Background Salt marshes are dominated by the smooth cordgrass Spartina alterniflora on the US Atlantic and Gulf of Mexico coastlines. Although soil microorganisms are well known to mediate important biogeochemical cycles in salt marshes, little is known about the role of root microbiomes in supporting the health and productivity of marsh plant hosts. Leveraging in situ gradients in aboveground plant biomass as a natural laboratory, we investigated the relationships between S. alterniflora primary productivity, sediment redox potential, and the physiological ecology of bulk sediment, rhizosphere, and root microbial communities at two Georgia barrier islands over two growing seasons. Results A marked decrease in prokaryotic alpha diversity with high abundance and increased phylogenetic dispersion was found in the S. alterniflora root microbiome. Significantly higher rates of enzymatic organic matter decomposition, as well as the relative abundances of putative sulfur (S)-oxidizing, sulfate-reducing, and nitrifying prokaryotes correlated with plant productivity. Moreover, these functional guilds were overrepresented in the S. alterniflora rhizosphere and root core microbiomes. Core microbiome bacteria from the Candidatus Thiodiazotropha genus, with the metabolic potential to couple S oxidation with C and N fixation, were shown to be highly abundant in the root and rhizosphere of S. alterniflora. Conclusions The S. alterniflora root microbiome is dominated by highly active and competitive species taking advantage of available carbon substrates in the oxidized root zone. Two microbially mediated mechanisms are proposed to stimulate S. alterniflora primary productivity: (i) enhanced microbial activity replenishes nutrients and terminal electron acceptors in higher biomass stands, and (ii) coupling of chemolithotrophic S oxidation with carbon (C) and nitrogen (N) fixation by root- and rhizosphere-associated prokaryotes detoxifies sulfide in the root zone while potentially transferring fixed C and N to the host plant.
The present study aimed to investigate the effects of sevoflurane post-conditioning in a rat brain cerebral ischemia-reperfusion (I/R) model and examine its possible mechanism. Rats were randomly divided into six groups: Sham control group (Sham), I/R group, sevoflurane group (Se), Toll-like receptor-4 (TLR4) inhibitor group (Tak-242), nuclear factor (NF)-κB inhibitor group (QNZ) and Sevoflurane post-conditioning combined with TLR4-NF-κB signaling pathway inhibitor group (Se + Tak-242). Morris water maze test and tetrazolium chloride staining were used to investigate the I/R injury. The nerve cell apoptosis and autophagy in cortical tissue were detected by TUNEL and transmission electron microscopy, respectively. The expression of TLR4 protein in cortical tissue was observed by immunohistochemical staining. The expression of autophagy and apoptotic associated proteins in cortical tissues and the activity of TLR4-NF-κB signaling pathway were assayed by western blot analysis. Sevoflurane post-conditioning improved the learning and memory dysfunction caused by cerebral I/R injury. The cerebral infarction area, nerve cell apoptosis and formation of autophagic vacuoles were reduced after sevoflurane administration. The expression of light chain 3II/I, Beclin-1, Bad and Cleaved-Caspase-3 proteins were inhibited and the expression of Bcl-2 protein was upregulated after sevoflurane administration. Sevoflurane post-conditioning also inhibited the TLR4 protein and NF-κB phosphorylation, and increased inhibitor of kBα phosphorylation. The treatment effect of Tak-242 and QNZ groups were not significantly different compared with the Se group (P>0.05), and the Se + Tak-242 group had the best results. The present study demonstrated that sevoflurane post-conditioning could protect middle cerebral artery occlusion-induced brain injury rats by inhibiting autophagy and apoptosis, and that its mechanism is related to the TLR4-NF-κB signaling pathway.
We show for the first time that PD-1 is palmitoylated, identify DHHC9 as the predominant enzyme for its palmitoylation, and reveal the molecular mechanisms underlying its effects on PD-1 stability and functions. Importantly, we also designed PD1-PALM, a competitive inhibitor of PD-1 palmitoylation, and this first-in-class molecule may inspire the development of new checkpoint inhibitors.
Summary Recent studies have shown that application of conductive materials including magnetite and carbon nanotubes (CNTs) can promote the methanogenic decomposition of short‐chain fatty acids and even more complex organic matter in anaerobic digesters and natural habitats. The linkage to microbial identity and the mechanisms, however, remain poorly understood. Here, we evaluate the effects of nanoscale magnetite (nanoFe3O4) and multiwalled CNTs on the syntrophic oxidation of propionate in an enrichment obtained from lake sediment. The microbial populations were composed mainly of Smithella, Syntrophomonas, Methanosaeta, Methanosarcina and Methanoregula. In addition to acetate, butyrate was transiently accumulated indicating that propionate was oxidized by Smithella via the dismutation pathway and part of the leaked butyrate was oxidized by Syntrophomonas. Propionate oxidation and CH4 production were significantly accelerated in the presence of nanoFe3O4 and CNTs. While propionate oxidation was suppressed upon H2 application and suspended completely upon formate application in the control, this suppressive effect was substantially compromised in the presence of nanoFe3O4 and CNTs. The tests on hydrogenotrophic methanogenesis of a pure culture methanogen and of the enrichment culture without propionate showed negative effect by both materials. The positive effect of nanoFe3O4 disappeared when it was insulated by surface‐coating with silica. Observations made with fluorescence in situ hybridization and scanning electron microscope indicated the extensive formation of microbial cell‐conductive material mixture aggregates. Our results suggest that direct interspecies electron transfer is likely activated by the conductive materials and operates in concert with H2/formate‐dependent electron transfer for syntrophic propionate oxidation in the sediment enrichment.
A number of cell fate determinations, including cell division, cell differentiation, and programmed cell death, intensely occur during plant germline development. How these cell fate determinations are regulated remains largely unclear. The transcription factor E2F is a core cell cycle regulator. Here we show that the Arabidopsis canonical E2Fs, including E2Fa, E2Fb, and E2Fc, play a redundant role in plant germline development. The e2fa e2fb e2fc (e2fabc) triple mutant is sterile, although its vegetative development appears normal. On the one hand, the e2fabc microspores undergo cell death during pollen mitosis. Microspores start to die at the bicellular stage. By the tricellular stage, the majority of the e2fabc microspores are degenerated. On the other hand, a wild type ovule often has one megaspore mother cell (MMC), whereas the majority of e2fabc ovules have two to three MMCs. The subsequent female gametogenesis of e2fabc mutant is aborted and the vacuole is severely impaired in the embryo sac. Analysis of transmission efficiency showed that the canonical E2Fs from both male and female gametophyte are essential for plant gametogenesis. Our study reveals that the canonical E2Fs are required for plant germline development, especially the pollen mitosis and the archesporial cell (AC)-MMC transition.
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