Apc1-mediated antagonism of Wnt/beta-catenin signaling is required for retino-tectal pathfinding in the zebrafish.

J.T.M. Paridaen; C. Danesin; A.T. Elas; S.G.P. van de Water; C. Houart; D. Zivkovic

doi:10.1089/zeb.2008.0561

Apc1-mediated antagonism of Wnt/beta-catenin signaling is required for retino-tectal pathfinding in the zebrafish.

J.T.M. Paridaen, C. Danesin, A.T. Elas, S.G.P. van de Water, C. Houart, D. Zivkovic

Hubrecht Institute

Research output: Contribution to journal/periodical › Article › Scientific › peer-review

9 Citations (Scopus)

Abstract

The tumor suppressor Apc1 is an intracellular antagonist of the Wnt/beta-catenin pathway. We examined the effects of an Apc1 loss-of-function mutation on retino-tectal axon pathfinding in zebrafish. In apc mutants, the retina is disorganized and optic nerves portray pathfinding defects at the optic chiasm and do not project properly to the tectum. Wild-type cells, transplanted into mutant retinae, acquire retinal ganglion cell fate and project axons that cross at the mispositioned optic chiasm and extend to the contralateral tectum, suggesting a function of apc1 in axon pathfinding. These defects are caused mainly by stabilization of beta-catenin. These data demonstrate that Apc1 function is required for correct patterning of the retina and proper retinal ganglion axon projections.

Original language	English
Pages (from-to)	41-47
Journal	Zebrafish
Volume	6
Issue number	1
DOIs	https://doi.org/10.1089/zeb.2008.0561
Publication status	Published - 2009

Access to Document

10.1089/zeb.2008.0561

Cite this

@article{96984b356cfe4e9782e27014f0e01d88,

title = "Apc1-mediated antagonism of Wnt/beta-catenin signaling is required for retino-tectal pathfinding in the zebrafish.",

abstract = "The tumor suppressor Apc1 is an intracellular antagonist of the Wnt/beta-catenin pathway. We examined the effects of an Apc1 loss-of-function mutation on retino-tectal axon pathfinding in zebrafish. In apc mutants, the retina is disorganized and optic nerves portray pathfinding defects at the optic chiasm and do not project properly to the tectum. Wild-type cells, transplanted into mutant retinae, acquire retinal ganglion cell fate and project axons that cross at the mispositioned optic chiasm and extend to the contralateral tectum, suggesting a function of apc1 in axon pathfinding. These defects are caused mainly by stabilization of beta-catenin. These data demonstrate that Apc1 function is required for correct patterning of the retina and proper retinal ganglion axon projections.",

author = "J.T.M. Paridaen and C. Danesin and A.T. Elas and {van de Water}, S.G.P. and C. Houart and D. Zivkovic",

note = "Reporting year: 2009",

year = "2009",

doi = "10.1089/zeb.2008.0561",

language = "English",

volume = "6",

pages = "41--47",

journal = "Zebrafish",

issn = "1545-8547",

publisher = "Mary Ann Liebert Inc.",

number = "1",

}

TY - JOUR

T1 - Apc1-mediated antagonism of Wnt/beta-catenin signaling is required for retino-tectal pathfinding in the zebrafish.

AU - Paridaen, J.T.M.

AU - Danesin, C.

AU - Elas, A.T.

AU - van de Water, S.G.P.

AU - Houart, C.

AU - Zivkovic, D.

N1 - Reporting year: 2009

PY - 2009

Y1 - 2009

N2 - The tumor suppressor Apc1 is an intracellular antagonist of the Wnt/beta-catenin pathway. We examined the effects of an Apc1 loss-of-function mutation on retino-tectal axon pathfinding in zebrafish. In apc mutants, the retina is disorganized and optic nerves portray pathfinding defects at the optic chiasm and do not project properly to the tectum. Wild-type cells, transplanted into mutant retinae, acquire retinal ganglion cell fate and project axons that cross at the mispositioned optic chiasm and extend to the contralateral tectum, suggesting a function of apc1 in axon pathfinding. These defects are caused mainly by stabilization of beta-catenin. These data demonstrate that Apc1 function is required for correct patterning of the retina and proper retinal ganglion axon projections.

AB - The tumor suppressor Apc1 is an intracellular antagonist of the Wnt/beta-catenin pathway. We examined the effects of an Apc1 loss-of-function mutation on retino-tectal axon pathfinding in zebrafish. In apc mutants, the retina is disorganized and optic nerves portray pathfinding defects at the optic chiasm and do not project properly to the tectum. Wild-type cells, transplanted into mutant retinae, acquire retinal ganglion cell fate and project axons that cross at the mispositioned optic chiasm and extend to the contralateral tectum, suggesting a function of apc1 in axon pathfinding. These defects are caused mainly by stabilization of beta-catenin. These data demonstrate that Apc1 function is required for correct patterning of the retina and proper retinal ganglion axon projections.

U2 - 10.1089/zeb.2008.0561

DO - 10.1089/zeb.2008.0561

M3 - Article

SN - 1545-8547

VL - 6

SP - 41

EP - 47

JO - Zebrafish

JF - Zebrafish

IS - 1

ER -

Apc1-mediated antagonism of Wnt/beta-catenin signaling is required for retino-tectal pathfinding in the zebrafish.

Abstract

Access to Document

Fingerprint

Cite this