Boundary cells regulate a switch in the expression of FGF3 in hindbrain rhombomeres

Dalit Sela-Donenfeld*, Galya Kayam, David G. Wilkinson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


Background. During formation of the vertebrate central nervous system, the hindbrain is organized into segmental units, called rhombomeres (r). These cell-lineage restricted segments are separated by a subpopulation of cells known as boundary cells. Boundary cells display distinct molecular and cellular properties such as an elongated shape, enriched extracellular matrix components and a reduced proliferation rate compared to intra-rhombomeric cells. However, little is known regarding their functions and the mechanisms that regulate their formation. Results. Hindbrain boundary cells express several signaling molecules, such as FGF3, which at earlier developmental stages is transiently expressed in specific rhombomeres. We show that chick embryos that lack boundary cells due to overexpression of truncated EphA4 receptor in the hindbrain have continued segmental expression of FGF3 at stages when it is normally restricted to hindbrain boundaries. Furthermore, surgical ablation of the boundary between r3 and r4, or blocking of the contact of r4 with boundary cells, results in sustained FGF3 expression in this segment. Conclusion. These findings suggest that boundary cells are required for the downregulation of segmental FGF3, presumably mediated by a soluble factor(s) that emanates from boundaries. We propose that this new function of boundary cells enables a switch in gene expression that may be required for stage-specific functions of FGF3 in the developing hindbrain.

Original languageAmerican English
Article number16
JournalBMC Developmental Biology
Issue number1
StatePublished - 2009

Bibliographical note

Funding Information:
We thank Dr. J. Briscoe and Dr. P. Charnay for plasmids and probes. We also thank M. Hazenfratz for summarizing parts of the data. This study was supported by THE ISRAEL SCIENCE FOUNDATION and by THE MEDICAL RESEARCH COUNCIL, UK. DSD was a recipient of an EMBO postdoctoral fellowship.


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