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Development 2010 Jul 01;13714:2329-39. doi: 10.1242/dev.048769.
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MID1 and MID2 are required for Xenopus neural tube closure through the regulation of microtubule organization.

Suzuki M , Hara Y , Takagi C , Yamamoto TS , Ueno N .

Closure of the neural tube requires both the change and maintenance of cell shape. The change occurs mainly through two coordinated morphogenetic events: cell elongation and apical constriction. How cytoskeletal elements, including microtubules, are regulated in this process in vivo is largely unknown. Here, we show that neural tube closure in Xenopus depends on orthologs of two proteins: MID1, which is responsible for Opitz G/BBB syndrome in humans, and its paralog MID2. Depletion of the Xenopus MIDs (xMIDs) by morpholino-mediated knockdown disrupted epithelial morphology in the neural plate, leading to neural tube defects. In the xMID-depleted neural plate, the normal epithelial organization was perturbed without affecting neural fate. Furthermore, the xMID knockdown destabilized and caused the disorganization of microtubules, which are normally apicobasally polarized, accounting for the abnormal phenotypes. We also found that the xMIDs and their interacting protein Mig12 were coordinately required for microtubule stabilization during remodeling of the neural plate. Finally, we showed that the xMIDs are required for the formation of multiple epithelial organs. We propose that similar MID-governed mechanisms underlie the normal morphogenesis of epithelial tissues and organs, including the tissues affected in patients with Opitz G/BBB syndrome.

PubMed ID: 20534674
Article link: Development

Species referenced: Xenopus laevis
Genes referenced: actb actl6a cad casp3.2 cat.2 cdh2 cdh3 ctnnb1 en1 fn1 foxa2 foxa4 gli1 gli3 h3-3a krt12.4 lamb2 mapt mid1 mid1ip1 mid2 ncam1 pax3 ptch2 shh shroom3 sox2 tbx2 tjp1 tub tuba4b tubb2b
Antibodies: Casp3 Ab3 Cdh3 Ab1 Ctnnb1 Ab6 H3f3a Ab9 Lama1 Ab1 Lama1 Ab2 Neuronal Ab5 Notochord Ab2 Sox2 Ab2 Tuba4b Ab2 Tuba4b Ab5
Morpholinos: mid1 MO1 mid1ip1 MO1

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