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.

Developmental plasticity of plant root systems has been intensively studied, but the mechanisms underpinning robustness remain unclear. Here, the authors show that DNA-methylation-mediated transcriptional repression serves as a backup system to control lateral root development when auxin signalling is perturbed.

Details

Title
Cryptic variation in RNA-directed DNA-methylation controls lateral root development when auxin signalling is perturbed
Author
Shahzad Zaigham 1 ; Eaglesfield Ross 1 ; Carr, Craig 1 ; Amtmann, Anna 1   VIAFID ORCID Logo 

 University of Glasgow, Institute of Molecular, Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, Glasgow, UK (GRID:grid.8756.c) (ISNI:0000 0001 2193 314X) 
Publication year
2020
Publication date
2020
Publisher
Nature Publishing Group
e-ISSN
20411723
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2342995916
Copyright
This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.