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Drosophila Vps35 function is necessary for normal endocytic trafficking and actin cytoskeleton organisation

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Drosophila Vps35 function is necessary for normal endocytic trafficking and actin cytoskeleton organisation. / Korolchuk, Viktor I.; Schütz, Martin M.; Gómez-Llorente, Carolina et al.
In: Journal of Cell Science, Vol. 120, No. 24, 15.12.2007, p. 4367-4376.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Korolchuk, VI, Schütz, MM, Gómez-Llorente, C, Rocha, J, Lansu, NR, Collins, SM, Wairkar, YP, Robinson, IM & O'Kane, CJ 2007, 'Drosophila Vps35 function is necessary for normal endocytic trafficking and actin cytoskeleton organisation', Journal of Cell Science, vol. 120, no. 24, pp. 4367-4376. https://doi.org/10.1242/jcs.012336

APA

Korolchuk, V. I., Schütz, M. M., Gómez-Llorente, C., Rocha, J., Lansu, N. R., Collins, S. M., Wairkar, Y. P., Robinson, I. M., & O'Kane, C. J. (2007). Drosophila Vps35 function is necessary for normal endocytic trafficking and actin cytoskeleton organisation. Journal of Cell Science, 120(24), 4367-4376. https://doi.org/10.1242/jcs.012336

Vancouver

Korolchuk VI, Schütz MM, Gómez-Llorente C, Rocha J, Lansu NR, Collins SM et al. Drosophila Vps35 function is necessary for normal endocytic trafficking and actin cytoskeleton organisation. Journal of Cell Science. 2007 Dec 15;120(24):4367-4376. doi: 10.1242/jcs.012336

Author

Korolchuk, Viktor I. ; Schütz, Martin M. ; Gómez-Llorente, Carolina et al. / Drosophila Vps35 function is necessary for normal endocytic trafficking and actin cytoskeleton organisation. In: Journal of Cell Science. 2007 ; Vol. 120, No. 24. pp. 4367-4376.

Bibtex

@article{896121fbee1a46b5a4c9af4fef6e870f,
title = "Drosophila Vps35 function is necessary for normal endocytic trafficking and actin cytoskeleton organisation",
abstract = "TO identify novel proteins required for receptor-mediated endocytosis, we have developed an RNAi-based screening method in Drosophila S2 cells, based on uptake of a scavenger receptor ligand. Some known endocytic proteins are essential for endocytosis in this assay, including clathrin and α-adaptin; however, other proteins important for synaptic vesicle endocytosis are not required. In a small screen for novel endocytic proteins, we identified the Drosophila homologue of Vps35, a component of the retromer complex, involved in endosome-to-Golgi trafficking. Loss of Vps35 inhibits scavenger receptor ligand endocytosis, and causes mislocalisation of a number of receptors and endocytic proteins. Vps35 has tumour suppressor properties because its loss leads to overproliferation of blood cells in larvae. Its loss also causes signalling defects at the neuromuscular junction, including upregulation of TGFβ/BMP signalling and excessive formation of synaptic terminals. Vps35 negatively regulates actin polymerisation, and genetic interactions suggest that some of the endocytic and signalling defects of vps35 mutants are due to this function.",
keywords = "Haemocytes, Neuromuscular junction, Rac1, Retromer, RNAi",
author = "Korolchuk, {Viktor I.} and Sch{\"u}tz, {Martin M.} and Carolina G{\'o}mez-Llorente and Jo{\~a}o Rocha and Lansu, {Nico R.} and Collins, {Stephanie M.} and Wairkar, {Yogesh P.} and Robinson, {Iain M.} and O'Kane, {Cahir J.}",
year = "2007",
month = dec,
day = "15",
doi = "10.1242/jcs.012336",
language = "English",
volume = "120",
pages = "4367--4376",
journal = "Journal of Cell Science",
issn = "0021-9533",
publisher = "Company of Biologists Ltd",
number = "24",

}

RIS

TY - JOUR

T1 - Drosophila Vps35 function is necessary for normal endocytic trafficking and actin cytoskeleton organisation

AU - Korolchuk, Viktor I.

AU - Schütz, Martin M.

AU - Gómez-Llorente, Carolina

AU - Rocha, João

AU - Lansu, Nico R.

AU - Collins, Stephanie M.

AU - Wairkar, Yogesh P.

AU - Robinson, Iain M.

AU - O'Kane, Cahir J.

PY - 2007/12/15

Y1 - 2007/12/15

N2 - TO identify novel proteins required for receptor-mediated endocytosis, we have developed an RNAi-based screening method in Drosophila S2 cells, based on uptake of a scavenger receptor ligand. Some known endocytic proteins are essential for endocytosis in this assay, including clathrin and α-adaptin; however, other proteins important for synaptic vesicle endocytosis are not required. In a small screen for novel endocytic proteins, we identified the Drosophila homologue of Vps35, a component of the retromer complex, involved in endosome-to-Golgi trafficking. Loss of Vps35 inhibits scavenger receptor ligand endocytosis, and causes mislocalisation of a number of receptors and endocytic proteins. Vps35 has tumour suppressor properties because its loss leads to overproliferation of blood cells in larvae. Its loss also causes signalling defects at the neuromuscular junction, including upregulation of TGFβ/BMP signalling and excessive formation of synaptic terminals. Vps35 negatively regulates actin polymerisation, and genetic interactions suggest that some of the endocytic and signalling defects of vps35 mutants are due to this function.

AB - TO identify novel proteins required for receptor-mediated endocytosis, we have developed an RNAi-based screening method in Drosophila S2 cells, based on uptake of a scavenger receptor ligand. Some known endocytic proteins are essential for endocytosis in this assay, including clathrin and α-adaptin; however, other proteins important for synaptic vesicle endocytosis are not required. In a small screen for novel endocytic proteins, we identified the Drosophila homologue of Vps35, a component of the retromer complex, involved in endosome-to-Golgi trafficking. Loss of Vps35 inhibits scavenger receptor ligand endocytosis, and causes mislocalisation of a number of receptors and endocytic proteins. Vps35 has tumour suppressor properties because its loss leads to overproliferation of blood cells in larvae. Its loss also causes signalling defects at the neuromuscular junction, including upregulation of TGFβ/BMP signalling and excessive formation of synaptic terminals. Vps35 negatively regulates actin polymerisation, and genetic interactions suggest that some of the endocytic and signalling defects of vps35 mutants are due to this function.

KW - Haemocytes

KW - Neuromuscular junction

KW - Rac1

KW - Retromer

KW - RNAi

U2 - 10.1242/jcs.012336

DO - 10.1242/jcs.012336

M3 - Journal article

C2 - 18057029

AN - SCOPUS:37749033461

VL - 120

SP - 4367

EP - 4376

JO - Journal of Cell Science

JF - Journal of Cell Science

SN - 0021-9533

IS - 24

ER -