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.

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.

Overexpression of ATG8/LC3 enhances wound-induced somatic reprogramming in Physcomitrium patens.

Animal and plant somatic cells have the capacity to switch states or reprogram into stem cells to adapt during stress and injury. This ability to deal with stochastic changes or reprogramming of somatic cells also needs macroautophagy/autophagy. Here, we expand on this notion and provide a primary example of how overexpression of ATG8/LC3 in the moss Physcomitrium patens enhances the ability to reprogram somatic cells into stem cells when subjected to severe wounding. This observation suggests that autophagy is not only required for cells to dedifferentiate but also makes cells more competent to do so.Abbreviation: ATG: autophagy related; atg5: AUTOPHAGY 5; ATG8/LC3: AUTOPHAGY 8/microtubule associated protein 1 light chain 3; GFP: green fluorescent protein.