Transcriptional mechanisms regulating MyoD expression in the mouse

1999 ◽  
Vol 296 (1) ◽  
pp. 213-219 ◽  
Author(s):  
Jennifer C. J. Chen ◽  
D. J. Goldhamer
Keyword(s):  
Myod Expression

scholarly journals Lipin1 is required for skeletal muscle development by regulating MEF2c and MyoD expression

2018 ◽  
Vol 597 (3) ◽  
pp. 889-901 ◽  
Author(s):  
Abdulrahman Jama ◽  
Dengtong Huang ◽  
Abdullah A. Alshudukhi ◽  
Roman Chrast ◽  
Hongmei Ren
Keyword(s):  
Skeletal Muscle ◽  
Muscle Development ◽  
Skeletal Muscle Development ◽  
Myod Expression

scholarly journals Sustained expression of HeyL is critical for the proliferation of muscle stem cells in overloaded muscle

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Sumiaki Fukuda ◽  
Akihiro Kaneshige ◽  
Takayuki Kaji ◽  
Yu-taro Noguchi ◽  
Yusei Takemoto ◽  
...  
Keyword(s):  
Stem Cells ◽  
Basal Lamina ◽  
Satellite Cells ◽  
Knockout Mice ◽  
Muscle Stem Cells ◽  
Muscle Satellite Cells ◽  
Effector Gene ◽  
Injury Model ◽  
Myod Expression

In overloaded and regenerating muscle, the generation of new myonuclei depends on muscle satellite cells (MuSCs). Because MuSC behaviors in these two environments have not been considered separately, MuSC behaviors in overloaded muscle remain unexamined. Here, we show that most MuSCs in overloaded muscle, unlike MuSCs in regenerating muscle, proliferate in the absence of MyoD expression. Mechanistically, MuSCs in overloaded muscle sustain the expression of Heyl, a Notch effector gene, to suppress MyoD expression, which allows effective MuSC proliferation on myofibers and beneath the basal lamina. Although Heyl-knockout mice show no impairment in an injury model, in a hypertrophy model, their muscles harbor fewer new MuSC-derived myonuclei due to increased MyoD expression and diminished proliferation, which ultimately causes blunted hypertrophy. Our results show that sustained HeyL expression is critical for MuSC proliferation specifically in overloaded muscle, and thus indicate that the MuSC-proliferation mechanism differs in overloaded and regenerating muscle.

Msx1 antagonizes the myogenic activity of Pax3 in migrating limb muscle precursors

Development ◽  
1999 ◽  
Vol 126 (22) ◽  
pp. 4965-4976 ◽  
Author(s):  
A.J. Bendall ◽  
J. Ding ◽  
G. Hu ◽  
M.M. Shen ◽  
C. Abate-Shen
Keyword(s):  
Protein Interactions ◽  
Myogenic Differentiation ◽  
Ectopic Expression ◽  
Homeobox Gene ◽  
Regulatory Elements ◽  
Limb Muscle ◽  
Chicken Embryos ◽  
Myogenic Activity ◽  
Myod Expression

The migration of myogenic precursors to the vertebrate limb exemplifies a common problem in development - namely, how migratory cells that are committed to a specific lineage postpone terminal differentiation until they reach their destination. Here we show that in chicken embryos, expression of the Msx1 homeobox gene overlaps with Pax3 in migrating limb muscle precursors, which are committed myoblasts that do not express myogenic differentiation genes such as MyoD. We find that ectopic expression of Msx1 in the forelimb and somites of chicken embryos inhibits MyoD expression as well as muscle differentiation. Conversely, ectopic expression of Pax3 activates MyoD expression, while co-ectopic expression of Msx1 and Pax3 neutralizes their effects on MyoD. Moreover, we find that Msx1 represses and Pax3 activates MyoD regulatory elements in cell culture, while in combination, Msx1 and Pax3 oppose each other's trancriptional actions on MyoD. Finally, we show that the Msx1 protein interacts with Pax3 in vitro, thereby inhibiting DNA binding by Pax3. Thus, we propose that Msx1 antagonizes the myogenic activity of Pax3 in migrating limb muscle precursors via direct protein-protein interaction. Our results implicate functional antagonism through competitive protein-protein interactions as a mechanism for regulating the differentiation state of migrating cells.

Cell heterogeneity upon myogenic differentiation: down-regulation of MyoD and Myf-5 generates ‘reserve cells’

1998 ◽  
Vol 111 (6) ◽  
pp. 769-779 ◽  
Author(s):  
N. Yoshida ◽  
S. Yoshida ◽  
K. Koishi ◽  
K. Masuda ◽  
Y. Nabeshima
Keyword(s):  
Cell Cycle ◽  
Myogenic Differentiation ◽  
Significant Proportion ◽  
Ectopic Expression ◽  
Terminal Differentiation ◽  
Growth Conditions ◽  
Down Regulation ◽  
Undifferentiated Cells ◽  
Myoblast Cells ◽  
Myod Expression

When a proliferating myoblast culture is induced to differentiate by deprivation of serum in the medium, a significant proportion of cells escape from terminal differentiation, while the rest of the cells differentiate. Using C2C12 mouse myoblast cells, this heterogeneity observed upon differentiation was investigated with an emphasis on the myogenic regulatory factors. The differentiating part of the cell population followed a series of well-described events, including expression of myogenin, p21(WAF1), and contractile proteins, permanent withdrawal from the cell cycle and cell fusion, whereas the rest of the cells did not initiate any of these events. Interestingly, the latter cells showed an undetectable or greatly reduced level of MyoD and Myf-5 expression, which had been originally expressed in the undifferentiated proliferating myoblasts. When these undifferentiated cells were isolated and returned to the growth conditions, they progressed through the cell cycle and regained MyoD expression. These cells demonstrated identical features with the original culture on the deprivation of serum. They produced both MyoD-positive differentiating and MyoD-negative undifferentiated populations once again. Thus the undifferentiated cells in the serum-deprived culture were designated ‘reserve cells’. Upon serum deprivation, MyoD expression rapidly decreased as a result of down-regulation in approximately 50% of the cells. After this heterogenization, MyoD positive cells expressed myogenin, which is the earliest known event of terminal differentiation and marks irreversible commitment to this, while MyoD-negative cells did not differentiate and became the reserve cells. We also demonstrated that ectopic expression of MyoD converted the reserve cells to differentiating cells, indicating that down-regulation of MyoD is a causal event in the formation of reserve cells.

scholarly journals Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer

2015 ◽  
Vol 35 (2) ◽  
Author(s):  
Yu Chih Pan ◽  
Xiao Wen Wang ◽  
Han Feng Teng ◽  
Yi Ju Wu ◽  
Hsuan Chia Chang ◽  
...  
Keyword(s):  
Signal Pathways ◽  
Cis Elements ◽  
Distal Enhancer ◽  
Wnt Pathways ◽  
Canonical Wnt ◽  
Myod Expression

We found that Wnt3a can directly activate MyoD expression through targeting cis-elements in the distal enhancer and in the upstream −8 to −9k region. A novel Pax3/Pax7-involved pathway and both canonical and non-canonical Wnt pathways are involved in this activation.

Sign in / Sign up

Export Citation Format

Share Document