However, the mechanisms controlling the proliferation potential of LRP cells at these stages remain poorly understood. The final LRP size depends on the balance between positive and negative signals that regulate cell proliferation. In addition, reactive oxygen species (ROS) have recently been implicated in lateral root development, although the complex gene network is still largely unknown (Manzano et al., 2014 Reyt et al., 2015 Orman-Ligeza et al., 2016). LRP emergence through the outer root cell layers involves active crosstalk with overlying layers such as the endodermis and cortex (Swarup et al., 2008 Marhavy et al., 2013 Porco et al., 2016). Several mechanisms contribute to the growth of LRP including a defined auxin transport (Marhavy et al., 2016). Later, cells continue dividing to produce new cell layers within the LRP. In the initial stages I–II, LRP founder cells divide anticlinally to increase the width of the LRP, a process restricted by ACR4 (De Smet et al., 2008). Initiation and progression of LRPs require a number of divisions of the lateral root founder cells in the pericycle (De Smet et al., 2008 Dubrovsky et al., 2008 Petricka et al., 2012 Lucas et al., 2013 Van Norman et al., 2013 Wachsman et al., 2015 von Wangenheim et al., 2016). Thus, LRPs are initiated from founder cells, by triggering new formative divisions that increase cell number within the LRP. Lateral root primordia (LRPs) arise from the pericycle cell layer where, at roughly regular intervals, a few cells become competent to divide in an auxin-dependent manner (De Smet et al., 2007 De Rybel et al., 2010 Moreno-Risueno et al., 2010). Development of lateral roots is one example of de novo organogenesis that is particularly relevant for root architecture. This entails a continuous recruitment of cells to form organ primordia (Gutierrez, 2005 Scheres, 2007). ![]() The post-embryonic mode of organogenesis in plants, unlike animals, involves the formation of new organs throughout adult life. Our results uncover a role for MYB36 outside the endodermis during LRP development through a mechanism analogous to regulating the proliferation/differentiation transition in the root meristem.Reducing the levels of hydrogen peroxide (H 2O 2) in myb36-5 significantly rescues the mutant phenotype. This was required to define the transition between proliferating and arrested cells inside the LRP, coinciding with the change from flat to dome-shaped primordia. MYB36 was expressed in the cells surrounding LRP where it controls a set of peroxidase genes, which maintain reactive oxygen species (ROS) balance. We found that MYB36 is a novel component of LR development at later stages.We found that Arabidopsis thaliana MYB36, which have been previously shown to regulate genes required for Casparian strip formation and the transition from proliferation to differentiation in the primary root, plays a new role in controlling LRP development at later stages. The mechanisms controlling proliferation potential of LRP cells remains poorly understood. ![]() The LRP size and shape depends on the balance between positive and negative signals that control cell proliferation. These are initiated from founder cells, triggering new formative divisions that generate lateral root primordia (LRP).
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