated repression in FCMs, whereas Lame duck activates a largely distinct transcriptional program in the same cells. Lineage-specific factors are therefore not sufficient to maintain FCM identity. Instead, their identity appears more plastic, requiring the combination of instructive repressive and activating programs to stabilize cell fate.
PubMed ID
PubMed Central ID
PMC4146391 (PMC) (EuropePMC)
Related Publication(s)
Personal communication to FlyBase
Furlong Lab EMBL TFBS contribution.
Monfort and Furlong, 2015.1.15, Furlong Lab EMBL TFBS contribution. [FBrf0227761]
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Development
    Title
    Development
    Publication Year
    1987-
    ISBN/ISSN
    0950-1991
    Data From Reference
    Aberrations (1)
    Alleles (7)
    Genes (42)
    Datasets (7)
    Sequence Features (1)
    Natural transposons (1)
    Insertions (1)
    Experimental Tools (1)
    Transgenic Constructs (4)