Recent progress in understanding the ecology and molecular genetics of soil mineral weathering bacteria.

Mineral weathering bacteria play essential roles in nutrient cycling and plant nutrition. However, we are far from having a comprehensive view of the factors regulating their distribution and the molecular mechanisms involved. In this review, we highlight the extrinsic factors (i.e., nutrient availability, carbon source) and the intrinsic properties of minerals explaining the distribution and functioning of these functional communities. We also present and discuss the progress made in understanding the molecular mechanisms and genes that are used by bacteria during the mineral weathering process, or regulated during their interaction with minerals, that have been recently unraveled by omics approaches.

The mineral weathering ability of Collimonas pratensis PMB3(1) involves a Malleobactin-mediated iron acquisition system.

Mineral weathering by microorganisms is considered to occur through a succession of mechanisms based on acidification and chelation. While the role of acidification is established, the role of siderophores is difficult to disentangle from the effect of the acidification. We took advantage of the ability of strain Collimonas pratensis PMB3(1) to weather minerals but not to acidify depending on the carbon source to address the role of siderophores in mineral weathering. We identified a single non-ribosomal peptide synthetase (NRPS) responsible for siderophore biosynthesis in the PMB3(1) genome. By combining iron-chelating assays, targeted mutagenesis and chemical analyses (HPLC and LC-ESI-HRMS), we identified the siderophore produced as malleobactin X and how its production depends on the concentration of available iron. Comparison with the genome sequences of other collimonads evidenced that malleobactin production seems to be a relatively conserved functional trait, though some collimonads harboured other siderophore synthesis systems. We also revealed by comparing the wild-type strain and its mutant impaired in the production of malleobactin that the ability to produce this siderophore is essential to allow the dissolution of hematite under non-acidifying conditions. This study represents the first characterization of the siderophore produced by collimonads and its role in mineral weathering.

Draft Genome Sequence of Collimonas pratensis Strain PMB3(1), an Effective Mineral-Weathering and Chitin-Hydrolyzing Bacterial Strain.

We announce the draft genome sequence of Collimonas pratensis PMB3(1), isolated from the Scleroderma citrinum mycorrhizosphere. In addition to its mineral-weathering effectiveness and antifungal activity, this strain is characterized by genomic features that give it great potential as a biocontrol and plant growth-promoting agent in nutrient-poor soils.

Dual transcriptomics and proteomics analyses of the early stage of interaction between Caballeronia mineralivorans PML1(12) and mineral.

Minerals and rocks represent essential reservoirs of nutritive elements for the long-lasting functioning of forest ecosystems developed on nutrient-poor soils. While the presence of effective mineral weathering bacteria was evidenced in the rhizosphere of different plants, the molecular mechanisms involved remain uncharacterized. To fill this gap, we combined transcriptomic, proteomics, geo-chemical and physiological analyses to decipher the potential molecular mechanisms explaining the mineral weathering effectiveness of strain PML1(12) of Caballeronia mineralivorans. Considering the early-stage of the interaction between mineral and bacteria, we identified the genes and proteins differentially expressed when: (i) the environment is depleted of certain essential nutrients (i.e., Mg and Fe), (ii) a mineral is added and (iii) the carbon source (i.e., glucose vs mannitol) differs. The integration of these data demonstrates that strain PML1(12) is capable of (i) mobilizing iron through the production of a non-ribosomal peptide synthetase-independent siderophore, (ii) inducing chemotaxis and motility in response to nutrient availability and (iii) strongly acidifying its environment in the presence of glucose using a suite of GMC oxidoreductases to weather mineral. These results provide new insights into the molecular mechanisms involved in mineral weathering and their regulation and highlight the complex sequence of events triggered by bacteria to weather minerals.

The antiviral drug tenofovir, an inhibitor of Pannexin-1-mediated ATP release, prevents liver and skin fibrosis by downregulating adenosine levels in the liver and skin.

BACKGROUND: Fibrosing diseases are a leading cause of morbidity and mortality worldwide and, therefore, there is a need for safe and effective antifibrotic therapies. Adenosine, generated extracellularly by the dephosphorylation of adenine nucleotides, ligates specific receptors which play a critical role in development of hepatic and dermal fibrosis. Results of recent clinical trials indicate that tenofovir, a widely used antiviral agent, reverses hepatic fibrosis/cirrhosis in patients with chronic hepatitis B infection. Belonging to the class of acyclic nucleoside phosphonates, tenofovir is an analogue of AMP. We tested the hypothesis that tenofovir has direct antifibrotic effects in vivo by interfering with adenosine pathways of fibrosis using two distinct models of adenosine and A2AR-mediated fibrosis. METHODS: Thioacetamide (100mg/kg IP)-treated mice were treated with vehicle, or tenofovir (75mg/kg, SubQ) (n = 5-10). Bleomycin (0.25U, SubQ)-treated mice were treated with vehicle or tenofovir (75mg/kg, IP) (n = 5-10). Adenosine levels were determined by HPLC, and ATP release was quantitated as luciferase-dependent bioluminescence. Skin breaking strength was analysed and H&E and picrosirus red-stained slides were imaged. Pannexin-1expression was knocked down following retroviral-mediated expression of of Pannexin-1-specific or scrambled siRNA. RESULTS: Treatment of mice with tenofovir diminished adenosine release from the skin of bleomycin-treated mice and the liver of thioacetamide-treated mice, models of diffuse skin fibrosis and hepatic cirrhosis, respectively. More importantly, tenofovir treatment diminished skin and liver fibrosis in these models. Tenofovir diminished extracellular adenosine concentrations by inhibiting, in a dose-dependent fashion, cellular ATP release but not in cells lacking Pannexin-1. CONCLUSIONS: These studies suggest that tenofovir, a widely used antiviral agent, could be useful in the treatment of fibrosing diseases.