Trichoderma-secreted anthranilic acid promotes lateral root development via auxin signaling and RBOHF-induced endodermal cell wall remodeling.

Cell Rep

Key Lab of Organic-Based Fertilizers of China and Jiangsu Provincial Key Lab for Solid Organic Waste Utilization, Nanjing Agricultural University, Nanjing 210095, China. Electronic address:

Published: April 2024

AI Article Synopsis

  • Trichoderma spp. produce secondary metabolites that help them communicate with plants and influence root development, although the specifics of how they do this are not well understood.
  • The compound anthranilic acid (2-AA), found in T. guizhouense NJAU4742, promotes the formation of lateral roots by enhancing auxin signaling and transport.
  • This study highlights 2-AA's role in lateral root development, showing that it works through mechanisms distinct from its known involvement in indole-3-acetic acid biosynthesis.

Article Abstract

Trichoderma spp. have evolved the capacity to communicate with plants by producing various secondary metabolites (SMs). Nonhormonal SMs play important roles in plant root development, while specific SMs from rhizosphere microbes and their underlying mechanisms to control plant root branching are still largely unknown. In this study, a compound, anthranilic acid (2-AA), is identified from T. guizhouense NJAU4742 to promote lateral root development. Further studies demonstrate that 2-AA positively regulates auxin signaling and transport in the canonical auxin pathway. 2-AA also partly rescues the lateral root numbers of CASP1:shy2-2, which regulates endodermal cell wall remodeling via an RBOHF-induced reactive oxygen species burst. In addition, our work reports another role for microbial 2-AA in the regulation of lateral root development, which is different from its better-known role in plant indole-3-acetic acid biosynthesis. In summary, this study identifies 2-AA from T. guizhouense NJAU4742, which plays versatile roles in regulating plant root development.

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Source
http://dx.doi.org/10.1016/j.celrep.2024.114030DOI Listing

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