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Dynamic expression of chicken cMeso2 in segmental plate and somites
Author(s) -
Buchberger Astrid,
Bonneick Sonja,
Klein Christian,
Arnold HansHenning
Publication year - 2002
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.1240
Subject(s) - somitogenesis , paraxial mesoderm , somite , biology , mesoderm , intermediate mesoderm , transactivation , microbiology and biotechnology , corepressor , transcription factor , genetics , myotome , primordium , repressor , gene , embryo , embryogenesis , embryonic stem cell
Abstract Somitogenesis in vertebrates involves prepatterning of paraxial mesoderm into somitomeres, establishing of anteroposterior polarity within somite primordia, and boundary formation between individual somites. cMeso2 is a newly identified chicken gene encoding a bHLH transcription factor, which is expressed in a transient stripe pattern in anterior presomitic mesoderm before segmentation of somites. The expression pattern overlaps with that of cMeso1 and correlates in time with the formation cycle of somites, suggesting that it may have a role in this process. Unlike its homologues in other organisms cMeso2 transcripts in chicken locate to the posterior aspects of somitomeres and constitute a marker for the caudal half of somites. Initiation of cMeso2 expression in presomitic mesoderm as well as its maintenance appears to be independent from influences by surrounding tissues, suggesting that it is part of the intrinsic program underlying segmentation. Although cMeso1 contains a C‐terminal activator domain that can be transferred onto an independent DNA‐binding domain, no evidence for such a transactivator domain can be found in cMeso2. In contrast, cMeso2 exerts transcriptional inhibition when coexpressed with the cMeso1 transactivator and seems to contain a repressor domain. Thus, cMeso1 and cMeso2 may function in an antagonistic manner during somitogenesis. © 2001 Wiley‐Liss, Inc.