English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo.

MPS-Authors
/persons/resource/persons219180

Gentzel,  Marc
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Kotini, M., Barriga, E. H., Leslie, J., Gentzel, M., Rauschenberger, V., Schambon, A., et al. (2018). Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo. Nature communications, 9(1): 3846. doi:10.1038/s41467-018-06368-x.


Cite as: https://hdl.handle.net/21.11116/0000-0003-F620-3
Abstract
Connexins are the primary components of gap junctions, providing direct links between cells under many physiological processes. Here, we demonstrate that in addition to this canonical role, Connexins act as transcriptional regulators. We show that Connexin 43 (Cx43) controls neural crest cell migration in vivo by directly regulating N-cadherin transcription. This activity requires interaction between Cx43 carboxy tail and the basic transcription factor-3, which drives the translocation of Cx43 tail to the nucleus. Once in the nucleus they form a complex with PolII which directly binds to the N-cadherin promoter. We found that this mechanism is conserved between amphibian and mammalian cells. Given the strong evolutionary conservation of connexins across vertebrates, this may reflect a common mechanism of gene regulation by a protein whose function was previously ascribed only to gap junctional communication.