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Transcriptional activation of auxin biosynthesis drives developmental reprogramming of differentiated cells. | LitMetric

AI Article Synopsis

  • Plant cells can change their differentiation state and regenerate, but the mechanism behind this reversion to pluripotency is not fully understood.
  • This study reveals that activating auxin biosynthesis is essential for reprogramming Arabidopsis leaf cells and that histone acetylation plays a key role in this process.
  • The research shows the importance of auxin signaling in restarting the cell cycle, highlighting the roles of specific genes and proteins in facilitating the regeneration of differentiated cells.

Article Abstract

Plant cells exhibit remarkable plasticity of their differentiation states, enabling regeneration of whole plants from differentiated somatic cells. How they revert cell fate and express pluripotency, however, remains unclear. In this study, we demonstrate that transcriptional activation of auxin biosynthesis is crucial for reprogramming differentiated Arabidopsis (Arabidopsis thaliana) leaf cells. Our data show that interfering with the activity of histone acetyltransferases dramatically reduces callus formation from leaf mesophyll protoplasts. Histone acetylation permits transcriptional activation of PLETHORAs, leading to the induction of their downstream YUCCA1 gene encoding an enzyme for auxin biosynthesis. Auxin biosynthesis is in turn required to accomplish initial cell division through the activation of G2/M phase genes mediated by MYB DOMAIN PROTEIN 3-RELATED (MYB3Rs). We further show that the AUXIN RESPONSE FACTOR 7 (ARF7)/ARF19 and INDOLE-3-ACETIC ACID INDUCIBLE 3 (IAA3)/IAA18-mediated auxin signaling pathway is responsible for cell cycle reactivation by transcriptionally upregulating MYB3R4. These findings provide a mechanistic model of how differentiated plant cells revert their fate and reinitiate the cell cycle to become pluripotent.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9614439PMC
http://dx.doi.org/10.1093/plcell/koac218DOI Listing

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