Faculty Profiles - MIYATA, Takaki

Papers - MIYATA, Takaki

Division display 1 - 20 of about 131 ／ All the affair displays >>

CD206+ macrophages transventricularly infiltrate the early embryonic cerebral wall to differentiate into microglia Reviewed International coauthorship

Yuki Hattori, Daisuke Kato, Futoshi Murayama, Sota Koike, Hisa Asai, Ayato Yamasaki, Yu Naito, Ayano Kawaguchi, Hiroyuki Konishi, Marco Prinz, Takahiro Masuda, Hiroaki Wake, Takaki Miyata

Cell Reports Vol. 42 ( 2 ) page： 112092 - 112092 2023.2

Transient microglial absence assists postmigratory neurons in proper differentiation. Reviewed

Hattori Y, Naito Y, Tsugawa Y, Nonaka S, Wake H, Nagasawa T, Kawaguchi A, Miyata T.

Nature Communications Vol. 11 page： 1631 2020.4

Dorsal-to-Ventral Cortical Expansion Is Physically Primed by Ventral Streaming of Early Embryonic Preplate Neurons. Reviewed

Saito K, Okamoto M, Watanabe Y, Noguchi N, Nagasaka A, Nishina Y, Shinoda T, Sakakibara A, Miyata T

Cell Reports Vol. 29 ( 6 ) page： 1555 - 1567.e5 2019.11

Authorship：Last author,　Corresponding author Language：English Publisher：Cell Reports

Embryonic radial glial fibers that guide most neocortical neurons are ventrally deflected near their terminal, contributing to further expansion of the neocortical area. Saito et al. demonstrate that this fiber deflection is induced physically by a previously unrecognized ventral stream of the earliest generated preplate neurons.

DOI： 10.1016/j.celrep.2019.09.075

Scopus

PubMed

Differentiating cells mechanically limit the interkinetic nuclear migration of progenitor cells to secure apical cytogenesis Reviewed

Watanabe Yuto, Kawaue Takumi, Miyata Takaki

DEVELOPMENT Vol. 145 ( 14 ) 2018.7

Elasticity-based boosting of neuroepithelial nucleokinesis via indirect energy transfer from mother to daughter. Reviewed

Shinoda T, Nagasaka A, Inoue Y, Higuchi R, Minami Y, Kato K, Suzuki M, Kondo T, Kawaue T, Saito K, Ueno N, Fukazawa Y, Nagayama M, Miura T, Adachi T, Miyata T

PLoS Biology Vol. 16 ( 4 ) page： e2004426 2018.4

TAG-1-assisted progenitor elongation streamlines nuclear migration to optimize subapical crowding Reviewed

Okamoto, M., Namba, T., Shinoda, T., Kondo, T., Watanabe, T., Inoue, Y., Takeuchi, K., Enomoto, Y., Ota, K., Oda, K., Wada, Y., Sagou, K., Saito, K., Sakakibara, A., Kawaguchi, A., Nakajima, K., Adachi, T., Fujimori, T., Ueda, M. Hayashi, S., Kaibuchi, K., Miyata, T.

Nature Neuroscience Vol. 16 page： 1556-1566 2013.9

Migration, early axonogenesis, and Reelin-dependent layer-forming behavior of early/posterior-born Purkinje cells in the developing mouse lateral cerebellum. Reviewed

Miyata, T., Ono Y, Okamoto M, Masaoka M, Sakakibara A, Kawaguchi A, Hashimoto M, Ogawa M

Neural Development Vol. 5 ( 3 ) page： 1-21 2010

Asymmetric production of surface-dividing and non-surface-dividing cortical progenitor cells. Reviewed

Miyata, T., Kawaguchi, A., Saito, K., Kawano, M., Muto, T., and Ogawa, M.

Development Vol. 131 page： 3133-3145 2004

Asymmetric inheritance of radial glial fibers by cortical neurons. Reviewed

Miyata, T., Kawaguchi, A., Okano, H., and Ogawa, M.

Neuron Vol. 31 page： 727-741 2001

NeuroD is required for differentiation of the granule cells in the cerebellum and hippocampus. Reviewed

Miyata, T., Maeda, T., and Lee, J.E.

Genes & Dev. Vol. 13 page： 1647-1652 1999

Regulation of Purkinje cell alignment by Reelin as revealed with CR-50 antibody. Reviewed

Miyata, T., Nakajima, K., Mikoshiba, K., and Ogawa, M.

J. Neurosci. Vol. 17 page： 3599-3609 1997

Quantitative in toto live imaging analysis of apical nuclear migration in the mouse telencephalic neuroepithelium Reviewed

Shimamura T, Miyata T.

Development, Growth, Differentiation 2024.12

A novel preparation for histological analyses of intraventricular macrophages in the embryonic brain Reviewed

Futoshi Murayama, Hisa Asai, Arya Kirone Patra, Hiroaki Wake, Takaki Miyata, Yuki Hattori

Development, Growth & Differentiation 2024.6

Endothelial cells regulate alveolar morphogenesis by constructing basement membranes acting as a scaffold for myofibroblasts Reviewed International journal

Haruko Watanabe-Takano, Katsuhiro Kato, Eri Oguri-Nakamura, Tomohiro Ishii, Koji Kobayashi, Takahisa Murata, Koichiro Tsujikawa, Takaki Miyata, Yoshiaki Kubota, Yasuyuki Hanada, Koichi Nishiyama, Tetsuro Watabe, Reinhard Fässler, Hirotaka Ishii, Naoki Mochizuki, Shigetomo Fukuhara

Nature Communications Vol. 15 ( 1 ) page： 1622 2024.3

Mechanical and physical interactions involving neocortical progenitor cells Invited Reviewed

Takaki Miyata

Neocortical Neurogenesis in Development and Evolution page： 119 - 136 2023.8

Analyzing the effect of cell rearrangement on Delta-Notch pattern formation

Toshiki Oguma, Hisako Takigawa-Imamura, Tomoyasu Shinoda, Shuntaro Ogura, Akiyoshi Uemura, Takaki Miyata, Philip K. Maini, Takashi Miura

Physical Review E Vol. 107 ( 6 ) page： 064404 2023.6

Actin crosslinking by α-actinin averts viscous dissipation of myosin force transmission in stress fibers. Reviewed

Katsuta H, Okuda S, Nagayama K, Machiyama H, Kidoaki S, Kato M, Sokabe M, Miyata T, Hirata H

iScience Vol. 26 ( 3 ) page： 106090 2023.3

Language：English Publishing type：Research paper (scientific journal) Publisher：iScience

Contractile force generated in actomyosin stress fibers (SFs) is transmitted along SFs to the extracellular matrix (ECM), which contributes to cell migration and sensing of ECM rigidity. In this study, we show that efficient force transmission along SFs relies on actin crosslinking by α-actinin. Upon reduction of α-actinin-mediated crosslinks, the myosin II activity induced flows of actin filaments and myosin II along SFs, leading to a decrease in traction force exertion to ECM. The fluidized SFs maintained their cable integrity probably through enhanced actin polymerization throughout SFs. A computational modeling analysis suggested that lowering the density of actin crosslinks caused viscous slippage of actin filaments in SFs and, thereby, dissipated myosin-generated force transmitting along SFs. As a cellular scale outcome, α-actinin depletion attenuated the ECM-rigidity-dependent difference in cell migration speed, which suggested that α-actinin-modulated SF mechanics is involved in the cellular response to ECM rigidity.

DOI： 10.1016/j.isci.2023.106090

Scopus

PubMed

Functional Cooperation of α-Synuclein and Tau Is Essential for Proper Corticogenesis. Reviewed

Wang S, Fu Y, Miyata T, Matsumoto S, Shinoda T, Itoh K, Harada A, Hirotsune S, Jin M

The Journal of neuroscience : the official journal of the Society for Neuroscience Vol. 42 ( 37 ) page： 7031 - 7046 2022.9

Language：English Publisher：Journal of Neuroscience

Alpha-synuclein (aSyn) and tau are abundant multifunctional neuronal proteins, and their intracellular deposits have been linked to many neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease. Despite the disease relevance, their physiological roles remain elusive, as mice with knock-out of either of these genes do not exhibit overt phenotypes. To reveal functional cooperation, we generated aSyn2/2tau2/2 double-knock-out mice and characterized the functional cross talk between these proteins during brain development. Intriguingly, deletion of aSyn and tau reduced Notch signaling and accelerated interkinetic nuclear migration of G2 phase at early embryonic stage. This significantly altered the balance between the proliferative and neurogenic divisions of progenitor cells, resulting in an overproduction of early born neurons and enhanced neurogenesis, by which the brain size was enlarged during the embryonic stage in both sexes. On the other hand, a reduction in the number of neural progenitor cells in the middle stage of corticogenesis diminished subsequent gliogenesis in the aSyn2/2tau2/2 cortex. Additionally, the expansion and maturation of macroglial cells (astrocytes and oligodendrocytes) were suppressed in the aSyn2/2tau2/2 postnatal brain, which in turn reduced the male aSyn2/2tau2/2 brain size and cortical thickness to less than the control values. Our study identifies important functional cooperation of aSyn and tau during corticogenesis.

DOI： 10.1523/JNEUROSCI.0396-22.2022

Scopus

PubMed

Border-associated macrophages transventricularly infiltrate the early embryonic cerebral wall to differentiate into microglia

Yuki Hattori, Daisuke Kato, Futoshi Murayama, Sota Koike, Yu Naito, Ayano Kawaguchi, Hiroaki Wake, Takaki Miyata

2022.7

Publisher：Cold Spring Harbor Laboratory

Summary

The relationships between microglia and macrophages, especially their lineage segregation outside the yolk sac, have been recently explored, providing a model in which a conversion from macrophages seeds microglia during brain development. However, spatiotemporal evidence to support such microglial seeding and to explain how it occurs has not been obtained. By cell tracking via slice culture, intravital imaging, and Flash tag-mediated labeling, we found that a group of intraventricular macrophages belonging to border-associated macrophages (BAMs), which were abundantly observed along the inner surface of the mouse cerebral wall at embryonic day 12, frequently entered the brain wall. Immunohistochemistry of the tracked cells showed that postinfiltrative BAMs acquired microglial properties while losing a macrophage phenotype. We also found that the intraventricular BAMs were supplied transepithelially from the roof plate. Thus, this study demonstrates that the “roof plate→ventricle→cerebral wall” route is an essential path for microglial colonization into the embryonic mouse brain.

DOI： 10.1101/2022.07.27.501563

Mid1 is associated with androgen-dependent axonal vulnerability of motor neurons in spinal and bulbar muscular atrophy. Reviewed

Ogura Y, Sahashi K, Hirunagi T, Iida M, Miyata T, Katsuno M

Cell death & disease Vol. 13 ( 7 ) page： 601 2022.7

Language：English Publisher：Cell Death and Disease

Spinal and bulbar muscular atrophy (SBMA) is an adult-onset hereditary neurodegenerative disease caused by the expansions of CAG repeats in the androgen receptor (AR) gene. Androgen-dependent nuclear accumulation of pathogenic AR protein causes degeneration of lower motor neurons, leading to progressive muscle weakness and atrophy. While the successful induction of SBMA-like pathology has been achieved in mouse models, mechanisms underlying motor neuron vulnerability remain unclear. In the present study, we performed a transcriptome-based screening for genes expressed exclusively in motor neurons and dysregulated in the spinal cord of SBMA mice. We found upregulation of Mid1 encoding a microtubule-associated RNA binding protein which facilitates the translation of CAG-expanded mRNAs. Based on the finding that lower motor neurons begin expressing Mid1 during embryonic stages, we developed an organotypic slice culture system of the spinal cord obtained from SBMA mouse fetuses to study the pathogenic role of Mid1 in SBMA motor neurons. Impairment of axonal regeneration arose in the spinal cord culture in SBMA mice in an androgen-dependent manner, but not in mice with non-CAG-expanded AR, and was either exacerbated or ameliorated by Mid1 overexpression or knockdown, respectively. Hence, an early Mid1 expression confers vulnerability to motor neurons, at least by inducing axonogenesis defects, in SBMA.

DOI： 10.1038/s41419-022-05001-6

Scopus

PubMed

　 PREV - NEXT 　

<MIYATA, Takaki>

Papers - MIYATA, Takaki