Aug 2026· Science Advances· Vol 12· 0 citations· 71 references
Medicine
TL;DR
Vitamin B3 secreted by plant roots shapes the assembly of a functionally specialized root microbiota, which metabolizes VB3 into an immune-active signal that enhances plant disease resistance and activation of systemic plant immunity.
Abstract
The microbiota is being increasingly recognized for its ability to regulate host physiology through the production of small bioactive molecules. However, how host-derived nutrients are metabolically transformed by root-associated microbes to influence plant immunity remains poorly understood. Here, we show that vitamin B3 (VB3; niacin) secreted by plant roots shapes the assembly of a functionally specialized root microbiota, which, in turn, metabolizes VB3 into an immune-active signal that enhances plant disease resistance. VB3 secretion selectively increases the abundance of root-associated bacteria harboring a conserved nic biosynthetic gene cluster (BGC), which enables the conversion of VB3 into 6-hydroxynicotinate (6-OHNA), a previously uncharacterized microbial metabolite involved in plant-microbe interactions. Microbially produced 6-OHNA is transported from roots to shoots, where it primes systemic immune responses in a salicylic acid–dependent manner. Disruption of the microbial nic BGC abolishes immune priming, whereas increased VB3 exudation from plant roots enhances disease resistance. Together, these findings reveal a metabolically mediated dialog between plant hosts and their microbiota that links host nutrient secretion to microbial functional specialization and the activation of systemic plant immunity.
Plants produce a diverse range of secondary metabolites [SMs] such as alkaloids, terpenoids and phenolics, which play crucial roles in defense, signalling and human health applications like pharmaceuticals and nutraceuticals. Traditionally viewed as autonomous plant biosynthetic processes, several evidence reveals that...
Priyanka Chauhan, P. Verma, A. Bhattacharya et al.· Discover Life· 0 citations
Induced systemic resistance (ISR) is activated in leaves upon root colonization by beneficial microbes, yet the signals linking rhizosphere perception to shoot immunity remain unknown. In the Arabidopsis thaliana-Pseudomonas simiae WCS417 model interaction, the root-specific transcription factor MYB72 and its target ge...
S. Hsu, Max J. J. Stassen, Kévin Robe et al.· bioRxiv· 0 citations
Microbial pathogens pose a serious challenge to food security under climate change. Microbiomes can filter out incoming pathogens. However, the specific microbial taxa and mechanisms that indicate the response of the microbiome and plant health to the invasion of pathogens remain largely unknown. Here, we combine multi...
Cheng-Jian Hong, Christian Sonne, Yun-Xia Li et al.· Plant, Cell and Environment· 0 citations
In plants, the development of soil-borne diseases has been shown to trigger the recruitment of beneficial microbes, which contribute to defense against pathogens. However, the underlying mechanisms driving this recruitment remain elusive. Here, we used a gnotobiotic system combined with a synthetic bacterial community...
Mohamed Zouaoui, Marie Solau, A. Amiel et al.· bioRxiv· 0 citations
Microbial pathogens require nutrients and water to support their growth and proliferation. Pathogen-mediated resource acquisition is orchestrated by the secretion of virulence factors that have evolved a diversity of forms (from effector proteins to small toxins), but which have converged in function (resource acquisit...
Faye Gaudreault-Lafleur, Charles Roussin-Lévéillée, Sabrina Gauthier et al.· bioRxiv· 0 citations
It is shown that the Arabidopsis NatA N-terminal-acetyltransferase complex acts as a leaf-intrinsic brake on these root-to-leaf systemic responses to ISR priming, enabling plants to sustain lifelong ISR priming without growth penalty.
Xiao-Jie Chen, Gu-Zi Chen, Yao Xu et al.· Proceedings of the National...· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.