| First Author | Ohmura T | Year | 2012 |
| Journal | Dev Dyn | Volume | 241 |
| Issue | 8 | Pages | 1350-64 |
| PubMed ID | 22689267 | Mgi Jnum | J:185597 |
| Mgi Id | MGI:5429465 | Doi | 10.1002/dvdy.23816 |
| Citation | Ohmura T, et al. (2012) Neural tube defects by NUAK1 and NUAK2 double mutation. Dev Dyn 241(8):1350-64 |
| abstractText | 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 alpha-tubulin-positive microtubules was poor. However, the distribution of F-actin, cortactin, Shroom3, Rho, myosin heavy chain IIB, phosphorylated myosin light chain 2, alpha-tubulin, gamma-tubulin, or acetylated alpha-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 alpha-tubulin-positive microtubules did not develop significantly. Developmental Dynamics 241:1350-1364, 2012. (c) 2012 Wiley Periodicals, Inc. |
