Abstract
Lateral root (LR) formation is an example of a plant post-embryonic organogenesis event. LRs are issued from non-dividing cells entering consecutive steps of formative divisions, proliferation and elongation. The chromatin remodeling protein PICKLE (PKL) negatively regulates auxin-mediated LR formation through a mechanism that is not yet known. Here we show that PKL interacts with RETINOBLASTOMA-RELATED 1 (RBR1) to repress the LATERAL ORGAN BOUNDARIES-DOMAIN 16 (LBD16) promoter activity. Since LBD16 function is required for the formative division of LR founder cells, repression mediated by the PKL–RBR1 complex negatively regulates formative division and LR formation. Inhibition of LR formation by PKL–RBR1 is counteracted by auxin, indicating that, in addition to auxin-mediated transcriptional responses, the fine-tuned process of LR formation is also controlled at the chromatin level in an auxin-signaling dependent manner.
Highlights
Lateral roots (LRs) are initiated in lateral root founder cells in the pericycle
This developmental process initiates by auxin signaling converging on protoxylem pericycle cells, which promotes the degradation of AUXIN/INDOLE-3ACETIC ACID (Aux/IAA) proteins involved in LR initiation (LRI) [6]
Elimination of Aux/IAA repressors through SKP-Cullin-F-box (TIR1/AFB) (SCFTIR1/AFB) ubiquitin ligase complexes and the 26S proteasome results in activation of AUXIN RESPONSE FACTOR (ARF)7/ARF19 transcription factors to drive the expression of LATERAL ORGAN BOUNDARIES DOMAIN/ASYMMETRIC LEAVES-LIKE (LBD/ASL) LATERAL ORGAN BOUNDARIESDOMAIN 16 (LBD16)/ASL18, LBD29/ASL16 and many other target genes required for auxin response, LRI and development [7]
Summary
Lateral roots (LRs) are initiated in lateral root founder cells in the pericycle. In the model plant Arabidopsis (Arabidopsis thaliana) and many other species, LRs arise from pericycle cells opposite the xylem pole [1]. PICKLE is a plant homologue of the animal chromatin remodeling ATPase Mi-2/CHD3/4 proteins, which in vertebrates form the Mi-2/nucleosome remodeling and deacetylase (NuRD) repressor complexes regulating chromatin organization, gene transcription and developmental signaling [12]. In vertebrates pRB is often present in chromatin repressor complexes that have roles in developmental transitions [17,18] These findings strongly suggest that the pRB protein regulates cellular differentiation separate from its function in cell cycle progression [19]. The RBR1–MSI1 interaction takes place at the RbA pocket domain of RBR1, leaving the LxCxE binding cleft that is located on the RbB pocket domain available for protein binding [23] This intera3ctoifo1n7 topology enables RBR1 to recruit histone deacetylases and simultaneously associate with transcription factors and chromatin modifiers containing the LxCxE motif.
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