This article shows a novel function for the MAP1B protein, related to the control of actin dynamics through interaction with Tiam1

Alfredo Cáceres

Arber S.

Bamburg J. R.

Bishop A. L.

Black M. M.

Bradke F.

Carolina Montenegro-Venegas

Christian Gonzalez-Billault

Cueille N.

Da Silva J. S.

Daub H.

Del Rio J. A.

Diego Peretti

DiTella M. C.

Edelmann W.

Elena Tortosa

Erika Holzbaur

Flavia Bollati

Fukata M.

Garvalov B. K.

Gonzalez-Billault C.

Ignacio Jausoro

Ik-Tsen Heng J.

Inagaki N.

Jesus Avila

Kodama A.

Krendel M.

Kunda P.

Luo L.

Maekawa M.

Mariano Bisbal

Meixner A.

Nakata T.

Ng J.

Nishimura T.

Paglini G.

Pedrotti B.

Riederer B. M.

Ruthel G.

Sander E. E.

Sarmiere P. D.

Silvana Rosso

Sosa L.

Takefuji M.

Takei Y.

Utreras E.

Watabe-Uchida M.

Waterman-Storer C. M.

Witte H.

Wittmann T.

Yang N.

Molecular Biology of the Cell

English

PubMed

Artículo de publicación ISICultured neurons obtained from MAP1B-deficient mice have a delay in axon outgrowth and a reduced rate of axonal
elongation compared with neurons from wild-type mice. Here we show that MAP1B deficiency results in a significant
decrease in Rac1 and cdc42 activity and a significant increase in Rho activity. We found that MAP1B interacted with
Tiam1, a guanosine nucleotide exchange factor for Rac1. The decrease in Rac1/cdc42 activity was paralleled by decreases
in the phosphorylation of the downstream effectors of these proteins, such as LIMK-1 and cofilin. The expression of a
constitutively active form of Rac1, cdc42, or Tiam1 rescued the axon growth defect of MAP1B-deficient neurons. Taken
together, these observations define a new and crucial function of MAP1B that we show to be required for efficient
cross-talk between microtubules and the actin cytoskeleton during neuronal polarization.This work was supported by FONDECYT (PICT 05-01697) and grants from
FONCyT (PICT 815), Agencia Cordoba Ciencia, and HHMI to A.C. J.A. was
supported by a Plan National Grant (SAF 2006-02424), CIBERNED and Comunidad
de Madrid (SAL 0202-2006). C.G.-B. was supported by Fondecyt
1095089 and ICM P05-001-F

Montenegro Venegas, Carolina

Tortosa, Elena

Rosso, Silvana

Peretti, Diego

Bollati, Flavia

Bisbal, Mariano

Jausoro, Ignacio

Avila, Jesús

Cáceres, Alfredo

González Billault, Christian

Name not available

MAP1B Regulates Axonal Development by Modulating Rho-GTPase Rac1 Activity

Cultured neurons obtained from MAP1B-deficient mice have a delay in axon outgrowth and a reduced rate of axonal elongation compared with neurons from wild-type mice. Here we show that MAP1B deficiency results in a significant decrease in Rac1 and cdc42 activity and a significant increase in Rho activity. We found that MAP1B interacted with Tiam1, a guanosine nucleotide exchange factor for Rac1. The decrease in Rac1/cdc42 activity was paralleled by decreases in the phosphorylation of the downstream effectors of these proteins, such as LIMK-1 and cofilin. The expression of a constitutively active form of Rac1, cdc42, or Tiam1 rescued the axon growth defect of MAP1B-deficient neurons. Taken together, these observations define a new and crucial function of MAP1B that we show to be required for efficient cross-talk between microtubules and the actin cytoskeleton during neuronal polarization.</jats:p

Crossref

Repositorio Académico de la Universidad de Chile

Cultured neurons obtained from MAP1B-deficient mice have a delay in axon outgrowth and a reduced rate of axonal elongation compared with neurons from wild-type mice. Here we show that MAP1B deficiency results in a significant decrease in Rac1 and cdc42 activity and a significant increase in Rho activity. We found that MAP1B interacted with Tiam1, a guanosine nucleotide exchange factor for Rac1. The decrease in Rac1/cdc42 activity was paralleled by decreases in the phosphorylation of the downstream effectors of these proteins, such as LIMK-1 and cofilin. The expression of a constitutively active form of Rac1, cdc42, or Tiam1 rescued the axon growth defect of MAP1B-deficient neurons. Taken together, these observations define a new and crucial function of MAP1B that we show to be required for efficient cross-talk between microtubules and the actin cytoskeleton during neuronal polarization.This work was supported by FONDECYT (PICT 05-01697) and grants from FONCyT (PICT 815), Agencia Cordoba Ciencia, and HHMI to A.C. J.A. was supported by a Plan National Grant (SAF 2006-02424), CIBERNED and Comunidad de Madrid (SAL 0202-2006). C.G.-B. was supported by Fondecyt 1095089 and ICM P05-001-F.Peer reviewe

Montenegro-Venegas, Carolina

Ávila, Jesús

González-Billault, Christian

Digital.CSIC

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http://www.repositorio.uchile.cl/handle/2250/119231

MAP1B Regulates Axonal Development by Modulating Rho-GTPase Rac1 Activity

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Repositorio Académico de la Universidad de Chile

Digital.CSIC