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Rab8, POSH, and TAK1 regulate synaptic growth in a Drosophila model of frontotemporal dementia

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Rab8, POSH, and TAK1 regulate synaptic growth in a Drosophila model of frontotemporal dementia. / West, Ryan John Hatcher; Lu, Yubing; Marie, Bruno; Gao, Fen-Baio; Sweeney, Sean.

In: Journal of Cell Biology, Vol. 208, No. 7, 30.03.2015, p. 931-947.

Research output: Contribution to journalArticle

Harvard

West, RJH, Lu, Y, Marie, B, Gao, F-B & Sweeney, S 2015, 'Rab8, POSH, and TAK1 regulate synaptic growth in a Drosophila model of frontotemporal dementia', Journal of Cell Biology, vol. 208, no. 7, pp. 931-947. https://doi.org/10.1083/jcb.201404066

APA

West, R. J. H., Lu, Y., Marie, B., Gao, F-B., & Sweeney, S. (2015). Rab8, POSH, and TAK1 regulate synaptic growth in a Drosophila model of frontotemporal dementia. Journal of Cell Biology, 208(7), 931-947. https://doi.org/10.1083/jcb.201404066

Vancouver

West RJH, Lu Y, Marie B, Gao F-B, Sweeney S. Rab8, POSH, and TAK1 regulate synaptic growth in a Drosophila model of frontotemporal dementia. Journal of Cell Biology. 2015 Mar 30;208(7):931-947. https://doi.org/10.1083/jcb.201404066

Author

West, Ryan John Hatcher ; Lu, Yubing ; Marie, Bruno ; Gao, Fen-Baio ; Sweeney, Sean. / Rab8, POSH, and TAK1 regulate synaptic growth in a Drosophila model of frontotemporal dementia. In: Journal of Cell Biology. 2015 ; Vol. 208, No. 7. pp. 931-947.

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@article{3b3ac8202e2c43c39aa7b915fd069779,
title = "Rab8, POSH, and TAK1 regulate synaptic growth in a Drosophila model of frontotemporal dementia",
abstract = "Mutations in genes essential for protein homeostasis have been identified in frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) patients. Why mature neurons should be particularly sensitive to such perturbations is unclear. We identified mutations in Rab8 in a genetic screen for enhancement of an FTD phenotype associated with ESCRT-III dysfunction. Examination of Rab8 mutants or motor neurons expressing a mutant ESCRT-III subunit, CHMP2BIntron5, at the Drosophila melanogaster neuromuscular junction synapse revealed synaptic overgrowth and endosomal dysfunction. Expression of Rab8 rescued overgrowth phenotypes generated by CHMP2BIntron5. In Rab8 mutant synapses, c-Jun N-terminal kinase (JNK)/activator protein-1 and TGF-β signaling were overactivated and acted synergistically to potentiate synaptic growth. We identify novel roles for endosomal JNK-scaffold POSH (Plenty-of-SH3s) and a JNK kinase kinase, TAK1, in regulating growth activation in Rab8 mutants. Our data uncover Rab8, POSH, and TAK1 as regulators of synaptic growth responses and point to recycling endosome as a key compartment for synaptic growth regulation during neurodegenerative processes.",
author = "West, {Ryan John Hatcher} and Yubing Lu and Bruno Marie and Fen-Baio Gao and Sean Sweeney",
note = "This content is made available by the publisher under a Creative Commons CC BY-NC-SA Licence.",
year = "2015",
month = "3",
day = "30",
doi = "10.1083/jcb.201404066",
language = "English",
volume = "208",
pages = "931--947",
journal = "Journal of Cell Biology",
issn = "0021-9525",
publisher = "Rockefeller University Press",
number = "7",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Rab8, POSH, and TAK1 regulate synaptic growth in a Drosophila model of frontotemporal dementia

AU - West, Ryan John Hatcher

AU - Lu, Yubing

AU - Marie, Bruno

AU - Gao, Fen-Baio

AU - Sweeney, Sean

N1 - This content is made available by the publisher under a Creative Commons CC BY-NC-SA Licence.

PY - 2015/3/30

Y1 - 2015/3/30

N2 - Mutations in genes essential for protein homeostasis have been identified in frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) patients. Why mature neurons should be particularly sensitive to such perturbations is unclear. We identified mutations in Rab8 in a genetic screen for enhancement of an FTD phenotype associated with ESCRT-III dysfunction. Examination of Rab8 mutants or motor neurons expressing a mutant ESCRT-III subunit, CHMP2BIntron5, at the Drosophila melanogaster neuromuscular junction synapse revealed synaptic overgrowth and endosomal dysfunction. Expression of Rab8 rescued overgrowth phenotypes generated by CHMP2BIntron5. In Rab8 mutant synapses, c-Jun N-terminal kinase (JNK)/activator protein-1 and TGF-β signaling were overactivated and acted synergistically to potentiate synaptic growth. We identify novel roles for endosomal JNK-scaffold POSH (Plenty-of-SH3s) and a JNK kinase kinase, TAK1, in regulating growth activation in Rab8 mutants. Our data uncover Rab8, POSH, and TAK1 as regulators of synaptic growth responses and point to recycling endosome as a key compartment for synaptic growth regulation during neurodegenerative processes.

AB - Mutations in genes essential for protein homeostasis have been identified in frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) patients. Why mature neurons should be particularly sensitive to such perturbations is unclear. We identified mutations in Rab8 in a genetic screen for enhancement of an FTD phenotype associated with ESCRT-III dysfunction. Examination of Rab8 mutants or motor neurons expressing a mutant ESCRT-III subunit, CHMP2BIntron5, at the Drosophila melanogaster neuromuscular junction synapse revealed synaptic overgrowth and endosomal dysfunction. Expression of Rab8 rescued overgrowth phenotypes generated by CHMP2BIntron5. In Rab8 mutant synapses, c-Jun N-terminal kinase (JNK)/activator protein-1 and TGF-β signaling were overactivated and acted synergistically to potentiate synaptic growth. We identify novel roles for endosomal JNK-scaffold POSH (Plenty-of-SH3s) and a JNK kinase kinase, TAK1, in regulating growth activation in Rab8 mutants. Our data uncover Rab8, POSH, and TAK1 as regulators of synaptic growth responses and point to recycling endosome as a key compartment for synaptic growth regulation during neurodegenerative processes.

U2 - 10.1083/jcb.201404066

DO - 10.1083/jcb.201404066

M3 - Article

VL - 208

SP - 931

EP - 947

JO - Journal of Cell Biology

JF - Journal of Cell Biology

SN - 0021-9525

IS - 7

ER -