High impact information on oep

• The zebrafish EGF-CFC gene one-eyed pinhead (oep) is required zygotically for the formation of the ventral neuroectoderm, endoderm, and prechordal plate [1].
• Mutations in oep eliminate the response to Squint and Cyclops overexpression but are suppressed by expression of Activin and activated forms of the type I receptor ActRIB and Smad2 [1].
• Widespread misexpression of both membrane-attached and secreted forms of oep rescues prechordal plate and forebrain development in mutant embryos but does not lead to the ectopic induction of these cell types in wild-type fish [2].
• The zebrafish one-eyed pinhead (oep) mutation disrupts embryonic development, resulting in cyclopia and defects in endoderm, prechordal plate, and ventral neuroectoderm formation [2].
• Here, we show that spt and oep genetically interact and are together essential for the formation of cardiac and somitic mesoderm [3].

Biological context of oep

• Second, combining zygotic mutations in ace/fgf8 and oep disrupts mesoderm formation, a phenotype that is not produced by either mutation alone and is consistent with our model of an interdependence of Fgf8 and Nodal pathways through the genetic regulation of the Nodal co-factor Oep and the cell propagation of Nodal signalling [4].
• We conclude that, in addition to a role in Nodal signaling, One-eyed pinhead is required for aspects of cell movement, possibly by regulating cell adhesion [5].
• To understand the cell behavior and cell-cell interaction during floor-plate development, the distribution and gene expression of wild-type and oep mutant cells in genetic mosaics were examined [6].

Anatomical context of oep

• Further decreasing Oep levels by removing maternal oep products aggravates the mesodermal defects in double mutants by disrupting the fate of the entire mesoderm [4].
• Overexpression of mixer induces ectopic sox17-expressing cells in wild-type embryos and promotes endoderm formation in oep mutants, but does not rescue sox17 expression or endoderm formation in casanova mutants [7].
• Following ubiquitous maternal and zygotic expression, highest levels of oep mRNA are found in the gastrula margin and in axial structures and forebrain [2].
• The sonic hedgehog (shh).gene is expressed in the notochord of oep animals [8].
• Our data suggest that both oep and ntl act in the blastoderm margin to specify mesendodermal cell fates [8].

Associations of oep with chemical compounds

• Lithium treatment of oep mutants still leads to ectopic gsc induction but not maintenance, suggesting that oep acts downstream of inducers of dorsal mesoderm [8].

Regulatory relationships of oep

• One-eyed pinhead regulates cell motility independent of Squint/Cyclops signaling [5].

Other interactions of oep

• Together, these results demonstrate synergy between oep and fgf8 that operates with regional differences and is involved in the induction, maintenance, movement and survival of mesodermal cell populations [4].
• Overexpression of a constitutively active form of the type I transforming growth factor beta (TGF-beta) receptor TARAM-A also promotes sox17 expression in wild-type and oep mutant embryos, but not in casanova mutants [7].
• These results reveal a redundant function of oep and ntl in mesoderm formation [8].
• Embryos lacking zygotic oep (Zoep mutants) display cardia bifida and, as we show here, also display reduced or absent nkx2.5 expression [9].
• In this paper, we investigate the relationships between bmp2b, oep, gata5, and nkx2 [9].

References