Format

Send to

Choose Destination
See comment in PubMed Commons below
Dev Dyn. 2012 Aug;241(8):1350-64. doi: 10.1002/dvdy.23816. Epub 2012 Jun 22.

Neural tube defects by NUAK1 and NUAK2 double mutation.

Author information

1
Laboratory for Vertebrate Body Plan, Center for Developmental Biology, RIKEN Kobe, Kobe, Japan.

Abstract

BACKGROUND:

NUAK1 and NUAK2, members of the AMP-activated protein kinase family of serine/threonine kinases, are prominently expressed in neuroectoderm, but their functions in neurulation have not been elucidated.

RESULTS:

NUAK1 and NUAK2 double mutants exhibited exencephaly, facial clefting, and spina bifida. Median hinge point was formed, but dorsolateral hinge point formation was not apparent in cranial neural plate; neither apical constriction nor apico-basal elongation took place efficiently in the double mutants during the 5-10-somite stages. Concomitantly, the apical concentration of phosphorylated myosin light chain 2, F-actin, and cortactin was insignificant, and development of acetylated α-tubulin-positive microtubules was poor. However, the distribution of F-actin, cortactin, Shroom3, Rho, myosin heavy chain IIB, phosphorylated myosin light chain 2, α-tubulin, γ-tubulin, or acetylated α-tubulin was apparently normal in the double mutant neuroepithelia at the 5-somite stage.

CONCLUSIONS:

NUAK1 and NUAK2 complementarily function in the apical constriction and apico-basal elongation that associate with the dorsolateral hinge point formation in cephalic neural plate during the 5- to 10-somite stages. In the double mutant neural plate, phosphorylated myosin light chain 2, F-actin, and cortactin did not concentrate efficiently in apical surfaces, and acetylated α-tubulin-positive microtubules did not develop significantly.

PMID:
22689267
DOI:
10.1002/dvdy.23816
[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Support Center