Portrait of author

Jonathan Chevalier:
Autophagy mediate cellular reprogramming. The role of the decay pathway during cellular reprogramming

Date: 17-01-2020    Supervisor: Morten Petersen

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 previous cellular 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 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.