Tumorhead distribution to cytoplasmic membrane of neural plate cells is positively regulated by Xenopus p21-activated kinase 1 (X-PAK1)
|Author(s)||Wu Chuan-Fen1, 4, Delsert Claude2, 3, Faure Sandrine2, Traverso Edwin E.1, Kloc Malgorzata1, 5, Kuang Jian4, Etkin Laurence D.1, Morin Nathalie2|
|Affiliation(s)||1 : Univ Texas, MD Anderson Canc Ctr, Dept Mol Genet, Houston, TX 77030 USA.
2 : CRBM, UMR 5237, CNRS, F-34291 Montpellier, France.
3 : IFREMER, LGP, F-17390 La Tremblade, France.
4 : Univ Texas, MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77030 USA.
5 : Univ Texas, MD Anderson Canc Ctr, Dept Biochem & Mol Biol, Houston, TX 77030 USA.
|Source||Developmental Biology (0012-1606) (Elsevier), 2007-08 , Vol. 308 , N. 1 , P. 169-186|
|WOS© Times Cited||3|
|Keyword(s)||Actin cytoskeleton, Differentiation, Proliferation, Neural plate, P21 activated kinase, Tumorhead|
|Abstract||Tumorhead (TH) regulates neural plate cell proliferation during Xenopus early development, and gain or loss of function prevents neural differentiation. TH shuttles between the nuclear and cytoplasmic/cortical cell compartments in embryonic cells. In this study, we show that subcellular distribution of TH is important for its functions. Targeting TH to the cell cortex/membrane potentiates a TH gain of function phenotype and results in neural plate expansion and inhibition of neuronal differentiation. We have found that TH subcellular localization is regulated, and that its shuttling between the nucleus and the cell cortex/cytoplasm is controlled by the catalytic activity of p21-activated kinase, X-PAK1. The phenotypes of embryos that lack, or have excess, X-PAK1 activity mimic the phenotypes induced by loss or gain of TH functions, respectively. We provide evidence that X-PAK1 is an upstream regulator of TH and discuss potential functions of TH at the cell cortex/cytoplasmic membrane and in the nucleus.