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First published online July 27, 2006
doi: 10.1242/10.1242/dev.02483
Department of Biology, University of Pennsylvania, Goddard Labs 316, Philadelphia, PA 19104-6017, USA.
* Author for correspondence (e-mail: eweinber{at}sas.upenn.edu)
Accepted 9 June 2006
We have used the maternal effect mutant ichabod, which is
deficient in maternal ß-catenin signaling, to test for the epistatic
relationship between ß-catenin activation, FGF signaling and bozozok,
squint and chordin expression. Injection of ß-catenin RNA
into ichabod embryos can completely rescue normal development. By
contrast, when FGF signaling is inhibited, ß-catenin did not induce
goosecoid and chordin, repress bmp4 expression or
induce a dorsal axis. These results demonstrate that FGF signaling is
necessary for ß-catenin induction of the zebrafish organizer. We show
that FGFs function downstream of squint and bozozok to turn
on chordin expression. Full rescue of ichabod by Squint is
dependent on FGF signaling, and partial rescue by FGFs is completely dependent
on chordin. By contrast, Bozozok can rescue the complete
anteroposterior axis, but not notochord, in embryos blocked in FGF signaling.
Surprisingly, accumulation of bozozok transcript in ß-catenin
RNA-injected ichabod embryos is also dependent on FGF signaling,
indicating a role of FGFs in maintenance of bozozok RNA. These
experiments show that FGF-dependent organizer function operates through both
bozozok RNA accumulation and a pathway consisting of
ß-catenin
Squint
FGF
Chordin, in which each component is
sufficient for expression of the downstream factors of the pathway, and in
which Nodal signaling is required for FGF gene expression and FGF signaling is
required for Squint induction of chordin.
Key words: ß-Catenin, FGF signaling, Dorsal axis formation, Neural induction, Dorsoventral patterning, Anteroposterior patterning, Organizer, Nodal, Chordin, Zebrafish
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