| Literature DB >> 31930531 |
Eleazar Rodriguez1, Jonathan Chevalier1, Jakob Olsen1, Jeppe Ansbøl1, Vaitsa Kapousidou1, Zhangli Zuo1, Steingrim Svenning2, Christian Loefke3, Stefanie Koemeda4, Pedro Serrano Drozdowskyj4, Jakub Jez4, Gerhard Durnberger3, Fabian Kuenzl3, Michael Schutzbier3, Karl Mechtler3, Elise Nagel Ebstrup1, Signe Lolle1, Yasin Dagdas3, Morten Petersen1.
Abstract
Somatic cells acclimate to changes in the environment by temporary reprogramming. Much has been learned about transcription factors that induce these cell-state switches in both plants and animals, but how cells rapidly modulate their proteome remains elusive. Here, we show rapid induction of autophagy during temporary reprogramming in plants triggered by phytohormones, immune, and danger signals. Quantitative proteomics following sequential reprogramming revealed that autophagy is required for timely decay of previous cellular states and for tweaking the proteome to acclimate to the new conditions. Signatures of previous cellular programs thus persist in autophagy-deficient cells, affecting cellular decision-making. Concordantly, autophagy-deficient cells fail to acclimatize to dynamic climate changes. Similarly, they have defects in dedifferentiating into pluripotent stem cells, and redifferentiation during organogenesis. These observations indicate that autophagy mediates cell-state switches that underlie somatic cell reprogramming in plants and possibly other organisms, and thereby promotes phenotypic plasticity.Entities:
Keywords: autophagy; cell state switching; de-differentiation; iPSC; temporary reprogramming
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Year: 2020 PMID: 31930531 PMCID: PMC7024839 DOI: 10.15252/embj.2019103315
Source DB: PubMed Journal: EMBO J ISSN: 0261-4189 Impact factor: 11.598