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Nap1l1  -  nucleosome assembly protein 1-like 1

Mus musculus

Synonyms: AA407126, AI256722, Brain protein DN38, D10Ertd68e, NAP-1, ...
 
 
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High impact information on Nap1l1

  • Axis specification and morphogenesis in the mouse embryo require Nap1, a regulator of WAVE-mediated actin branching [1].
  • Thus, the Nap1 mutant phenotypes define the crucial roles of Nap1/WAVE-mediated actin regulation in tissue organization and establishment of the body plan of the mammalian embryo [1].
  • The axis duplications arise because Nap1 is required for the normal polarization and migration of cells of the Anterior Visceral Endoderm (AVE), an early extraembryonic organizer tissue [1].
  • Other morphogenetic processes appear to proceed normally in the absence of Nap1/WAVE activity: the notochord, the layers of the heart, and the epithelial-to-mesenchymal transition (EMT) at gastrulation appear normal [1].
  • Nap1 mutants show specific morphogenetic defects: they fail to close the neural tube, fail to form a single heart tube (cardia bifida), and show delayed migration of endoderm and mesoderm [1].
 

Biological context of Nap1l1

  • TSPY contains a SET/NAP domain that is present in a family of cyclin B and/or histone binding proteins represented by the oncoprotein SET and the nucleosome assembly protein 1 (NAP1), involved in cell cycle regulation and replication [2].
  • A striking phenotype seen in approximately one quarter of Nap1 mutants is the duplication of the anteroposterior body axis [1].
 

Anatomical context of Nap1l1

  • Here, we show that mouse embryos that lack Nap1, a regulatory component of the WAVE complex, arrest at midgestation and have defects in morphogenesis of all three embryonic germ layers [1].

References

 
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