NBR1-mediated selective autophagy of ARF7 modulates root branching.

Auxin dictates root architecture via the Auxin Response Factor (ARF) family of transcription factors, which control lateral root (LR) formation. In Arabidopsis, ARF7 regulates the specification of prebranch sites (PBS) generating LRs through gene expression oscillations and plays a pivotal role during LR initiation. Despite the importance of ARF7 in this process, there is a surprising lack of knowledge about how ARF7 turnover is regulated and how this impacts root architecture. Here, we show that ARF7 accumulates in autophagy mutants and is degraded through NBR1-dependent selective autophagy. We demonstrate that the previously reported rhythmic changes to ARF7 abundance in roots are modulated via autophagy and might occur in other tissues. In addition, we show that the level of co-localization between ARF7 and autophagy markers oscillates and can be modulated by auxin to trigger ARF7 turnover. Furthermore, we observe that autophagy impairment prevents ARF7 oscillation and reduces both PBS establishment and LR formation. In conclusion, we report a novel role for autophagy during development, namely by enacting auxin-induced selective degradation of ARF7 to optimize periodic root branching.

Going through changes - the role of autophagy during reprogramming and differentiation.

Somatic cell reprogramming is a complex feature that allows differentiated cells to undergo fate changes into different cell types. This process, which is conserved between plants and animals, is often achieved via dedifferentiation into pluripotent stem cells, which have the ability to generate all other types of cells and tissues of a given organism. Cellular reprogramming is thus a complex process that requires extensive modification at the epigenetic and transcriptional level, unlocking cellular programs that allow cells to acquire pluripotency. In addition to alterations in the gene expression profile, cellular reprogramming requires rearrangement of the proteome, organelles and metabolism, but these changes are comparatively less studied. In this context, autophagy, a cellular catabolic process that participates in the recycling of intracellular constituents, has the capacity to affect different aspects of cellular reprogramming, including the removal of protein signatures that might hamper reprogramming, mitophagy associated with metabolic reprogramming, and the supply of energy and metabolic building blocks to cells that undergo fate changes. In this Review, we discuss advances in our understanding of the role of autophagy during cellular reprogramming by drawing comparisons between plant and animal studies, as well as highlighting aspects of the topic that warrant further research.

Autophagy mediates temporary reprogramming and dedifferentiation in plant somatic cells.

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.