Abstract

Lateral roots (LRs) dominate the overall root surface of adult plants and are crucial for soil exploration and nutrient acquisition. When grown under mild nitrogen (N) deficiency, flowering plants develop longer LRs to enhance nutrient acquisition. This response is partly mediated by brassinosteroids (BR) and yet unknown mechanisms. Here, we show that local auxin biosynthesis modulates LR elongation while allelic coding variants of YUCCA8 determine the extent of elongation under N deficiency. By up-regulating the expression of YUCCA8/3/5/7 and of Tryptophan Aminotransferase of Arabidopsis 1 (TAA1) under mild N deficiency auxin accumulation increases in LR tips. We further demonstrate that N-dependent auxin biosynthesis in LRs acts epistatic to and downstream of a canonical BR signaling cascade. The uncovered BR-auxin hormonal module and its allelic variants emphasize the importance of fine-tuning hormonal crosstalk to boost adaptive root responses to N availability and offer a path to improve soil exploration by expanded root systems in plants.

Highlights

  • Lateral roots (LRs) dominate the overall root surface of adult plants and are crucial for soil exploration and nutrient acquisition

  • Whereas previous studies have shown that low N availability increases auxin levels in roots[32,33,34], our results indicated that this relies on a YUCCA-dependent increase in local auxin biosynthesis

  • We show that coding variation in the YUC8 gene determines the extent of LR elongation under mild N deficiency and that Tryptophan Aminotransferase of Arabidopsis 1 (TAA1)- and YUC5/7/8-dependent local auxin biosynthesis acts downstream of BR signaling to regulate this response (Fig. 6)

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Summary

Introduction

Lateral roots (LRs) dominate the overall root surface of adult plants and are crucial for soil exploration and nutrient acquisition. When grown under mild nitrogen (N) deficiency, flowering plants develop longer LRs to enhance nutrient acquisition This response is partly mediated by brassinosteroids (BR) and yet unknown mechanisms. While PR and LR responses to low N were in overall attenuated in BR-deficient mutants of Arabidopsis thaliana, loss of BRASSINOSTEROID SIGNALING KINASE 3 (BSK3) completely suppressed the response of PR but not of LRs24. These results indicate that additional signaling or regulatory components mediate N-dependent LR elongation. Our results reveal the importance of hormonal crosstalk in LRs where BRs and auxin act synergistically to stimulate cell elongation in response to low N availability

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