In chicken pectoral muscle cell cultures, FST enhanced muscle cell development (Link and Nishi 1997).
Genetic Srf deletion studies showed SRF to be indispensable for in vivo skeletal and cardiac muscle cell development.
FST's inhibition of MSTN binding to its receptors has been demonstrated in vitro (Lee and McPherron 2001), supporting that the enhancement of muscle cell development by FST was probably due to FST's suppression of MSTN.
Moreover, muscle cell development in Ciona mirrors many aspects of muscle cell gene regulation and morphogenesis documented in other organisms, and as such may serve as a paradigm for related studies of in vivo cellular behaviors.
To analyze muscle cell development in a perturbed developmental context we misexpressed the Xenopus homeodomain-containing transcription factor Bix1 [21] in muscle precursors, using the sna>Bix construct, which had previously been shown to cause shortening and/or bending of the tail when electroporated in Ciona embryos [22].
Up-regulated genes are involved mainly in muscle cell development (10 of 41 BP terms).
In addition, endoglin-/ and Smad5-/ mice exhibit impaired vascular smooth muscle cell development.
However, these species are complex, which makes it difficult to work out the general principles that control muscle cell development.
From all of this, it can be inferred that myocardin is the master regulator of smooth muscle cell development and is responsible for the tissue-specific function of SRF in smooth muscle cells during development.
Early studies conducted in mouse embryonic cells [ 22] identified 5-azacytidine as a differentiating agent that induces muscle cell development, along with the global loss of DNA methylation.
In contrast, metabolic processes, generation of precursor metabolites/energy and oxidation reduction were positively correlated categories, while muscle cell development and skeletal myofibril assembly were negatively correlated.
