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Research group Group Büttner

We study how different organelles within a cell communicate and how this interorganellar connectivity contributes to protein homeostasis and cellular fitness during aging.

Group description

We are interested in different aspects of cellular aging and organellar connectivity. Using a combination of molecular and cell biology, genetics, biochemistry and imaging, we apply yeast as a model to understand age-associated cellular decay. The causes of aging are intertwined, and interdependent organelle subsystems and networks cooperate to sustain viability over time. Communication between organelles is ensured by dedicated signal transduction pathways or by direct physical contact at so-called membrane contact sites. We are interested in membrane contact site dynamics in response to aging, altered metabolic regimes and cell stress and the impact of organellar communication on cellular fitness and proteostasis in aging cells. The capacity of a cell to balance protein synthesis, folding and degradation progressively declines during aging, and long-lived cells are particularly sensitive to the deterioration of protein quality control. The accumulation of abnormal proteins in the course of aging expedites the sequential decay of different proteostatic subsystems maintaining cellular homeostasis, including autophagy. The different projects in our lab are centered around interorganellar communication during cellular aging, facilitated by signal transduction pathways and by direct physical contact between distinct organelles. We complement our studies in yeast with Drosophila research to extend our findings from the cellular to the organismal level.

Our funding

The Swedish Research Council
Knut and Alice Wallenberg Foundation
Stiftelsen Olle Engkvist Byggmästare
The Austrian Science Fund
Carl Tryggesr Stiftelse
Åke Wibergs Stiftelse

Group members

Group managers

Sabrina Büttner

Professor

Department of Molecular Biosciences, The Wenner-Gren Institute

08-16 41 70

sabrina.buettner@su.se

Members

Maja Sjödahl

Student

Department of Molecular Biosciences, Wenner-Grens institute

maja.sjodahl@su.se

Carmela Vazquez Calvo

Praktikant

Department of Molecular Biosciences, The Wenner-Gren Institute

carmela.calvo@su.se

Emma Block

PhD student

Department of Molecular Biosciences, The Wenner-Gren Institute

emma.block@su.se

Filomena Broeskamp

Post doctor

Department of Molecular Biosciences, The Wenner-Gren Institute

filomena.broeskamp@su.se

Irene Alvarez Guerra

PhD student

Department of Molecular Biosciences, The Wenner-Gren Institute

irene.alvarezguerra@su.se

Lukas Habernig

Researcher

Department of Molecular Biosciences, The Wenner-Gren Institute

08-16 41 95

lukas.habernig@su.se

Simon Prokisch-Chalas

PhD student

Department of Molecular Biosciences, The Wenner-Gren Institute

simon.prokisch@su.se

Publications

Sterol Metabolism Differentially Contributes to Maintenance and Exit of Quiescence.

Peselj C, Ebrahimi M, Broeskamp F, Prokisch S, Habernig L, Alvarez-Guerra I, Kohler V, Vögtle FN, Büttner S.* Front. Cell Dev. Biol. 2022 Feb 14. doi.org/10.3389/fcell.2022.788472.

Phosphate Restriction Promotes Longevity via Activation of Autophagy and the Multivesicular Body

Pathway. Ebrahimi M, Habernig L, Broeskamp F, Aufschnaiter A, Diessl J, Atienza I, Matz S, Ruiz FA, Büttner S*. Cells. 2021 Nov 13;10(11):3161. doi: 10.3390/cells10113161.

Ca2+ administration prevents α-synuclein proteotoxicity by stimulating calcineurin-dependent lysosom

proteolysis. Habernig L, Broeskamp F, Aufschnaiter A, Diessl J, Peselj C, Urbauer E, Eisenberg T, de Ory A, Büttner S*. PLoS Genet. 2021 Nov 15;17(11):e1009911. doi: 10.1371/journal.pgen.1009911.

Snd3 controls nucleus-vacuole junctions in response to glucose signaling.

Tosal-Castano S, Peselj C, Kohler V, Habernig L, Berglund LL, Ebrahimi M, Vögtle FN, Höög J, Andréasson C, Büttner S*. Cell Rep. 2021 Jan 19;34(3):108637. doi: 10.1016/j.celrep.2020.108637.

Respiratory supercomplexes enhance electron transport by decreasing cytochrome c diffusion distance.

Berndtsson J, Aufschnaiter A, Rathore S, Marin-Buera L, Dawitz H, Diessl J, Kohler V, Barrientos A, Büttner S*, Fontanesi F*, Ott M*. EMBO Rep. 2020 Oct 5;:e51015.

Bab2 functions as an ecdysone-responsive transcriptional repressor during Drosophila development.

Duan J, Zhao Y, Li H, Habernig L, Gordon MD, Miao X, Engström Y, and Büttner S.* Cell Reports. 2020 Jul 28;32(4):107972

An Early mtUPR: Redistribution of the Nuclear Transcription Factor Rox1 to Mitochondria Protects

against Intramitochondrial Proteotoxic Aggregates. Poveda-Huertes D, Matic S, Marada A, Haberni L, Licheva M, Myketin L, Gilsbach R, Tosal-Castano S, Papinski D, Mulica P, Kretz O, Kücükköse C, Taskin AA, Hein L, Kraft C, Büttner S, Meisinger C, and Vögtle FN. Mol. Cell. 2020; 77, 180-188.e9.

The enzymatic core of the Parkinson’s Disease-associated protein LRRK2 impairs mitochondrial

biogenesis in aging yeast. Aufschnaiter A., Kohler V, Walter C, Tosal-Castano S, Habernig L, Wolinski H, Keller W, Vögtle FN, Büttner S*. Front. Mol. Neurosci., 2018 June 21. doi.org/10.3389/fnmol.2018.00205.

Mitochondrial translation efficiency controls cytoplasmic protein homeostasis.

Suhm T, Kaimal JM, Dawitz H, Peselj C, Masser AE, Hanzén S, Ambrozic M, Smialowska A, Björck ML, Brzezinski P, Nyström T, Büttner S, Andréasson C, Ott M. Cell Metab. 2018 doi.org/10.1016/j.cmet.2018.04.011

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