Molecular hydrogen (H₂) is crucial for agricultural microbial systems. However, the mechanisms underlying its influence on crop yields is yet to be fully elucidated. This study observed that H₂-based irrigation significantly increased strawberry (Fragaria × ananassa Duch.) yield with/without nutrient fertilization. The reduction in soil available nitrogen (N), phosphorus (P), potassium (K), and organic matter was consistent with the increased expression levels of N/P/K-absorption-related genes in root tissues at the fruiting stage. Metagenomics profiling showed the alterations in rhizosphere microbial community composition achieved by H₂, particularly under the conditions without fertilizers. These included the enrichment of plant-growth-promoting rhizobacteria, such as Burkholderia, Pseudomonas, and Cupriavidus genera. Rhizobacteria with the capability to oxidize H₂ (group 2a [NiFe] hydrogenase) were also enriched. Consistently, genes related to soil carbon (C) fixation (i.e., rbcL, porD, frdAB, etc.), dissimilar nitrate reduction (i.e., napAB and nrfAH), and P solublization, mineralization, and transportation (i.e., ppx-gppA, appA, and ugpABCE) exhibited higher abundance. Contrary tendencies were observed in the soil C degradation and N denitrification genes. Together, these results clearly indicate that microbe-mediated soil C, N, and P cycles might be functionally altered by H₂, thus increasing plant nutrient uptake capacity and horticultural crop yield.

Chili veinal mottle virus (ChiVMV) causes severe yield losses in solanaceous crops across Asia, making the exploration of host resistance imperative. Although GTPase-activating proteins (GAPs) are known to modulate host-pathogen interactions and participate in plant defense against bacterial and fungal pathogens, their role in antiviral immunity remains largely unexplored. Here, we demonstrate that NtRhoGAP1, a RhoGAP protein from Nicotiana tabacum, confers resistance to ChiVMV by potentiating salicylic acid (SA) defense signaling. SA binding protein 3 (SABP3) as a key regulatory hub integrating NtRhoGAP1-mediated immunity into SA signaling. NtRhoGAP1 interacts with NtSABP3 and modulates its expression and subcellular localization. Importantly, NtRhoGAP1 and NtSABP3 exert antagonistic effects on SA signaling during ChiVMV infection, highlighting their opposing roles in modulating plant immunity. Furthermore, we find that ChiVMV nuclear inclusion protease a (NIa-Pro) specifically binds to NtSABP3. NtSABP3 fails to compromise plant immunity against ChiVMV when it cannot interact with NIa-Pro. These findings unveil that NtRhoGAP1 positively regulates plant immunity by engaging the SA signaling pathway, representing a novel arms race between plants and pathogens.