Disentangling the molecular mechanisms of disease suppression by endophytic Flavobacterium sp. 98

TY - JOUR

T1 - Disentangling the molecular mechanisms of disease suppression by endophytic Flavobacterium sp. 98

AU - Pan, Xinya

AU - Elsayed, Somayah S.

AU - van Wezel, Gilles P.

AU - Raaijmakers, Jos M.

AU - Carrión, Víctor J.

N1 - Data archiving: no NIOO data

PY - 2026/3

Y1 - 2026/3

N2 - Endophytic microorganisms colonize internal plant tissues and enhance host resistance to pathogens. We previously showed that endophytic Flavobacterium sp. 98 (Fl98) protects sugar beet against the fungal root pathogen Rhizoctonia solani via biosynthetic gene cluster 298 (BGC298) . However, the molecular mechanisms underlying this protection remained poorly understood. Here, comparative metabolomic analyses revealed that knockout of BGC298 led to reduced production of the antifungal compound 5,6-dimethylbenzimidazole (DMB) in Fl98. We hypothesized that BGC298 is involved in regulating DMB biosynthesis and therefore contributes to Fl98’s disease suppression as a novel protective mechanism. Subsequent site-directed mutagenesis of the DMB-synthase gene bluB abolished DMB production by Fl98, and both ΔBGC298 and Δ bluB mutants were compromised in protecting sugar beet seedlings in greenhouse bioassays. Bioinformatic analyses further indicated that bluB is widespread across Flavobacterium , while BGC298 is limited to a small subset of plant-associated strains. Together, our findings highlight the pivotal role of BGC298 and DMB biosynthesis in plant protection by endophytic Flavobacterium sp. 98.

AB - Endophytic microorganisms colonize internal plant tissues and enhance host resistance to pathogens. We previously showed that endophytic Flavobacterium sp. 98 (Fl98) protects sugar beet against the fungal root pathogen Rhizoctonia solani via biosynthetic gene cluster 298 (BGC298) . However, the molecular mechanisms underlying this protection remained poorly understood. Here, comparative metabolomic analyses revealed that knockout of BGC298 led to reduced production of the antifungal compound 5,6-dimethylbenzimidazole (DMB) in Fl98. We hypothesized that BGC298 is involved in regulating DMB biosynthesis and therefore contributes to Fl98’s disease suppression as a novel protective mechanism. Subsequent site-directed mutagenesis of the DMB-synthase gene bluB abolished DMB production by Fl98, and both ΔBGC298 and Δ bluB mutants were compromised in protecting sugar beet seedlings in greenhouse bioassays. Bioinformatic analyses further indicated that bluB is widespread across Flavobacterium , while BGC298 is limited to a small subset of plant-associated strains. Together, our findings highlight the pivotal role of BGC298 and DMB biosynthesis in plant protection by endophytic Flavobacterium sp. 98.

KW - 5,6-dimethylbenzimidazole

KW - Comparative genomics

KW - Disease-suppressive soil

KW - Endophytic microbiome

KW - Flavobacterium

KW - Molecular mechanisms

U2 - 10.1016/j.micres.2025.128415

DO - 10.1016/j.micres.2025.128415

M3 - Article

AN - SCOPUS:105024379499

SN - 0944-5013

VL - 304

JO - Microbiological Research

JF - Microbiological Research

M1 - 128415

ER -