Biology subjects

Chevalier, J.

Publications and source records attributed to Chevalier, J..

5 recordsLinked to original sources

bioRxiv2025

Autophagic degradation of EIN3 ensures developmental plasticity and recovery from environmental stress in Arabidopsis

Ethylene signaling, mediated by the key transcription factor EIN3, regulates diverse developmental processes and stress adaptations, including hypocotyl growth, aging, and submergence tolerance. Autophagy, a cellular recycling process, also facilitates adaptation by reprogramming cellular components. While EIN3 degradation via the proteasome is well established, its connection to autophagy remains unclear. Here, we show that EIN3 turnover is directly regulated by ATG8-mediated autophagy. Consistently, autophagy-deficient plants exhibit impaired EIN3-dependent hypocotyl growth during light-to-dark transitions. Additionally, EIN3 accumulation contributes to the premature senescence observed in atg mutants. Beyond development, our combination of cell imaging, phenotypic analyses, and proteomics reveals that autophagy is essential for EIN3-driven transcriptional reprogramming during submergence. Together, our findings uncover a direct role for autophagy in regulating EIN3 stability, providing mechanistic insight into how this process fine-tunes ethylene responses in growth and stress adaptation.

plant biology↗

bioRxiv2022

Autophagy regulates ARF7 degradation to facilitate 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. Additionally, we prove that the level of co- localization between ARF7 and autophagy markers oscillates and can be modulated by auxin to trigger ARF7 turnover. Furthermore, we observed 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.

plant biology↗

bioRxiv2022

mRNA decapping machinery targets LBD3/ASL9 transcripts to allow developmental changes in Arabidopsis

Multicellular organisms perceive and transduce multiple cues to optimize development. Key transcription factors drive developmental changes, but RNA processing also contributes to tissue development. Here, we report that multiple decapping deficient mutants share developmental defects in apical hook, primary and lateral root growth. More specifically, LATERAL ORGAN BOUNDARIES DOMAIN 3 (LBD3)/ASYMMETRIC LEAVES 2-LIKE 9 (ASL9) transcripts accumulate in decapping deficient plants and can be found in complexes with decapping components. Accumulation of ASL9 inhibits apical hook, primary root growth and lateral root formation. Interestingly, exogenous auxin application restores lateral roots formation in both ASL9 over-expressors and mRNA decay-deficient mutants. Likewise, mutations in the cytokinin transcription factors type-B ARABIDOPSIS RESPONSE REGULATORS (B-ARRs) ARR10 and ARR12 restore the developmental defects caused by over-accumulation of capped ASL9 transcript upon ASL9 overexpression. Most importantly, loss-of-function of asl9 partially restores apical hook and lateral root formation in decapping deficient mutants. Thus, the mRNA decay machinery directly targets ASL9 transcripts for decay, possibly to interfere with cytokinin/auxin responses, during development.

developmental biology↗

bioRxiv2020

Natural selection and the advantage of recombination

The ubiquity of sex and recombination in nature is widely viewed as enigmatic, despite an abundance of limited-scope explanations. Natural selection, it seems, should amplify well-matched combinations of genes. Recombination would break up these well-matched combinations and should thus be suppressed. We show, to the contrary, that on average: 1) natural selection amplifies poorly-matched gene combinations and 2) creates time-averaged negative associations in the process. Recombination breaks up these poorly-matched combinations, neutralizes the negative associations, and should thus be passively and universally favored.

evolutionary biology↗

bioRxiv2019

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.

plant biology↗