A prion accelerates proliferation at the expense of lifespan

In fluctuating environments, switching between different growth strategies, such as those affecting cell size and proliferation, can be advantageous to an organism. Trade-offs arise, however. Mechanisms that aberrantly increase cell size or proliferation—such as mutations or chemicals that interfere...

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Autores principales:	David M Garcia, Edgar A Campbell, Christopher M Jakobson, Mitsuhiro Tsuchiya, Ethan A Shaw, Acadia L DiNardo, Matt Kaeberlein, Daniel F Jarosz
Formato:	article
Lenguaje:	EN
Publicado:	eLife Sciences Publications Ltd 2021
Materias:	prions aging cell size protein synthesis epigenetics RNA modification Medicine R Science Q Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/418f66c5630d4db19a8f8ec90c1a9440
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spelling	oai:doaj.org-article:418f66c5630d4db19a8f8ec90c1a94402021-11-23T13:03:17ZA prion accelerates proliferation at the expense of lifespan10.7554/eLife.609172050-084Xe60917https://doaj.org/article/418f66c5630d4db19a8f8ec90c1a94402021-09-01T00:00:00Zhttps://elifesciences.org/articles/60917https://doaj.org/toc/2050-084XIn fluctuating environments, switching between different growth strategies, such as those affecting cell size and proliferation, can be advantageous to an organism. Trade-offs arise, however. Mechanisms that aberrantly increase cell size or proliferation—such as mutations or chemicals that interfere with growth regulatory pathways—can also shorten lifespan. Here we report a natural example of how the interplay between growth and lifespan can be epigenetically controlled. We find that a highly conserved RNA-modifying enzyme, the pseudouridine synthase Pus4/TruB, can act as a prion, endowing yeast with greater proliferation rates at the cost of a shortened lifespan. Cells harboring the prion grow larger and exhibit altered protein synthesis. This epigenetic state, [BIG+] (better in growth), allows cells to heritably yet reversibly alter their translational program, leading to the differential synthesis of dozens of proteins, including many that regulate proliferation and aging. Our data reveal a new role for prion-based control of an RNA-modifying enzyme in driving heritable epigenetic states that transform cell growth and survival.David M GarciaEdgar A CampbellChristopher M JakobsonMitsuhiro TsuchiyaEthan A ShawAcadia L DiNardoMatt KaeberleinDaniel F JaroszeLife Sciences Publications Ltdarticleprionsagingcell sizeprotein synthesisepigeneticsRNA modificationMedicineRScienceQBiology (General)QH301-705.5ENeLife, Vol 10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	prions aging cell size protein synthesis epigenetics RNA modification Medicine R Science Q Biology (General) QH301-705.5
spellingShingle	prions aging cell size protein synthesis epigenetics RNA modification Medicine R Science Q Biology (General) QH301-705.5 David M Garcia Edgar A Campbell Christopher M Jakobson Mitsuhiro Tsuchiya Ethan A Shaw Acadia L DiNardo Matt Kaeberlein Daniel F Jarosz A prion accelerates proliferation at the expense of lifespan
description	In fluctuating environments, switching between different growth strategies, such as those affecting cell size and proliferation, can be advantageous to an organism. Trade-offs arise, however. Mechanisms that aberrantly increase cell size or proliferation—such as mutations or chemicals that interfere with growth regulatory pathways—can also shorten lifespan. Here we report a natural example of how the interplay between growth and lifespan can be epigenetically controlled. We find that a highly conserved RNA-modifying enzyme, the pseudouridine synthase Pus4/TruB, can act as a prion, endowing yeast with greater proliferation rates at the cost of a shortened lifespan. Cells harboring the prion grow larger and exhibit altered protein synthesis. This epigenetic state, [BIG+] (better in growth), allows cells to heritably yet reversibly alter their translational program, leading to the differential synthesis of dozens of proteins, including many that regulate proliferation and aging. Our data reveal a new role for prion-based control of an RNA-modifying enzyme in driving heritable epigenetic states that transform cell growth and survival.
format	article
author	David M Garcia Edgar A Campbell Christopher M Jakobson Mitsuhiro Tsuchiya Ethan A Shaw Acadia L DiNardo Matt Kaeberlein Daniel F Jarosz
author_facet	David M Garcia Edgar A Campbell Christopher M Jakobson Mitsuhiro Tsuchiya Ethan A Shaw Acadia L DiNardo Matt Kaeberlein Daniel F Jarosz
author_sort	David M Garcia
title	A prion accelerates proliferation at the expense of lifespan
title_short	A prion accelerates proliferation at the expense of lifespan
title_full	A prion accelerates proliferation at the expense of lifespan
title_fullStr	A prion accelerates proliferation at the expense of lifespan
title_full_unstemmed	A prion accelerates proliferation at the expense of lifespan
title_sort	prion accelerates proliferation at the expense of lifespan
publisher	eLife Sciences Publications Ltd
publishDate	2021
url	https://doaj.org/article/418f66c5630d4db19a8f8ec90c1a9440
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A prion accelerates proliferation at the expense of lifespan

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