High impact information on mpp5

• Mosaic analysis indicates that the nok retinal patterning phenotype is not cell-autonomous [1].
• We show that nok encodes a membrane-associated guanylate kinase-family scaffolding protein [1].
• We propose that nok function in patterning of postmitotic neurons is mediated through neuroepithelial cells and is necessary for guiding neurons to their proper destinations in retinal laminae [1].
• The zebrafish heart and mind (had) mutation, which disrupts the alpha1B1 subunit of Na(+),K(+) ATPase, causes heart tube elongation defects and other developmental abnormalities that are reminiscent of several epithelial cell polarity mutants, including nagie oko (nok) [2].
• Heart and soul/PRKCi and nagie oko/Mpp5 regulate myocardial coherence and remodeling during cardiac morphogenesis [3].

Biological context of mpp5

• This study defines three steps that are required for brain ventricle development and that occur independently of circulation: (1) morphogenesis of the neural tube, requiring nok function; (2) lumen inflation requiring atp1a1a.1 function; and (3) localized cell proliferation [4].

Anatomical context of mpp5

• Here, by analyzing the adhering properties of photoreceptors in zebrafish N-cad and nok mutants, we demonstrated for the first time that the nok gene is essential for the establishment and/or maintenance of the OLM [5].

Other interactions of mpp5

• Initial formation of zebrafish brain ventricles occurs independently of circulation and requires the nagie oko and snakehead/atp1a1a.1 gene products [4].

References