Autophagy mediate cellular reprogramming

Publikation: Bog/antologi/afhandling/rapportPh.d.-afhandlingForskning

Standard

Autophagy mediate cellular reprogramming. / Chevalier, Jonathan Renaud.

Department of Biology, Faculty of Science, University of Copenhagen, 2020.

Publikation: Bog/antologi/afhandling/rapportPh.d.-afhandlingForskning

Harvard

Chevalier, JR 2020, Autophagy mediate cellular reprogramming. Department of Biology, Faculty of Science, University of Copenhagen.

APA

Chevalier, J. R. (2020). Autophagy mediate cellular reprogramming. Department of Biology, Faculty of Science, University of Copenhagen.

Vancouver

Chevalier JR. Autophagy mediate cellular reprogramming. Department of Biology, Faculty of Science, University of Copenhagen, 2020.

Author

Chevalier, Jonathan Renaud. / Autophagy mediate cellular reprogramming. Department of Biology, Faculty of Science, University of Copenhagen, 2020.

Bibtex

@phdthesis{95b82c607363443a90e1916e771df5b2,
title = "Autophagy mediate cellular reprogramming",
abstract = "Going through their life cycle plants, as all organisms, face numerous developmental cues in addition to environmental challenges. All those stimuli require rapid response to adapt and survive. Somatic cells acclimate to changes in the environment by temporary reprogramming. Much has been learned about transcription factors that induce these cellstate switches in both plants and animals, but how cells rapidly modulate their proteome remains elusive. In this study we show that autophagy, and decay machinery, are necessary to efficiently adjust to new conditions. In plants, autophagy is rapidly induced during temporary reprogramming triggered by phytohormones, immune, and danger signals. Quantitative proteomics following sequential reprogramming revealed that autophagy is required for timely removal of the previouscellular states allowing the new program to unfold and preventing contradictory information being relay to the nucleus. Signatures of previous cellular programs thus persist in autophagy-deficient cells, affecting cellular decision-making. Autophagy appears to be needed to keep the new program into physiological range and prevent accumulation of newly synthesized protein. Concordantly, autophagy deficient cells fail to acclimatize to dynamic climate changes. Similarly, they have defects in dedifferentiating into pluripotent stem cells, and redifferentiation duringorganogenesis. 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 .",
author = "Chevalier, {Jonathan Renaud}",
year = "2020",
language = "English",
publisher = "Department of Biology, Faculty of Science, University of Copenhagen",

}

RIS

TY - BOOK

T1 - Autophagy mediate cellular reprogramming

AU - Chevalier, Jonathan Renaud

PY - 2020

Y1 - 2020

N2 - Going through their life cycle plants, as all organisms, face numerous developmental cues in addition to environmental challenges. All those stimuli require rapid response to adapt and survive. Somatic cells acclimate to changes in the environment by temporary reprogramming. Much has been learned about transcription factors that induce these cellstate switches in both plants and animals, but how cells rapidly modulate their proteome remains elusive. In this study we show that autophagy, and decay machinery, are necessary to efficiently adjust to new conditions. In plants, autophagy is rapidly induced during temporary reprogramming triggered by phytohormones, immune, and danger signals. Quantitative proteomics following sequential reprogramming revealed that autophagy is required for timely removal of the previouscellular states allowing the new program to unfold and preventing contradictory information being relay to the nucleus. Signatures of previous cellular programs thus persist in autophagy-deficient cells, affecting cellular decision-making. Autophagy appears to be needed to keep the new program into physiological range and prevent accumulation of newly synthesized protein. Concordantly, autophagy deficient cells fail to acclimatize to dynamic climate changes. Similarly, they have defects in dedifferentiating into pluripotent stem cells, and redifferentiation duringorganogenesis. 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 .

AB - Going through their life cycle plants, as all organisms, face numerous developmental cues in addition to environmental challenges. All those stimuli require rapid response to adapt and survive. Somatic cells acclimate to changes in the environment by temporary reprogramming. Much has been learned about transcription factors that induce these cellstate switches in both plants and animals, but how cells rapidly modulate their proteome remains elusive. In this study we show that autophagy, and decay machinery, are necessary to efficiently adjust to new conditions. In plants, autophagy is rapidly induced during temporary reprogramming triggered by phytohormones, immune, and danger signals. Quantitative proteomics following sequential reprogramming revealed that autophagy is required for timely removal of the previouscellular states allowing the new program to unfold and preventing contradictory information being relay to the nucleus. Signatures of previous cellular programs thus persist in autophagy-deficient cells, affecting cellular decision-making. Autophagy appears to be needed to keep the new program into physiological range and prevent accumulation of newly synthesized protein. Concordantly, autophagy deficient cells fail to acclimatize to dynamic climate changes. Similarly, they have defects in dedifferentiating into pluripotent stem cells, and redifferentiation duringorganogenesis. 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 .

M3 - Ph.D. thesis

BT - Autophagy mediate cellular reprogramming

PB - Department of Biology, Faculty of Science, University of Copenhagen

ER -

ID: 237194174