The pattern of MyoD and contractile protein localization in primary epaxial myotome reflects the dynamic progression of nascent myoblast differentiation

2006 ◽  
Vol 235 (2) ◽  
pp. 382-394 ◽  
Author(s):  
Yagai Yang ◽  
Charles P. Ordahl
Keyword(s):  
Protein Localization ◽  
Contractile Protein ◽  
Myoblast Differentiation

Complex regulation of the muscle-specific contractile protein (troponin I) gene

1987 ◽  
Vol 7 (9) ◽  
pp. 3065-3075
Author(s):  
S F Konieczny ◽  
C P Emerson
Keyword(s):  
Transcriptional Activation ◽  
Troponin I ◽  
Protein Gene ◽  
Regulatory Elements ◽  
Developmental Expression ◽  
Contractile Protein ◽  
Upstream Region ◽  
Myoblast Differentiation ◽  
Quantitative Expression ◽  
I Gene

A cloned quail troponin I contractile protein gene, stably transfected into a mouse myogenic cell line, exhibits appropriate developmental activation and quantitative expression during myoblast differentiation. Deletion mutagenesis analyses reveal that the troponin I gene has two distinct cis regulatory elements required for its developmental expression, as measured by mRNA accumulation and nuclear runoff transcription assays. One element in the 5' flanking region is required for maximum quantitative expression, and a second larger regulatory element (1.5 kilobases) within the first intron is responsible for differentiation-specific transcription. The upstream region is highly sensitive to negative repression by interaction with pBR322 sequences. The larger intragenic region retains some activity when moved to the 5' and 3' flanking regions and when inverted but is maximally active in its native intragenic site. The concerted activities of these two regulatory regions produce a 100- to 200-fold transcriptional activation during myoblast differentiation. The conserved 5' exon-intron organization of troponin I and other contractile protein genes suggests a possible mechanism by which intragenic control elements coordinate contractile protein gene regulation during skeletal myogenesis.

scholarly journals Complex regulation of the muscle-specific contractile protein (troponin I) gene.

1987 ◽  
Vol 7 (9) ◽  
pp. 3065-3075 ◽  
Author(s):  
S F Konieczny ◽  
C P Emerson
Keyword(s):  
Transcriptional Activation ◽  
Troponin I ◽  
Protein Gene ◽  
Regulatory Elements ◽  
Developmental Expression ◽  
Contractile Protein ◽  
Upstream Region ◽  
Myoblast Differentiation ◽  
Quantitative Expression ◽  
I Gene

A cloned quail troponin I contractile protein gene, stably transfected into a mouse myogenic cell line, exhibits appropriate developmental activation and quantitative expression during myoblast differentiation. Deletion mutagenesis analyses reveal that the troponin I gene has two distinct cis regulatory elements required for its developmental expression, as measured by mRNA accumulation and nuclear runoff transcription assays. One element in the 5' flanking region is required for maximum quantitative expression, and a second larger regulatory element (1.5 kilobases) within the first intron is responsible for differentiation-specific transcription. The upstream region is highly sensitive to negative repression by interaction with pBR322 sequences. The larger intragenic region retains some activity when moved to the 5' and 3' flanking regions and when inverted but is maximally active in its native intragenic site. The concerted activities of these two regulatory regions produce a 100- to 200-fold transcriptional activation during myoblast differentiation. The conserved 5' exon-intron organization of troponin I and other contractile protein genes suggests a possible mechanism by which intragenic control elements coordinate contractile protein gene regulation during skeletal myogenesis.

Actin-like contractile protein in carbon tetrachloride-induced cirrhosis in the rat

Pathology ◽  
1977 ◽  
Vol 9 (3) ◽  
pp. 187-194 ◽  
Author(s):  
B.H. Toh ◽  
M.N. Cauchi ◽  
H.K. Muller
Keyword(s):  
Carbon Tetrachloride ◽  
Contractile Protein

Lighting a path: genetic studies pinpoint neurodevelopmental mechanisms in autism and related disorders

2012 ◽  
Vol 14 (3) ◽  
pp. 239-252
Keyword(s):  
Molecular Mechanisms ◽  
Protein Localization ◽  
Regulation Of Gene Expression ◽  
Neuronal Cell ◽  
Mrna Splicing ◽  
Genetic Mutations ◽  
Scaffolding Proteins ◽  
Molecular Processes ◽  
Genetic Studies ◽  
Novel Treatments

In this review, we outline critical molecular processes that have been implicated by discovery of genetic mutations in autism. These mechanisms need to be mapped onto the neurodevelopment step(s) gone awry that may be associated with cause in autism. Molecular mechanisms include: (i) regulation of gene expression; (ii) pre-mRNA splicing; (iii) protein localization, translation, and turnover; (iv) synaptic transmission; (v) cell signaling; (vi) the functions of cytoskeletal and scaffolding proteins; and (vii) the function of neuronal cell adhesion molecules. While the molecular mechanisms appear broad, they may converge on only one of a few steps during neurodevelopment that perturbs the structure, function, and/or plasticity of neuronal circuitry. While there are many genetic mutations involved, novel treatments may need to target only one of few developmental mechanisms.

Sign in / Sign up

Export Citation Format

Share Document