Plexin-B1 is a GTPase activating protein for M-Ras, remodelling dendrite morphology

Yasuhiro Saito, Izumi Oinuma, Satoshi Fujimoto, Manabu Negishi

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

Plexins are receptors for axonal guidance molecules known as semaphorins. We recently reported that the semaphorin 4D (Sema4D) receptor, Plexin-B1, induces axonal growth cone collapse by functioning as an R-Ras GTPase activating protein (GAP). Here, we report that Plexin-B1 shows GAP activity for M-Ras, another member of the Ras family of GTPases. In cortical neurons, the expression of M-Ras was upregulated during dendritic development. Knockdown of endogenous M-Ras-but not R-Ras-reduced dendritic outgrowth and branching, whereas overexpression of constitutively active M-Ras, M-Ras(Q71L), enhanced dendritic outgrowth and branching. Sema4D suppressed M-Ras activity and reduced dendritic outgrowth and branching, but this reduction was blocked by M-Ras(Q71L). M-Ras(Q71L) stimulated extracellular signal-regulated kinase (ERK) activation, inducing dendrite growth, whereas Sema4D suppressed ERK activity and down-regulation of ERK was required for a Sema4D-induced reduction of dendrite growth. Thus, we conclude that Plexin-B1 is a dual functional GAP for R-Ras and M-Ras, remodelling axon and dendrite morphology, respectively.

Original languageEnglish
Pages (from-to)614-621
Number of pages8
JournalEMBO Reports
Volume10
Issue number6
DOIs
Publication statusPublished - May 18 2009
Externally publishedYes

Fingerprint

ras GTPase-Activating Proteins
GTPase-Activating Proteins
Dendrites
Extracellular Signal-Regulated MAP Kinases
Semaphorins
ras Proteins
Growth Cones
GTP Phosphohydrolases
Growth
Neurons
Axons
Cones
Down-Regulation
Chemical activation
Molecules
CD100 antigen
plexin

All Science Journal Classification (ASJC) codes

  • Genetics
  • Molecular Biology
  • Biochemistry

Cite this

Plexin-B1 is a GTPase activating protein for M-Ras, remodelling dendrite morphology. / Saito, Yasuhiro; Oinuma, Izumi; Fujimoto, Satoshi; Negishi, Manabu.

In: EMBO Reports, Vol. 10, No. 6, 18.05.2009, p. 614-621.

Research output: Contribution to journalArticle

Saito, Yasuhiro ; Oinuma, Izumi ; Fujimoto, Satoshi ; Negishi, Manabu. / Plexin-B1 is a GTPase activating protein for M-Ras, remodelling dendrite morphology. In: EMBO Reports. 2009 ; Vol. 10, No. 6. pp. 614-621.
@article{2a8be02c99714e0d99d80089a393ebbb,
title = "Plexin-B1 is a GTPase activating protein for M-Ras, remodelling dendrite morphology",
abstract = "Plexins are receptors for axonal guidance molecules known as semaphorins. We recently reported that the semaphorin 4D (Sema4D) receptor, Plexin-B1, induces axonal growth cone collapse by functioning as an R-Ras GTPase activating protein (GAP). Here, we report that Plexin-B1 shows GAP activity for M-Ras, another member of the Ras family of GTPases. In cortical neurons, the expression of M-Ras was upregulated during dendritic development. Knockdown of endogenous M-Ras-but not R-Ras-reduced dendritic outgrowth and branching, whereas overexpression of constitutively active M-Ras, M-Ras(Q71L), enhanced dendritic outgrowth and branching. Sema4D suppressed M-Ras activity and reduced dendritic outgrowth and branching, but this reduction was blocked by M-Ras(Q71L). M-Ras(Q71L) stimulated extracellular signal-regulated kinase (ERK) activation, inducing dendrite growth, whereas Sema4D suppressed ERK activity and down-regulation of ERK was required for a Sema4D-induced reduction of dendrite growth. Thus, we conclude that Plexin-B1 is a dual functional GAP for R-Ras and M-Ras, remodelling axon and dendrite morphology, respectively.",
author = "Yasuhiro Saito and Izumi Oinuma and Satoshi Fujimoto and Manabu Negishi",
year = "2009",
month = "5",
day = "18",
doi = "10.1038/embor.2009.63",
language = "English",
volume = "10",
pages = "614--621",
journal = "EMBO Reports",
issn = "1469-221X",
publisher = "Nature Publishing Group",
number = "6",

}

TY - JOUR

T1 - Plexin-B1 is a GTPase activating protein for M-Ras, remodelling dendrite morphology

AU - Saito, Yasuhiro

AU - Oinuma, Izumi

AU - Fujimoto, Satoshi

AU - Negishi, Manabu

PY - 2009/5/18

Y1 - 2009/5/18

N2 - Plexins are receptors for axonal guidance molecules known as semaphorins. We recently reported that the semaphorin 4D (Sema4D) receptor, Plexin-B1, induces axonal growth cone collapse by functioning as an R-Ras GTPase activating protein (GAP). Here, we report that Plexin-B1 shows GAP activity for M-Ras, another member of the Ras family of GTPases. In cortical neurons, the expression of M-Ras was upregulated during dendritic development. Knockdown of endogenous M-Ras-but not R-Ras-reduced dendritic outgrowth and branching, whereas overexpression of constitutively active M-Ras, M-Ras(Q71L), enhanced dendritic outgrowth and branching. Sema4D suppressed M-Ras activity and reduced dendritic outgrowth and branching, but this reduction was blocked by M-Ras(Q71L). M-Ras(Q71L) stimulated extracellular signal-regulated kinase (ERK) activation, inducing dendrite growth, whereas Sema4D suppressed ERK activity and down-regulation of ERK was required for a Sema4D-induced reduction of dendrite growth. Thus, we conclude that Plexin-B1 is a dual functional GAP for R-Ras and M-Ras, remodelling axon and dendrite morphology, respectively.

AB - Plexins are receptors for axonal guidance molecules known as semaphorins. We recently reported that the semaphorin 4D (Sema4D) receptor, Plexin-B1, induces axonal growth cone collapse by functioning as an R-Ras GTPase activating protein (GAP). Here, we report that Plexin-B1 shows GAP activity for M-Ras, another member of the Ras family of GTPases. In cortical neurons, the expression of M-Ras was upregulated during dendritic development. Knockdown of endogenous M-Ras-but not R-Ras-reduced dendritic outgrowth and branching, whereas overexpression of constitutively active M-Ras, M-Ras(Q71L), enhanced dendritic outgrowth and branching. Sema4D suppressed M-Ras activity and reduced dendritic outgrowth and branching, but this reduction was blocked by M-Ras(Q71L). M-Ras(Q71L) stimulated extracellular signal-regulated kinase (ERK) activation, inducing dendrite growth, whereas Sema4D suppressed ERK activity and down-regulation of ERK was required for a Sema4D-induced reduction of dendrite growth. Thus, we conclude that Plexin-B1 is a dual functional GAP for R-Ras and M-Ras, remodelling axon and dendrite morphology, respectively.

UR - http://www.scopus.com/inward/record.url?scp=67349193305&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67349193305&partnerID=8YFLogxK

U2 - 10.1038/embor.2009.63

DO - 10.1038/embor.2009.63

M3 - Article

VL - 10

SP - 614

EP - 621

JO - EMBO Reports

JF - EMBO Reports

SN - 1469-221X

IS - 6

ER -