title: Fgfr2 and Fgfr3 are not required for patterning and maintenance of the midbrain and anterior hindbrain.
abstract: The mid-/hindbrain organizer (MHO) is characterized by the expression of a network of genes, which controls the patterning and development of the prospective midbrain and anterior hindbrain. One key molecule acting at the MHO is the fibroblast growth factor (Fgf) 8. Ectopic expression of Fgf8 induces genes that are normally expressed at the mid-/hindbrain boundary followed by the induction of midbrain and anterior hindbrain structures. Inactivation of the Fgf receptor (Fgfr) 1 gene, which was thought to be the primary transducer of the Fgf8 signal at the MHO, in the mid-/hindbrain region, leads to a deletion of dorsal structures of the mid-/hindbrain region, whereas ventral tissues are less severely affected. This suggests that other Fgfrs might be responsible for ventral mid-/hindbrain region development. Here we report the analysis of Fgfr2 conditional knockout mice, lacking the Fgfr2 in the mid-/hindbrain region and of Fgfr3 knockout mice with respect to the mid-/hindbrain region. In both homozygous mouse mutants, patterning of the mid-/hindbrain region is not altered, neuronal populations develop normal and are maintained into adulthood. This analysis shows that the Fgfr2 and the Fgfr3 on their own are dispensable for the development of the mid-/hindbrain region. We suggest functional redundancy of Fgf receptors in the mid-/hindbrain region.
authors.affiliation: GSF-National Research Center for Environment and Health, Institute of Developmental Genetics, Ingolstadter Landstrasse 1, 85764 Neuherberg, Germany.
authors.forename: Alexandra A
authors.initials: AA
authors.lastname: Blak
authors.forename: Thorsten
authors.initials: T
authors.lastname: Naserke
authors.forename: Jonna
authors.initials: J
authors.lastname: Saarimäki-Vire
authors.forename: Paula
authors.initials: P
authors.lastname: Peltopuro
authors.forename: Mario
authors.initials: M
authors.lastname: Giraldo-Velasquez
authors.forename: Daniela M
authors.initials: DM
authors.lastname: Vogt Weisenhorn
authors.forename: Nilima
authors.initials: N
authors.lastname: Prakash
authors.forename: Michael
authors.initials: M
authors.lastname: Sendtner
authors.forename: Juha
authors.initials: J
authors.lastname: Partanen
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Wurst
mesh_terms: D000818:Animals; D019521:Body Patterning / Q000502:physiology*; D051524:Fibroblast Growth Factor 8 / Q000378:metabolism; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008636:Mesencephalon / Q000196:embryology*; D051379:Mice; D018345:Mice, Knockout; D051497:Receptor, Fibroblast Growth Factor, Type 2 / Q000235:genetics / Q000378:metabolism*; D051498:Receptor, Fibroblast Growth Factor, Type 3 / Q000235:genetics / Q000378:metabolism*; D012249:Rhombencephalon / Q000196:embryology*
chemical_list: C496457:Fgf8 protein, mouse; D051524:Fibroblast Growth Factor 8; C496354:Fgfr2 protein, mouse; C496366:Fgfr3 protein, mouse; D051497:Receptor, Fibroblast Growth Factor, Type 2; D051498:Receptor, Fibroblast Growth Factor, Type 3