FGF3 and FGF8 mediate a rhombomere 4 signaling activity in the zebrafish hindbrain.
AuthorsMaves L, Jackman W, Kimmel CB,
JournalDevelopment
PubMed ID12135921
'The segmentation of the vertebrate hindbrain into rhombomeres is highly conserved, but how early hindbrain patterning is established is not well understood. We show that rhombomere 4 (r4) functions as an early-differentiating signaling center in the zebrafish hindbrain. Time-lapse analyses of zebrafish hindbrain development show that r4 forms first and ... More
vhnf1 and Fgf signals synergize to specify rhombomere identity in the zebrafish hindbrain.
AuthorsWiellette EL, Sive H,
JournalDevelopment
PubMed ID12835397
'Vertebrate hindbrain segmentation is a highly conserved process but the mechanism of rhombomere determination is not well understood. Recent work in the zebrafish has shown a requirement for fibroblast growth factor (Fgf) signaling and for the transcription factor variant hepatocyte nuclear factor 1 (vhnf1) in specification of rhombomeres 5 and ... More
The zebrafish Iroquois gene iro7 positions the r4/r5 boundary and controls neurogenesis in the rostral hindbrain.
AuthorsLecaudey V, Anselme I, Rosa F, Schneider-Maunoury S,
JournalDevelopment
PubMed ID15175248
Early brain regionalisation involves the activation of genes coding for transcription factors in distinct domains of the neural plate. The limits of these domains often prefigure morphological boundaries. In the hindbrain, anteroposterior patterning depends on a segmentation process that leads to the formation of seven bulges called rhombomeres (r). The ... More
Abnormal neurofilament transport caused by targeted disruption of neuronal kinesin heavy chain KIF5A.
AuthorsXia CH, Roberts EA, Her LS, Liu X, Williams DS, Cleveland DW, Goldstein LS,
JournalJ Cell Biol
PubMed ID12682084
To test the hypothesis that fast anterograde molecular motor proteins power the slow axonal transport of neurofilaments (NFs), we used homologous recombination to generate mice lacking the neuronal-specific conventional kinesin heavy chain, KIF5A. Because null KIF5A mutants die immediately after birth, a synapsin-promoted Cre-recombinase transgene was used to direct inactivation ... More