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This paper reports a novel skull phenotype in a ciliopathic mutant mouse in which only a single calvarial bone plate encases the forebrain in mice lacking Fuz, an essential regulator of ciliogenesis.
Fuzzy appears to control subcellular localization of the core PCP (Montrer BMP1 Kits ELISA) protein Dishevelled (Montrer DVL2 Kits ELISA), recruiting it to Rab8 (Montrer RAB8A Kits ELISA)-positive vesicles and to the basal body and cilium. We show that loss of Fuzzy results in inhibition of PCP (Montrer BMP1 Kits ELISA) signaling
Using the ciliopathic Fuz mutant mouse, we find that high arched palate does not, as commonly suggested, arise from midface hypoplasia; rather, increased neural crest expands the maxillary primordia.
The data demonstrate a new model for coordination of Hh and Wnt (Montrer WNT2 Kits ELISA) signaling and reveal a Fuz-dependent negative feedback loop controlling Wnt (Montrer WNT2 Kits ELISA)/beta-catenin (Montrer CTNNB1 Kits ELISA) signaling.
Fuz controls the morphogenesis and differentiation of hair follicles through the formation of primary cilia.
Fuz plays an important role in cilia formation, Hh signal transduction, and embryonic development in mammals.
This gene encodes a planar cell polarity protein that is involved in ciliogenesis and directional cell movement. Knockout studies in mice exhibit neural tube defects and defective cilia, and mutations in this gene are associated with neural tube defects in humans. Alternatively spliced transcript variants have been found for this gene.
fuzzy homolog (Drosophila)
, protein fuzzy homolog
, fuzzy homolog