The inner ear develops from the otic placode, one of the cranial placodes that arise from a region of ectoderm adjacent to the anterior neural plate called the pre-placodal domain. We have identified a Forkhead family transcription factor, Foxi3, that is expressed in the pre-placodal domain and down-regulated when the otic placode is induced. We now show that Foxi3 mutant mice do not form otic placodes as evidenced by expression changes in early molecular markers and the lack of thickened placodal ectoderm, an otic cup or otocyst. Some preplacodal genes downstream of Foxi3 - Gata3, Six1 and Eya1 - are not expressed in the ectoderm of Foxi3 mutant mice, and the ectoderm exhibits signs of increased apoptosis. We also show that Fgf signals from the hindbrain and cranial mesoderm, which are necessary for otic placode induction, are received by pre-placodal ectoderm in Foxi3 mutants, but do not initiate otic induction. Finally, we show that the epibranchial placodes that develop in close proximity to the otic placode and the mandibular division of the trigeminal ganglion are missing in Foxi3 mutants. Our data suggest that Foxi3 is necessary to prime pre-placodal ectoderm for the correct interpretation of inductive signals for the otic and epibranchial placodes.
Although spatiotemporal changes of the glycome (full set of glycans, otherwise known as saccharides or carbohydrates) during placenta formation (placentation) are functionally and clinically important, they are poorly defined. Here, we elucidated novel aspects of the glycome during mouse placentation, from embryonic day 6.5 (E6.5) to E12.5, by investigating the largely unexplored binding distribution of lectin I from Bandeiraea simplicifolia (BS-I lectin), a glycan-binding protein that recognizes the DGalNAc and DGal glycans found at the terminal ends of specific oligosaccharides attached to lipids or proteins. We show that BS-I lectin binding marks all trophoblast cells during early placentation (E7.5 and E8.5 stages), continues in labyrinthine and junctional zone trophoblast but is lost from parietal trophoblast giant cells by E10.5/E11.5 (definitive placenta stage) and is lost from all trophoblast types, but marks the fetal capillary endothelium of the labyrinth, by E12.5. In the decidua basalis (the maternal part of the placenta), BS-I lectin positivity mainly marks the decidual stroma cells of the venous sinusoid area (E7.5 and E8.5 stages) and the entire decidua basalis by E10.5, as well as the osteopontin-positive subset of uterine natural killer (uNK) cells from E7.5 onwards. This work provides the first comprehensive description of the hitherto ill-defined spatiotemporal binding distribution of BS-I lectin in the fetal and maternal placenta between E6.5 and E12.5, thereby contributing to glycome elucidation during placentation. It also establishes BS-I lectin positivity as a novel pan-trophoblast marker during early placentation and as a new marker for mature uNK cells from E7.5 onwards. Anat Rec, 296:921-932, 2013. V C 2013 Wiley Periodicals, Inc.Key words: glycome; Bandeiraea simplicifolia lectin I; placenta; trophoblast development; uNK cellsThe glycome, or complete set of glycans (sugars or saccharides), of an organ includes the glycan part of all glycoconjugates (proteins or lipids covalently attached to glycans) present in it. Although glycans are best known for their ubiquitous role in energy metabolism, they also have more specific functions during embryonic development by
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