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Dial M( RF ) for myogenesis
Author(s) -
Moncaut Natalia,
Rigby Peter W. J.,
Carvajal Jaime J.
Publication year - 2013
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12379
Subject(s) - myod , myogenesis , myf5 , biology , transcription factor , microbiology and biotechnology , myogenic regulatory factors , ctcf , genetics , mef2 , pax3 , computational biology , gene , enhancer
The transcriptional regulatory network that controls the determination and differentiation of skeletal muscle cells in the embryo has at its core the four myogenic regulatory factors ( MRF s) Myf5, MyoD, Mrf4 and MyoG. These basic helix–loop–helix transcription factors act by binding, as obligate heterodimers with the ubiquitously expressed E proteins, to the E‐box sequence CANNTG . While all skeletal muscle cells have the same underlying function their progenitors arise at many sites in the embryo and it has become apparent that the upstream activators of the cascade differ in these various populations so that it can be switched on by a variety of inductive signals, some of which act by initiating transcription, some by maintaining it. The application of genome‐wide approaches has provided important new information as to how the MRF s function to activate the terminal differentiation programme and some of these data provide significant mechanistic insights into questions which have exercised the field for many years. We also consider the emerging roles played by micro‐ RNA s in the regulation of both upstream activators and terminal differentiation genes.