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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Publikationen des W. G. Kerckhoff-Instituts     Display Documents



ID: 474490.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Publikationen des W. G. Kerckhoff-Instituts
VITO-2, a new SID domain protein, is expressed in the myogenic lineage during early mouse embryonic development
Authors:Mielcarek, M.; Piotrowska, I.; Schneider, A.; Gunther, S.; Braun, T.
Date of Publication (YYYY-MM-DD):2009
Title of Journal:Gene Expr Patterns
Volume:9
Issue / Number:3
Start Page:129
End Page:37
Audience:Not Specified
Abstract / Description:MCAT elements and its cognate binding partners, the transcription enhancer factors (TEFs) play important roles in the regulation of expression of several muscle-specific genes. The biological effects of TEFs strongly depend on different co-factors, which might act as co-activators or anti-repressors to enable transcriptional activation of target genes by TEFs. Previously, we have cloned and characterized VITO-1, which acts as a skeletal muscle-specific transcriptional co-activator of TEFs. Here we describe the cloning and expression profile of a related gene, VITO-2 (also termed Vgl-3), which shares a high homology with VITO-1 in the SID domain responsible for interaction with TEFs. During early embryonic and fetal development VITO-2 is mainly expressed in the myogenic lineage with an onset of expression in the myotomes of somites VI at E9.5 slightly later than VITO-1. At later developmental stages VITO-2 is predominantly found in the nervous system. In adult mice VITO-2 was detected in different tissues, including skeletal muscle, heart, kidney, liver and brain, where it was found in cortical and cerebellar neurons as well as in Purkinje cells. The expression of VITO-2 in the mesoderm was repressed by the notch/delta pathway and activated by Myf-5 since Dll-1 mutant showed an aberrant expression of VITO-2 but not VITO-1 in the tail bud and in the caudal neural tube at E10.5 while Myf-5 mutant mice lack expression of VITO-1 and VITO-2 in somites until E10.5.
Free Keywords:Animals; Base Sequence; Brain/metabolism; Branchial Region/metabolism; Cerebral Cortex/metabolism; Ganglia, Spinal/embryology/metabolism; Gene Expression Profiling; Intercellular Signaling Peptides and Proteins/deficiency; Kidney/metabolism; Liver/metabolism; Mice; Molecular Sequence Data; Muscle Development/*genetics; *Muscle Proteins/biosynthesis/genetics; Muscle, Skeletal/embryology/metabolism; Myocardium/metabolism; Myogenic Regulatory Factor 5/deficiency; Neuroepithelial Cells/metabolism; Purkinje Cells/metabolism; Somites/metabolism; Transcription Factors/*biosynthesis/*genetics
External Publication Status:published
Document Type:Article
Communicated by:N. N.
Affiliations:MPI für physiologische und klinische Forschung
External Affiliations:Max-Planck-Institute for Heart and Lung Research, Department of Cardiac Development and Remodelling, Parkstr. 1, D-61231 Bad Nauheim, Hessen, Germany.
Identifiers:ISSN:1567-133X (Print) 1567-133X (Linking)
URL:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=..
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