Increased copper toxicity in Saccharomyces cerevisiae lacking VPS35, a component of the retromer and monogenic Parkinson disease gene in humans

Nadine Sowada; Barbara Stiller; Christian Kubisch

doi:10.1016/j.bbrc.2016.05.157

Increased copper toxicity in Saccharomyces cerevisiae lacking VPS35, a component of the retromer and monogenic Parkinson disease gene in humans

Standard

Increased copper toxicity in Saccharomyces cerevisiae lacking VPS35, a component of the retromer and monogenic Parkinson disease gene in humans. / Sowada, Nadine; Stiller, Barbara; Kubisch, Christian.

In: BIOCHEM BIOPH RES CO, Vol. 476, No. 4, 05.08.2016, p. 528-33.

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

Harvard

Sowada, N, Stiller, B & Kubisch, C 2016, 'Increased copper toxicity in Saccharomyces cerevisiae lacking VPS35, a component of the retromer and monogenic Parkinson disease gene in humans', BIOCHEM BIOPH RES CO, vol. 476, no. 4, pp. 528-33. https://doi.org/10.1016/j.bbrc.2016.05.157

APA

Sowada, N., Stiller, B., & Kubisch, C. (2016). Increased copper toxicity in Saccharomyces cerevisiae lacking VPS35, a component of the retromer and monogenic Parkinson disease gene in humans. BIOCHEM BIOPH RES CO, 476(4), 528-33. https://doi.org/10.1016/j.bbrc.2016.05.157

Vancouver

Sowada N, Stiller B, Kubisch C. Increased copper toxicity in Saccharomyces cerevisiae lacking VPS35, a component of the retromer and monogenic Parkinson disease gene in humans. BIOCHEM BIOPH RES CO. 2016 Aug 5;476(4):528-33. https://doi.org/10.1016/j.bbrc.2016.05.157

Bibtex

@article{10b2c50b6b644844be9424957a96b765,

title = "Increased copper toxicity in Saccharomyces cerevisiae lacking VPS35, a component of the retromer and monogenic Parkinson disease gene in humans",

abstract = "The Saccharomyces cerevisiae gene VPS35 encodes a component of the retromer complex which is involved in vesicle transport from endosomes to the trans-Golgi network. Yeast and human VPS35 orthologs are highly conserved and mutations in human VPS35 cause an autosomal dominant form of late-onset Parkinson disease (PD). We now show that deletion of VPS35 in yeast (vps35Δ) leads to a dose-dependent growth defect towards copper. This increased sensitivity could be rescued by transformation with yeast wild-type VPS35 but not by the expression of a construct harboring the yeast equivalent (i.e. D686N) of the most commonly identified VPS35-associated PD mutation, p.D620N. In addition, we show that expression of one copy of α-synuclein, which is known to directly interact with copper, leads to a pronounced aggravation of copper toxicity in vps35Δ cells, thereby linking the regulation of copper homeostasis by Vps35p in yeast to one of the key molecules in PD pathophysiology.",

keywords = "Journal Article",

author = "Nadine Sowada and Barbara Stiller and Christian Kubisch",

year = "2016",

month = aug,

day = "5",

doi = "10.1016/j.bbrc.2016.05.157",

language = "English",

volume = "476",

pages = "528--33",

journal = "BIOCHEM BIOPH RES CO",

issn = "0006-291X",

publisher = "Academic Press Inc.",

number = "4",

}

RIS

TY - JOUR

T1 - Increased copper toxicity in Saccharomyces cerevisiae lacking VPS35, a component of the retromer and monogenic Parkinson disease gene in humans

AU - Sowada, Nadine

AU - Stiller, Barbara

AU - Kubisch, Christian

PY - 2016/8/5

Y1 - 2016/8/5

N2 - The Saccharomyces cerevisiae gene VPS35 encodes a component of the retromer complex which is involved in vesicle transport from endosomes to the trans-Golgi network. Yeast and human VPS35 orthologs are highly conserved and mutations in human VPS35 cause an autosomal dominant form of late-onset Parkinson disease (PD). We now show that deletion of VPS35 in yeast (vps35Δ) leads to a dose-dependent growth defect towards copper. This increased sensitivity could be rescued by transformation with yeast wild-type VPS35 but not by the expression of a construct harboring the yeast equivalent (i.e. D686N) of the most commonly identified VPS35-associated PD mutation, p.D620N. In addition, we show that expression of one copy of α-synuclein, which is known to directly interact with copper, leads to a pronounced aggravation of copper toxicity in vps35Δ cells, thereby linking the regulation of copper homeostasis by Vps35p in yeast to one of the key molecules in PD pathophysiology.

AB - The Saccharomyces cerevisiae gene VPS35 encodes a component of the retromer complex which is involved in vesicle transport from endosomes to the trans-Golgi network. Yeast and human VPS35 orthologs are highly conserved and mutations in human VPS35 cause an autosomal dominant form of late-onset Parkinson disease (PD). We now show that deletion of VPS35 in yeast (vps35Δ) leads to a dose-dependent growth defect towards copper. This increased sensitivity could be rescued by transformation with yeast wild-type VPS35 but not by the expression of a construct harboring the yeast equivalent (i.e. D686N) of the most commonly identified VPS35-associated PD mutation, p.D620N. In addition, we show that expression of one copy of α-synuclein, which is known to directly interact with copper, leads to a pronounced aggravation of copper toxicity in vps35Δ cells, thereby linking the regulation of copper homeostasis by Vps35p in yeast to one of the key molecules in PD pathophysiology.

KW - Journal Article

U2 - 10.1016/j.bbrc.2016.05.157

DO - 10.1016/j.bbrc.2016.05.157

M3 - SCORING: Journal article

C2 - 27262440

VL - 476

SP - 528

EP - 533

JO - BIOCHEM BIOPH RES CO

JF - BIOCHEM BIOPH RES CO

SN - 0006-291X

IS - 4

ER -