Activation of the mitochondrial unfolded protein response does not predict longevity in Caenorhabditis elegans

Christopher F. Bennett, Helen Vander Wende, Marissa Simko, Shannon Klum, Sarah Barfield, Haeri Choi, Victor V. Pineda and Matt Kaeberlein ()
Additional contact information
Christopher F. Bennett: University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA
Helen Vander Wende: University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA
Marissa Simko: University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA
Shannon Klum: University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA
Sarah Barfield: University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA
Haeri Choi: University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA
Victor V. Pineda: University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA
Matt Kaeberlein: University of Washington, 1959 NE Pacific Street, D-514, Box 357470, Seattle, Washington 98195-7470, USA

Nature Communications, 2014, vol. 5, issue 1, 1-10

Abstract: Abstract Recent studies have propagated the model that the mitochondrial unfolded protein response (UPRmt) is causal for lifespan extension from inhibition of the electron transport chain (ETC) in Caenorhabditis elegans. Here we report a genome-wide RNAi screen for negative regulators of the UPRmt. Lifespan analysis of nineteen RNAi clones that induce the hsp-6p::gfp reporter demonstrate differential effects on longevity. Deletion of atfs-1, which is required for induction of the UPRmt, fails to prevent lifespan extension from knockdown of two genes identified in our screen or following knockdown of the ETC gene cco-1. RNAi knockdown of atfs-1 also has no effect on lifespan extension caused by mutation of the ETC gene isp-1. Constitutive activation of the UPRmt by gain of function mutations in atfs-1 fails to extend lifespan. These observations identify several new factors that promote mitochondrial homoeostasis and demonstrate that the UPRmt, as currently defined, is neither necessary nor sufficient for lifespan extension.

Date: 2014
References: Add references at CitEc
Citations: View citations in EconPapers (2)

Downloads: (external link)
https://www.nature.com/articles/ncomms4483 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4483

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms4483

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().