During vertebrate development, a unique population of cells, termed neural crest cells,
migrates throughout the developing embryo, generating various cell types, for example,
the smooth muscle that divides the aorta and pulmonary artery where they connect to
the heart, and the autonomic neurons, which coordinate organ function. The distinctions
between neural crest cells that will form smooth muscle and those that will become
neurons are thought to occur prior to migration. Here, we show that in mice with mutations
of the transcription factor Twist1, a subpopulation of presumptive smooth muscle cells, following migration to the heart,
instead mis-specify to resemble autonomic neurons. Twist1 represses transcription
of the pro-neural factor Phox2b both through antagonism of its upstream effector, Sox10, and through direct binding
to its promoter. Phox2b is absolutely required for autonomic neuron development, and
indeed, the aberrant neurons in Twist1 mutants disappear when Phox2b is also mutated. Ectopic Twist1 expression within all neural crest cells disrupts
the specification of normal autonomic neurons. Collectively, these data reveal that
neural crest cells can alter their cell fate from mesoderm to ectoderm after they
have migrated and that Twist1 functions to maintain neural crest cell potency during
embryonic development.
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Autonomic Neuroscience: Basic and ClinicalAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
Article info
Publication history
Received:
May 15,
2013
Identification
Copyright
© 2013 Published by Elsevier Inc.
