Faculty Profiles - HISAMOTO, Naoki

Papers - HISAMOTO, Naoki

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The C. elegans BRCA2-ALP/Enigma Complex Regulates Axon Regeneration via a Rho GTPase-ROCK-MLC Phosphorylation Pathway Reviewed

Shimizu Tatsuhiro, Pastuhov Strahil Iv, Hanafusa Hiroshi, Matsumoto Kunihiro, Hisamoto Naoki

Cell reports Vol. 24 ( 7 ) page： 1880 - 1889 2018.8

Phosphatidylserine exposure mediated by ABC transporter activates the integrin signaling pathway promoting axon regeneration Reviewed

Hisamoto Naoki, Tsuge Anna, Pastuhov Strahil Iv, Shimizu Tatsuhiro, Hanafusa Hiroshi, Matsumoto Kunihiro

NATURE COMMUNICATIONS Vol. 9 ( 1 ) page： 3099 2018.8

UNC-16/JIP3 regulates early events in synaptic vesicle protein trafficking via LRK-1/LRRK2 and AP complexes

Choudhary Bikash, Kamak Madhushree, Ratnakaran Neena, Kumar Jitendra, Awasthi Anjali, Li Chun, Nguyen Ken, Matsumoto Kunihiro, Hisamoto Naoki, Koushika Sandhya P.

PLOS GENETICS Vol. 13 ( 11 ) page： e1007100 2017.11

Signal transduction cascades in axon regeneration: insights from C. elegans

Hisamoto Naoki, Matsumoto Kunihiro

CURRENT OPINION IN GENETICS & DEVELOPMENT Vol. 44 page： 54 - 60 2017.6

Higher Precision Rotational Manipulation of C. elegans by Microchannel

Nakajima Masahiro, Igarashi Yu, Takeuchi Masaru, Hisamoto Nagoki, Hasegawa Yasuhisa, Fukuda Toshio

2017 IEEE 17TH INTERNATIONAL CONFERENCE ON NANOTECHNOLOGY (IEEE-NANO) page： 297 - 298 2017

The C. elegans Discoidin Domain Receptor DDR-2 Modulates the Met-like RTK-JNK Signaling Pathway in Axon Regeneration. Reviewed

Hisamoto N, Nagamori Y, Shimizu T, Pastuhov SI, Matsumoto K.

PLoS Genetics Vol. 12 ( 12 ) page： e1006475 2016.12

Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal)

The ability of specific neurons to regenerate their axons after injury is governed by cell-intrinsic regeneration pathways. However, the signaling pathways that orchestrate axon regeneration are not well understood. In Caenorhabditis elegans, initiation of axon regeneration is positively regulated by SVH-2 Met-like growth factor receptor tyrosine kinase (RTK) signaling through the JNK MAPK pathway. Here we show that SVH-4/DDR-2, an RTK containing a discoidin domain that is activated by collagen, and EMB-9 collagen type IV regulate the regeneration of neurons following axon injury. The scaffold protein SHC-1 interacts with both DDR-2 and SVH-2. Furthermore, we demonstrate that overexpression of svh-2 and shc-1 suppresses the delay in axon regeneration observed in ddr-2 mutants, suggesting that DDR-2 functions upstream of SVH-2 and SHC-1. These results suggest that DDR-2 modulates the SVH-2-JNK pathway via SHC-1. We thus identify two different RTK signaling networks that play coordinated roles in the regulation of axonal regeneration.

DOI： 10.1371/journal.pgen.1006475

The core molecular machinery used for engulfment of apoptotic cells regulates the JNK pathway mediating axon regeneration in Caenorhabditis elegans. Reviewed

Pastuhov, S.I., Fujiki, K., Tsuge, A., Asai, K., Ishikawa, S., Hirose, K., Matsumoto, K., Hisamoto, N.

Journal of Neuroscience Vol. 36 ( 37 ) page： 9710-9721 2016.9

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

The mechanisms that govern the ability of specific neurons to regenerate their axons after injury are not well understood. In Caenorhabditis elegans, the initiation of axon regeneration is positively regulated by the JNK-MAPK pathway. In this study, we identify two components functioning upstream of the JNK pathway: the Ste20-related protein kinase MAX-2 and the Rac-type GTPase CED-10. CED-10, when bound by GTP, interacts with MAX-2 and functions as its upstream regulator in axon regeneration. CED-10, in turn, is activated by axon injury via signals initiated from the integrin α-subunit INA-1 and the nonreceptor tyrosine kinase SRC-1 and transmitted via the signaling module CED-2/CrkII-CED-5/Dock180-CED-12/ELMO. This module is also known to regulate the engulfment of apoptotic cells during development. Our findings thus reveal that the molecular machinery used for engulfment of apoptotic cells also promotes axon regeneration through activation of the JNK pathway.

DOI： 10.1523/JNEUROSCI.0453-16.2016

Axotomy-induced HIF/serotonin signaling axis promotes axon regeneration in C. elegans. Reviewed

Alam T, Maruyama H, Li C, Pastuhov SI, Nix P, Bastiani M, Hisamoto N, Matsumoto K.

NATURE COMMUNICATIONS Vol. 7 page： 10388 2016.1

Axon regeneration is regulated by Ets-C/EBP transcription complexes generated by activation of the cAMP/Ca²⁺-p38 MAPK signaling pathways. Reviewed

Chun Li, Naoki Hisamoto, Kunihiro Matsumoto

PLoS Genetics Vol. 11 page： e1005603 2015.10

The C. elegans HGF/plasminogen-like protein SVH-1 has protease-dependent and -independent functions Reviewed

Naoki Hisamoto, Chun Li, Motoki Yoshida, Kunihiro Matsumoto

Cell reports 2014

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

脊椎動物の肝細胞増殖因子(HGF)とプラスミノーゲンは、それぞれ増殖因子と細胞外マトリクス(ECM)を切断するプロテアーゼという全く異なる機能を持つが、構造およびアミノ酸配列の類似性から、共通の祖先遺伝子から分岐したと考えられている。しかし、これらの因子が２つの機能を同時に持つ祖先遺伝子からそれぞれ機能分化したのか、それとも脊椎動物で増殖因子の機能が後発的に獲得されたのか、その進化的経緯は不明であった。我々は以前、線虫C. エレガンスにおいてHGF/プラスミノーゲン様因子SVH-1がHGF受容体ホモログであるSVH-2を介して神経軸索再生を制御することを報告した。今回、我々はSVH-1およびSVH-2遺伝子が他の無脊椎動物でも広く保存されていること、さらにSVH-1がSVH-2非依存的に幼虫の生育を制御することを見出した。SVH-1は機能的なプロテアーゼドメインを持ち、その活性は生育に必須であるが軸索再生には必須ではない。svh-1遺伝子の欠損はECMタンパク質FBL-1の咽頭筋への異常な蓄積を引き起こす。またsvh-1変異体の幼虫期での生育停止の表現型は、fbl-1遺伝子の欠損により部分的に抑圧された。以上の結果から、SVH-1は増殖因子かつプロテアーゼという２つの異なる機能を持った因子であること、またHGFとプラスミノーゲンは両方の機能を持つ祖先型から分岐した可能性が示唆された。

DOI： http://dx.doi.org/10.1016/j.celrep.2014.10.056

Endocannabinoid-Goα signalling inhibits axon regeneration in Caenorhabditis elegans by antagonizing Gqα-PKC-JNK signalling Reviewed

Strahil Iv. Pastuhov, Kota Fujiki, Paola Nix, Shuka Kanao, Michael Bastiani, Kunihiro Matsumoto and Naoki Hisamoto

Nature Communications 2012.10

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

The ability of neurons to regenerate their axons after injury is determined by a balance between cellular pathways that promote and those that inhibit regeneration. In Caenorhabditis elegans, axon regeneration is positively regulated by the c-Jun N-terminal kinase mitogen activated protein kinase pathway, which is activated by growth factor-receptor tyrosine kinase signalling. Here we show that fatty acid amide hydrolase-1, an enzyme involved in the degradation of the endocannabinoid anandamide (arachidonoyl ethanolamide), regulates the axon regeneration response of γ-aminobutyric acid neurons after laser axotomy. Exogenous arachidonoyl ethanolamide inhibits axon regeneration via the Goα subunit GOA-1, which antagonizes the Gqα subunit EGL-30. We further demonstrate that protein kinase C functions downstream of Gqα and activates the MLK-1-MEK-1-KGB-1 c-Jun N-terminal kinase pathway by phosphorylating MLK-1. Our results show that arachidonoyl ethanolamide induction of a G protein signal transduction pathway has a role in the inhibition of post-development axon regeneration.

DOI： 10.1038/ncomms2136

C. elegans growth factor-receptor tyrosine kinase signaling regulates axon regeneration. Reviewed

Li C, Hisamoto N, Nix P, Kanao S, Mizuno T, Bastiani M and Matsumoto K.

Nature Neuroscience Vol. 15 ( 4 ) page： 551-557 2012.4

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

The ability of neurons to undergo regenerative growth after injury is governed by cell-intrinsic and cell-extrinsic regeneration pathways. These pathways represent potential targets for therapies to enhance regeneration. However, the signaling pathways that orchestrate axon regeneration are not well understood. In Caenorhabditis elegans, the Jun N-terminal kinase (JNK) and p38 MAP kinase (MAPK) pathways are important for axon regeneration. We found that the C. elegans SVH-1 growth factor and its receptor, SVH-2 tyrosine kinase, regulate axon regeneration. Loss of SVH-1-SVH-2 signaling resulted in a substantial defect in the ability of neurons to regenerate, whereas its activation improved regeneration. Furthermore, SVH-1-SVH-2 signaling was initiated extrinsically by a pair of sensory neurons and functioned upstream of the JNK-MAPK pathway. Thus, SVH-1-SVH-2 signaling via activation of the MAPK pathway acts to coordinate neuron regeneration response after axon injury.

DOI： 10.1038/nn.3052

Heavy Metal Stress Assay of Caenorhabditis elegans

Pastuhov Strahil Iv, Shimizu Tatsuhiro, Hisamoto Naoki

BIO-PROTOCOL Vol. 7 ( 11 ) page： e2312 2017.6

Endocannabinoid signaling regulates regenerative axon navigation in Caenorhabditis elegans via the GPCRs NPR-19 and NPR-32. Reviewed

Pastuhov SI, Matsumoto K, Hisamoto N.

Genes to Cells Vol. 21 ( 7 ) page： 696-705 2016.7

The chaperone complex BAG2-HSC70 regulates localization of C. elegans Leucine-rich repeat kinase LRK-1 in the Golgi Reviewed

Fukuzono T, Pastuhov SI, Fukushima O, Li C, Hattori A, Iemura S, Natsume T, Shibuya H, Hanafusa H, Matsumoto K, Hisamoto N.

Genes to Cells page： in press 2016

MAP kinase cascades regulating axon regeneration in C. elegans. Invited Reviewed

Pastuhov SI, Hisamoto N., Matsumoto K.

Proc. Jpn. Acad. Ser. B. Phys. Biol. Sci. Vol. 91 page： 63-75 2015

he Caenorhabditis elegans JNK Signaling Pathway Activates Expression of Stress Response Genes by Derepressing the Fos/HDAC Repressor Complex Reviewed

Hattori A, Mizuno T, Akamatsu M, Hisamoto N, Matsumoto K.

PLoS Genetics Vol. 9 page： e1003315 2013.2

Forgetting in C. elegans is accelerated by neuronal communication via the TIR-1/JNK-1 pathway. Reviewed

Inoue A, Sawatari E, Hisamoto N, Kitazono T, Teramoto T, Fujiwara M, Matsumoto K, Ishihara T.

Cell Reports Vol. 3 page： 808-816 2013.2

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

The control of memory retention is important for proper responses to constantly changing environments, but the regulatory mechanisms underlying forgetting have not been fully elucidated. Our genetic analyses in C. elegans revealed that mutants of the TIR-1/JNK-1 pathway exhibited prolonged retention of olfactory adaptation and salt chemotaxis learning. In olfactory adaptation, conditioning induces attenuation of odor-evoked Ca(2+) responses in olfactory neurons, and this attenuation is prolonged in the TIR-1/JNK-1-pathway mutant animals. We also found that a pair of neurons in which the pathway functions is required for the acceleration of forgetting, but not for sensation or adaptation, in wild-type animals. In addition, the neurosecretion from these cells is important for the acceleration of forgetting. Therefore, we propose that these neurons accelerate forgetting through the TIR-1/JNK-1 pathway by sending signals that directly or indirectly stimulate forgetting.

DOI： 10.1016/j.celrep.2013.02.019

Dysregulated LRRK2 signaling in response to endoplasmic reticulum stress leads to dopaminergic neuron degeneration in C. elegans. Reviewed

Yuan Y, Cao P, Smith MA, Kramp K, Huang Y, Hisamoto N, Matsumoto K, Hatzoglou M, Jin H, Feng Z.

PLoS One Vol. 6 ( 8 ) page： e22354 2011.8

Axon regeneration requires coordinate activation of p38 and JNK MAPK pathways. Reviewed

Nix P, Hisamoto N, Matsumoto K, Bastiani M.

Proceedings of the National Academy of Sciences of the United States of America Vol. 108 ( 26 ) page： 10738-10743 2011.6

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Papers - HISAMOTO, Naoki