ABSTRACT
The plant microbes are an integral part of the host and play fundamental roles in plant growth and health. There is evidence indicating that plants have the ability to attract beneficial microorganisms through their roots in order to defend against pathogens. However, the mechanisms of plant microbial community assembly from below- to aboveground compartments under pathogen infection remain unclear. In this study, we investigated the bacterial and fungal communities in bulk soil, rhizosphere soil, root, stem, and leaf of both healthy and infected (Potato virus Y disease, PVY) plants. The results indicated that bacterial and fungal communities showed different recruitment strategies in plant organs. The number and abundance of shared bacterial ASVs between bulk and rhizosphere soils decreased with ascending migration from below- to aboveground compartments, while the number and abundance of fungal ASVs showed no obvious changes. Field type, plant compartments, and PVY infection all affected the diversity and structures of microbial community, with stronger effects observed in the bacterial community than the fungal community. Furthermore, PVY infection, rhizosphere soil pH, and water content (WC) contributed more to the assembly of the bacterial community than the fungal community. The analysis of microbial networks revealed that the bacterial communities were more sensitive to PVY infection than the fungal communities, as evidenced by the lower network stability of the bacterial community, which was characterized by a higher proportion of positive edges. PVY infection further increased the bacterial network stability and decreased the fungal network stability. These findings advance our understanding of how microbes respond to pathogen infections and provide a rationale and theoretical basis for biocontrol technology in promoting sustainable agriculture. KEY POINTS: ⢠Different recruitment strategies between plant bacterial and fungal communities. ⢠Bacterial community was more sensitive to PVY infection than fungal community. ⢠pH and WC drove the microbial community assembly under PVY infection.
Subject(s)
Bacteria , Fungi , Plant Diseases , Plant Roots , Rhizosphere , Soil Microbiology , Fungi/physiology , Bacteria/classification , Bacteria/genetics , Bacteria/isolation & purification , Bacteria/metabolism , Plant Diseases/microbiology , Plant Roots/microbiology , Microbiota , Plant Leaves/microbiology , Hydrogen-Ion Concentration , Mycobiome , Plants/microbiologyABSTRACT
Plant health states may influence the distribution of rhizosphere microorganisms, which regulate plant growth and development. In this study, the response of rhizosphere bacteria and fungi of healthy and diseased plants compared to bulk microbes was analyzed using high-throughput sequencing. Plant adaptation strategies of plants under potato virus Y (PVY) infection have been studied from a microbial perspective. The diversity and community structure of bacteria and fungi varied between bulk and rhizosphere soils, but not between healthy and diseased rhizosphere soils. A LEfSe analysis revealed the significant differences between different treatments on bacterial and fungal community compositions and identified Roseiflexaceae, Sphingomonas, and Sphingobium as the bacterial biomarkers of bulk (BCK), healthy rhizosphere (BHS), and diseased rhizosphere (BIS) soils, respectively; Rhodotorula and Ascomycota_unidentified_1_1 were identified as the fungal biomarkers of bulk (FCK) and healthy rhizosphere (FHS) soils. Bacterial networks were found to be more complex and compact than fungal networks and revealed the roles of biomarkers as network keystone taxa. PVY infection further increased the connectedness among microbial taxa to improve rhizosphere microbial community stability and resistance to environmental stress. Additionally, water content (WC) played an apparent influence on bacterial community structure and diversity, and pH showed significant effects on fungal community diversity. WC and pH greatly affected the biomarkers of bacterial rhizosphere communities, whereas the biomarkers of bulk bacterial communities were significantly affected by soil nutrients, especially for Sphingobium. Overall, the rhizosphere microbial community enrichment processes were different between healthy and diseased plants by changing the community compositions and identifying different biomarkers. These findings provide insight into the assemblage of rhizosphere microbial communities and soil physicochemical properties, which contributes to a deeper understanding of the establishment of an artificial core root microbiota to facilitate plant growth and bolstering resistance mechanisms. This knowledge contributes to a deeper understanding of the establishment of an artificial core root microbiota, thereby facilitating plant growth and bolstering resistance mechanisms.
ABSTRACT
Purpose: Atherosclerosis is the main cause of atherosclerotic cardiovascular disease (CVD). Here, we aimed to uncover the role and mechanisms of fat mass and obesity-associated genes (FTO) in the regulation of vascular smooth muscle cell (VSMC) senescence in atherosclerotic plaques. Methods: ApoE-/- mice fed a high-fat diet (HFD) were used to establish an atherosclerotic animal model. Immunohistochemistry, and the staining of hematoxylin-eosin, Oil Red O, Sirius red, and Masson were performed to confirm the role of FTO in atherosclerosis in vivo. Subsequently, FTO expression in primary VSMCs is either upregulated or downregulated. Oxidized low-density lipoprotein (ox-LDL) was used to treat VSMCs, followed by EdU staining, flow cytometry, senescence-associated ß-galactosidase (SA-ß-gal) staining, immunofluorescence, telomere detection, RT-qPCR, and Western blotting to determine the molecular mechanisms by which FTO inhibits VSMC senescence. Results: Decreased FTO expression was observed in progressive atherosclerotic plaques of ApoE-/- mice fed with HFD. FTO upregulation inhibits atherosclerotic lesions in mice. FTO inhibits VSMC aging in atherosclerotic plaques by helping VSMC withstand ox-LDL-induced cell cycle arrest and senescence. This process is achieved by stabilizing the MIS12 protein in VSMC through a proteasome-mediated pathway. Conclusion: FTO inhibits VSMC senescence and subsequently slows the progression of atherosclerotic plaques by stabilizing the MIS12 protein.