Year-end Sale % OFF 
Abstract
Maintaining the right balance between plasticity and robustness in biological systems is important to allow adaptation while maintaining essential functions. Developmental plasticity of plant root systems has been the subject of intensive research, but the mechanisms underpinning robustness remain unclear. Here, we show that potassium deficiency inhibits lateral root organogenesis by delaying early stages in the formation of lateral root primordia. However, the severity of the symptoms arising from this perturbation varies within a natural population of Arabidopsis and is associated with the genetic variation in CLSY1, a key component of the RNA-directed DNA-methylation machinery. Mechanistically, CLSY1 mediates the transcriptional repression of a negative regulator of root branching, IAA27, and promotes lateral root development when the auxin-dependent proteolysis pathway fails. Our study identifies DNA-methylation-mediated transcriptional repression as a backup system for post-translational protein degradation which ensures robust development and performance of plants in a challenging environment.
Highlights
Maintaining the right balance between plasticity and robustness in biological systems is important to allow adaptation while maintaining essential functions
lateral roots (LRs) emerge from xylem-pole cell triplets, so-called founder cells (FCs), which occur at regular longitudinal intervals in the pericycle layer that surrounds the central vasculature[6]
The transcriptional programmes that underpin the different stages of LR development are activated by auxin responsive factors (ARFs), which bind to auxin responsive elements (AuxRe) in the promoters of their target genes
Summary
Maintaining the right balance between plasticity and robustness in biological systems is important to allow adaptation while maintaining essential functions. Based on a genome-wide association (GWA) study of lateral root development under low-K conditions, we report here that genetic variation in a CLASSY chromatin remodelling factor (CLSY1) determines the robustness of LR development against perturbation of the auxin pathway by low K. Using a combination of cell biology and molecular genetics experiments we provide evidence that CLSY1-mediated silencing of IAA27 provides a ‘backup switch’ for maintaining lateral root development when the canonical auxin-mediated pathway is disrupted. Genetic variation in this backup circuit is cryptic and only becomes apparent under environmental or genetic challenge
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
