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The GET pathway can increase the risk of mitochondrial outer membrane proteins to be mistargeted to the ER

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The GET pathway can increase the risk of mitochondrial outer membrane proteins to be mistargeted to the ER. / Vitali, Daniela G; Sinzel, Monika; Bulthuis, Elianne P; Kolb, Antonia; Zabel, Susanne; Mehlhorn, Dietmar G; Figueiredo Costa, Bruna; Farkas, Ákos; Clancy, Anne; Schuldiner, Maya; Grefen, Christopher; Schwappach, Blanche; Borgese, Nica; Rapaport, Doron.

In: J CELL SCI, Vol. 131, No. 10, 16.05.2018.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Vitali, DG, Sinzel, M, Bulthuis, EP, Kolb, A, Zabel, S, Mehlhorn, DG, Figueiredo Costa, B, Farkas, Á, Clancy, A, Schuldiner, M, Grefen, C, Schwappach, B, Borgese, N & Rapaport, D 2018, 'The GET pathway can increase the risk of mitochondrial outer membrane proteins to be mistargeted to the ER', J CELL SCI, vol. 131, no. 10. https://doi.org/10.1242/jcs.211110

APA

Vitali, D. G., Sinzel, M., Bulthuis, E. P., Kolb, A., Zabel, S., Mehlhorn, D. G., Figueiredo Costa, B., Farkas, Á., Clancy, A., Schuldiner, M., Grefen, C., Schwappach, B., Borgese, N., & Rapaport, D. (2018). The GET pathway can increase the risk of mitochondrial outer membrane proteins to be mistargeted to the ER. J CELL SCI, 131(10). https://doi.org/10.1242/jcs.211110

Vancouver

Vitali DG, Sinzel M, Bulthuis EP, Kolb A, Zabel S, Mehlhorn DG et al. The GET pathway can increase the risk of mitochondrial outer membrane proteins to be mistargeted to the ER. J CELL SCI. 2018 May 16;131(10). https://doi.org/10.1242/jcs.211110

Bibtex

@article{7915b96593f14e06b7deff281fec6b2e,
title = "The GET pathway can increase the risk of mitochondrial outer membrane proteins to be mistargeted to the ER",
abstract = "Tail-anchored (TA) proteins are anchored to their corresponding membrane via a single transmembrane segment (TMS) at their C-terminus. In yeast, the targeting of TA proteins to the endoplasmic reticulum (ER) can be mediated by the guided entry of TA proteins (GET) pathway, whereas it is not yet clear how mitochondrial TA proteins are targeted to their destination. It has been widely observed that some mitochondrial outer membrane (MOM) proteins are mistargeted to the ER when overexpressed or when their targeting signal is masked. However, the mechanism of this erroneous sorting is currently unknown. In this study, we demonstrate the involvement of the GET machinery in the mistargeting of suboptimal MOM proteins to the ER. These findings suggest that the GET machinery can, in principle, recognize and guide mitochondrial and non-canonical TA proteins. Hence, under normal conditions, an active mitochondrial targeting pathway must exist that dominates the kinetic competition against other pathways.",
keywords = "Adaptor Proteins, Vesicular Transport/genetics, Adenosine Triphosphatases/metabolism, Endoplasmic Reticulum/genetics, Guanine Nucleotide Exchange Factors/metabolism, Membrane Proteins/genetics, Mitochondrial Membrane Transport Proteins/genetics, Mitochondrial Membranes/metabolism, Protein Transport, Saccharomyces cerevisiae/genetics, Saccharomyces cerevisiae Proteins/genetics",
author = "Vitali, {Daniela G} and Monika Sinzel and Bulthuis, {Elianne P} and Antonia Kolb and Susanne Zabel and Mehlhorn, {Dietmar G} and {Figueiredo Costa}, Bruna and {\'A}kos Farkas and Anne Clancy and Maya Schuldiner and Christopher Grefen and Blanche Schwappach and Nica Borgese and Doron Rapaport",
note = "{\textcopyright} 2018. Published by The Company of Biologists Ltd.",
year = "2018",
month = may,
day = "16",
doi = "10.1242/jcs.211110",
language = "English",
volume = "131",
journal = "J CELL SCI",
issn = "0021-9533",
publisher = "Company of Biologists Ltd",
number = "10",

}

RIS

TY - JOUR

T1 - The GET pathway can increase the risk of mitochondrial outer membrane proteins to be mistargeted to the ER

AU - Vitali, Daniela G

AU - Sinzel, Monika

AU - Bulthuis, Elianne P

AU - Kolb, Antonia

AU - Zabel, Susanne

AU - Mehlhorn, Dietmar G

AU - Figueiredo Costa, Bruna

AU - Farkas, Ákos

AU - Clancy, Anne

AU - Schuldiner, Maya

AU - Grefen, Christopher

AU - Schwappach, Blanche

AU - Borgese, Nica

AU - Rapaport, Doron

N1 - © 2018. Published by The Company of Biologists Ltd.

PY - 2018/5/16

Y1 - 2018/5/16

N2 - Tail-anchored (TA) proteins are anchored to their corresponding membrane via a single transmembrane segment (TMS) at their C-terminus. In yeast, the targeting of TA proteins to the endoplasmic reticulum (ER) can be mediated by the guided entry of TA proteins (GET) pathway, whereas it is not yet clear how mitochondrial TA proteins are targeted to their destination. It has been widely observed that some mitochondrial outer membrane (MOM) proteins are mistargeted to the ER when overexpressed or when their targeting signal is masked. However, the mechanism of this erroneous sorting is currently unknown. In this study, we demonstrate the involvement of the GET machinery in the mistargeting of suboptimal MOM proteins to the ER. These findings suggest that the GET machinery can, in principle, recognize and guide mitochondrial and non-canonical TA proteins. Hence, under normal conditions, an active mitochondrial targeting pathway must exist that dominates the kinetic competition against other pathways.

AB - Tail-anchored (TA) proteins are anchored to their corresponding membrane via a single transmembrane segment (TMS) at their C-terminus. In yeast, the targeting of TA proteins to the endoplasmic reticulum (ER) can be mediated by the guided entry of TA proteins (GET) pathway, whereas it is not yet clear how mitochondrial TA proteins are targeted to their destination. It has been widely observed that some mitochondrial outer membrane (MOM) proteins are mistargeted to the ER when overexpressed or when their targeting signal is masked. However, the mechanism of this erroneous sorting is currently unknown. In this study, we demonstrate the involvement of the GET machinery in the mistargeting of suboptimal MOM proteins to the ER. These findings suggest that the GET machinery can, in principle, recognize and guide mitochondrial and non-canonical TA proteins. Hence, under normal conditions, an active mitochondrial targeting pathway must exist that dominates the kinetic competition against other pathways.

KW - Adaptor Proteins, Vesicular Transport/genetics

KW - Adenosine Triphosphatases/metabolism

KW - Endoplasmic Reticulum/genetics

KW - Guanine Nucleotide Exchange Factors/metabolism

KW - Membrane Proteins/genetics

KW - Mitochondrial Membrane Transport Proteins/genetics

KW - Mitochondrial Membranes/metabolism

KW - Protein Transport

KW - Saccharomyces cerevisiae/genetics

KW - Saccharomyces cerevisiae Proteins/genetics

U2 - 10.1242/jcs.211110

DO - 10.1242/jcs.211110

M3 - SCORING: Journal article

C2 - 29661846

VL - 131

JO - J CELL SCI

JF - J CELL SCI

SN - 0021-9533

IS - 10

ER -