Influence of the neural tube/notochord complex on MyoD expression and cellular proliferation in chicken embryos

Abstract

Important advances have been made in understanding the genetic processes that control skeletal muscle formation. Studies conducted on quails detected a delay in the myogenic program of animals selected for high growth rates. These studies have led to the hypothesis that a delay in myogenesis would allow somitic cells to proliferate longer and consequently increase the number of embryonic myoblasts. To test this hypothesis, recently segmented somites and part of the unsegmented paraxial mesoderm were separated from the neural tube/ notochord complex in HH12 chicken embryos. In situ hybridization and competitive RT-PCR revealed that MyoD transcripts, which are responsible for myoblast determination, were absent in somites separated from neural tube/notochord (1.06 and 0.06 10 -3 attomol MyoD/ 1 attomol ß-actin for control and separated somites, respectively; P<0.01). However, reapproximation of these structures allowed MyoD to be expressed in somites. Cellular proliferation was analyzed by immunohistochemical detection of incorporated BrdU, a thymidine analogue. A smaller but not significant (P = 0.27) number of proliferating cells was observed in somites that had been separated from neural tube/notochord (27 and 18 for control and separated somites, respectively). These results confirm the influence of the axial structures on MyoD activation but do not support the hypothesis that in the absence of MyoD transcripts the cellular proliferation would be maintained for a longer period of time.

Neural crest and the patterning of vertebrate craniofacial muscles

“…How these broad, sequential, partially overlapping expression domains then become restricted to discrete myogenic foci ( Figure 7) is less well understood (Buckingham, 2016;Tzahor, 2015). Signals from the brain and notochord are likely candidates, analogous to processes well described for myotome development in the trunk (Alves et al, 2003;Deries & Thorsteinsd ottir, 2016;Musumeci et al, 2015;Stern & Hauschka, 1995). To date the only identified site-specific locus that initiates myogenesis within head mesoderm is the isthmus (midbrain-hindbrain junction), beside which the lateral rectus muscle develops; the signaling molecules have not been identified.…”

Normal and aberrant craniofacial myogenesis by grafted trunk somitic and segmental plate mesoderm

“…Orchestrating myogenic initiation, differentiation, movements, proliferation and survival among trunk muscle precursors requires a consortium of extrinsic signals from adjacent tissues (Alves et al, 2003;Borycki and Emerson, 2000;Christ and Brand-Saberi, 2002;Pownall et al, 2002), as well as intra-somitic signals. Some signals are distinct for medial and lateral myogenic zones of the dermamyotome, and maintaining the ratio among signals is essential for proper spatio-temporal coordination of myogenesis (e.g.…”

Study on the transcriptional regulatory mechanism of the MyoD1 gene in Guanling bovine

“…The MyoD gene family (MyoD1, Myf5, MyoG, and Myf6) has been shown to act as a key regulator that controls the expression of specic proteins in the proliferation and differentiation of muscle cells. [8][9][10][11]18,27 Among them, MyoD1 plays an important role in muscle growth in the transcriptional regulation of muscle-specic genes, 38 while Myf6 (MRF4) primarily functions in a downstream role in myogenesis, including myober formation 19,39 and the maintenance of the muscle phenotype. 39 The Myf6 and MyoD1 promoters are regulated quite differently, leading to opposite roles of MRF4 and MyoD in cell proliferation and myogenic differentiation, 40 in which MyoD is a potential negative intercessor of MRF4 in regulating the cell cycle.…”