Yuko Nishiwaki
Okinawa Institute of Science and Technology
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Featured researches published by Yuko Nishiwaki.
Development | 2003
Ichiro Masai; Zsolt Lele; Masahiro Yamaguchi; Atsuko Komori; Asuka Nakata; Yuko Nishiwaki; Hironori Wada; Hideomi Tanaka; Yasuhiro Nojima; Matthias Hammerschmidt; Stephen W. Wilson; Hitoshi Okamoto
The complex, yet highly ordered and predictable, structure of the neural retina is one of the most conserved features of the vertebrate central nervous system. In all vertebrate classes, retinal neurons are organized into laminae with each neuronal class adopting specific morphologies and patterns of connectivity. Using genetic analyses in zebrafish, we demonstrate that N-cadherin (Ncad) has several distinct and crucial functions during the establishment of retinal organization. Although the location of cell division is disorganized in embryos with reduced or no Ncad function, different classes of retinal neurons are generated. However, these neurons fail to organize into correct laminae, most probably owing to compromised adhesion between retinal cells. In addition, amacrine cells exhibit exuberant and misdirected outgrowth of neurites that contributes to severe disorganization of the inner plexiform layer. Retinal ganglion cells also exhibit defects in process outgrowth, with axons exhibiting fasciculation defects and adopting incorrect ipsilateral trajectories. At least some of these defects are likely to be due to a failure to maintain compartment boundaries between eye, optic nerve and brain. Although in vitro studies have implicated Fgf receptors in modulating the axon outgrowth promoting properties of Ncad, most aspects of the Ncad mutant phenotype are not phenocopied by treatments that block Fgf receptor function.
Development | 2005
Hironori Wada; Miki Iwasaki; Tomomi Sato; Ichiro Masai; Yuko Nishiwaki; Hideomi Tanaka; Atsushi Sato; Yasuhiro Nojima; Hitoshi Okamoto
In the developing vertebrate hindbrain, the characteristic trajectory of the facial (nVII) motor nerve is generated by caudal migration of the nVII motor neurons. The nVII motor neurons originate in rhombomere (r) 4, and migrate caudally into r6 to form the facial motor nucleus. In this study, using a transgenic zebrafish line that expresses green fluorescent protein (GFP) in the cranial motor neurons, we isolated two novel mutants, designated landlocked (llk) and off-road (ord), which both show highly specific defects in the caudal migration of the nVII motor neurons. We show that the landlocked locus contains the gene scribble1 (scrb1), and that its zygotic expression is required for migration of the nVII motor neurons mainly in a non cell-autonomous manner. Taking advantage of the viability of the llk mutant embryos, we found that maternal expression of scrb1 is required for convergent extension (CE) movements during gastrulation. Furthermore, we show a genetic interaction between scrb1 and trilobite(tri)/strabismus(stbm) in CE. The dual roles of the scrb1 gene in both neuronal migration and CE provide a novel insight into the underlying mechanisms of cell movement in vertebrate development.
Developmental Cell | 2013
Yuko Nishiwaki; Asuka Yoshizawa; Yutaka Kojima; Eri Oguri; Shohei Nakamura; Shohei Suzuki; Junichi Yuasa-Kawada; Mariko Kinoshita-Kawada; Toshiaki Mochizuki; Ichiro Masai
Intracellular vesicular transport is important for photoreceptor function and maintenance. However, the mechanism underlying photoreceptor degeneration in response to vesicular transport defects is unknown. Here, we report that photoreceptors undergo apoptosis in a zebrafish β-soluble N-ethylmaleimide-sensitive factor attachment protein (β-SNAP) mutant. β-SNAP cooperates with N-ethylmaleimide-sensitive factor to recycle the SNAP receptor (SNARE), a key component of the membrane fusion machinery, by disassembling the cis-SNARE complex generated in the vesicular fusion process. We found that photoreceptor apoptosis in the β-SNAP mutant was dependent on the BH3-only protein BNip1. BNip1 functions as a component of the syntaxin-18 SNARE complex and regulates retrograde transport from the Golgi to the endoplasmic reticulum. Failure to disassemble the syntaxin-18 cis-SNARE complex caused BNip1-dependent apoptosis. These data suggest that the syntaxin-18 cis-SNARE complex functions as an alarm factor that monitors vesicular fusion competence and that BNip1 transforms vesicular fusion defects into photoreceptor apoptosis.
Scientific Reports | 2017
Maria Iribarne; Yuko Nishiwaki; Shohei Nakamura; Masato Araragi; Eri Oguri; Ichiro Masai
Genetic mutations in aryl hydrocarbon receptor interacting protein-like 1 (AIPL1) cause photoreceptor degeneration associated with Leber congenital amaurosis 4 (LCA4) in human patients. Here we report retinal phenotypes of a zebrafish aipl1 mutant, gold rush (gosh). In zebrafish, there are two aipl1 genes, aipl1a and aipl1b, which are expressed mainly in rods and cones, respectively. The gosh mutant gene encodes cone-specific aipl1, aipl1b. Cone photoreceptors undergo progressive degeneration in the gosh mutant, indicating that aipl1b is required for cone survival. Furthermore, the cone-specific subunit of cGMP phosphodiesterase 6 (Pde6c) is markedly decreased in the gosh mutant, and the gosh mutation genetically interacts with zebrafish pde6c mutation eclipse (els). These data suggest that Aipl1 is required for Pde6c stability and function. In addition to Pde6c, we found that zebrafish cone-specific guanylate cyclase, zGc3, is also decreased in the gosh and els mutants. Furthermore, zGc3 knockdown embryos showed a marked reduction in Pde6c. These observations illustrate the interdependence of cGMP metabolism regulators between Aipl1, Pde6c, and Gc3 in photoreceptors.
Development | 2018
Toshiaki Mochizuki; Yutaka Kojima; Yuko Nishiwaki; Tetsuya Harakuni; Ichiro Masai
ABSTRACT In vertebrate lens, lens epithelial cells cover the anterior half of the lens fiber core. Lens epithelial cells proliferate, move posteriorly and start to differentiate into lens fiber cells at the lens equator. Although FGF signaling promotes this equatorial commencement of lens fiber differentiation, the underlying mechanism is not fully understood. Here, we show that lens epithelial cells abnormally enter lens fiber differentiation without passing through the equator in zebrafish vps45 mutants. VPS45 belongs to the Sec1/Munc18-like protein family and promotes endosome trafficking, which differentially modulates signal transduction. Ectopic lens fiber differentiation in vps45 mutants does not depend on FGF, but is mediated through activation of TGFβ signaling and inhibition of canonical Wnt signaling. Thus, VPS45 normally suppresses lens fiber differentiation in the anterior region of lens epithelium by modulating TGFβ and canonical Wnt signaling pathways. These data indicate a novel role of endosome trafficking to ensure equator-dependent commencement of lens fiber differentiation. Summary: The endocytic regulator VPS45 suppresses FGF-independent lens fiber differentiation and ensures the spatial pattern of lens development.
Mechanisms of Development | 2008
Yuko Nishiwaki; Atsuko Komori; Hiroshi Sagara; Emiko Suzuki; Tomonori Manabe; Toshihiko Hosoya; Yasuhiro Nojima; Hironori Wada; Hideomi Tanaka; Hitoshi Okamoto; Ichiro Masai
Developmental Biology | 2014
Fumiyasu Imai; Asuka Yoshizawa; Ayako Matsuzaki; Eri Oguri; Masato Araragi; Yuko Nishiwaki; Ichiro Masai
The Japanese Biochemical Society/The Molecular Biology Society of Japan | 2017
Yuko Nishiwaki; Ichiro Masai
The Molecular Biology Society of Japan | 2016
Yuko Nishiwaki; Miyuki Suenaga; Masato Araragi; Ichiro Masai
The Molecular Biology Society of Japan | 2016
Nishtha Ranawat; Yuko Nishiwaki; Ichiro Masai