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The interesting problem in the research area based on previous research is that the rocks have been changed due to hydrothermal alteration processes and many ore mineralizations are found. This research was conducted to study alteration due to hydrothermal processes, as well as to determine the distribution of alteration zones and their relationship to metal mineralization. The research location is located in the Beruang Kanan area, Tumbang Miri District, Gunung Mas Regency, Central Kalimantan Province. Ore mineral paragenesis is a sequential stage in the formation of ore minerals from the initial phase of formation to the final phase. The stage of mineralization can be identified from the identification of ore mineral paragenesis. Identification of ore mineral paragenesis is identified using an ore microscope. The stages of metal mineral paragenesis at the research location itself are divided into 4, namely: early, middle, late, and supergene. The early to late stages are the stages of metal mineral formation hypogenely. These three stages include the process of metal mineral deposition in the magmatic to hydrothermal phases. The early stages and main mineralization are referred to as the hypogene stage.

Although biomineralization of CaCO 3 is widespread in Bacteria and Archaea, the molecular mechanisms involved in this process remain less known than those used by Eukaryotes. A better understanding of these mechanisms is crucial for a broad diversity of studies including those (i) aiming at assessing the role of bacteria in the geochemical cycles of Ca and C, (ii) investigating the process of fossilization, and (iii) engineering applications using bacterially mediated CaCO 3 mineralization. Different types of bacterially-mediated mineralization modes have been distinguished depending on whether they are influenced (by extracellular organic molecules), induced (by metabolic activity) or controlled (by specific genes). In the first two types, mineralization is usually extracellular, while it is intracellular for the two ascertained cases of controlled bacterial mineralization. In this review, we list a large number of cases illustrating the three different modes of bacterially-mediated CaCO 3 mineralization. Overall, this shows the broad diversity of metabolic pathways, organic molecules and thereby microorganisms that can biomineralize CaCO 3 . Providing an improved understanding of the mechanisms involved and a good knowledge of the molecular drivers of carbonatogenesis, the increasing number of (meta)-omics studies may help in the future to estimate the significance of bacterially mediated CaCO 3 mineralization.

Abstract Disclosure: J. Höppner: None. P. Hanna: None. M.N. Wein: None. H. Jueppner: None. T.J. Gardella: None. R. Civitelli: None. I.A. Portales-Castillo: None. Abstract The parathyroid hormone receptor-1 (PTH1R) plays a key role in bone development and acts in the growth plates in response to PTHrP ligand. Eiken syndrome is characterized by a delay in bone mineralization and is caused by homozygous PTH1R mutations. One such mutation, R485X, truncates the receptor's C-tail and removes serine phosphorylation sites involved in βarrestin binding. In HEK293 cells, R485X-hPTH1R exhibits deficient interaction with βarrestin and increased cAMP signaling both basally and in response to PTHrP (Portales-Castillo et al., Comms. Biology 2023). To understand how the R485X mutation causes delayed bone mineralization, we generated humanized R485X-hPTH1R knock-in mice. Homozygous hPTH1RR485X/R485X mice closely recapitulate the delayed bone mineralization seen in Eiken patients, as skeletal whole mount preparations from neonatal mutant mice showed reduced Alizarin red staining compared to WT controls, and metatarsal explants from the mutant mice showed a pronounced absence of mineralized bone. Tails of hPTH1RR485X/R485X mice were ∼50% shorter than those of WT littermates, and H&E-stained sections revealed only proliferative chondrocytes in the growth plates of mutant mice. This delay in growth plate chondrocyte maturation in hPTH1RR485X/R485X mice resolved with age, although older long bones and tails remained smaller in size than WT controls (Höppner et al. Presented at ASBMR 2023).Based on our in vitro findings and initial mouse characterization, we reasoned that the phenotype of Eiken mice may be explained by increased PTHrP/PTH1R signaling in growth plate chondrocyte. The class IIa histone deacetylase HDAC4 suppresses chondrocyte maturation downstream of PTH1R signaling. Therefore, we generated compound mutant mice bearing both Hdac4 deletion and the mutant R485X PTH1R allele. Indeed, Hdac4 deletion largely rescued the mineralization defect apparent in metatarsals of P1 hPTH1RR485X/R485X mice. We then assessed the contribution of endogenous PTHrP to the Eiken-like phenotype by generating hPTH1RR485X/R485X/PTHrPflox/+/Col2-Cre(tg) mice. Remarkably, these mice exhibit approximately the same tail lengths as hPTH1R-WT littermate controls, indicating that reduced PTHrP production can rescue the effects of homozygosity for R485X-PTH1R. In line, vertebral growth plates of the rescued mice exhibited normal zones of chondrocytes, including hypertrophic cells. The overall results support a disease mechanism for Eiken syndrome by which excess cAMP signaling by PTH1R-R485X, as induced in part by endogenous PTHrP, results in delayed chondrocyte differentiation and bone mineralization. Further studies employing βarr1/2-KO mice may help shed light on the specific roles of βarrestins in growth plate development by PTH1R in Eiken syndrome. Presentation: 6/3/2024

Nutrient contents of soil organic matter in forests vary with regional differences in soil types and parent material, and can be modified by forest type and management intensity. Variation of organic carbon (OC)-to-nutrient ratios in soils supposedly alters microbial carbon and nutrient use efficiencies and the rates of OC-to-nutrient mineralization. Here, we studied mineralization rates of carbon (C), nitrogen (N), phosphorus (P), and sulfur (S) for topsoil samples from differently managed forest plots in Germany. Samples were incubated for two weeks in microlysimeters under controlled conditions. CO2 respiration, leachable dissolved organic carbon (DOC), nitrate (NO3–), ammonium (NH4+), sulfate (SO42–), and phosphate (PO43–) were determined as net organic C (OC) and nutrient mineralization rates. We hypothesized that in soils with high C-to-nutrient ratios, soil microbes may mobilize relatively more OC as CO2 or DOC than nutrients to meet their nutrient requirements. Further, we hypothesized that forest management practices, such as tree species selection and harvest intensity, potentially affect the stoichiometry of SOM mineralization by altering the ratios of C-to-nutrients in soils. Results showed that CO2-release rates were proportional to soil OC, but when normalized to microbial biomass C, they increased, similar to DOC leaching rates, with soil OC-to-N ratios. However, contrary to our expectation, higher soil OC-to-nutrient ratios did not go along with reduced nutrient leaching. Instead, when normalized to soil OC, the largest amounts of N, P, and S were leached in the most nutrient poor region, so that sites with highest soil OC-to-nutrient ratios had the smallest OC-to-nutrient mineralization ratio. Forest type and tree species selection affected soil stoichiometry only in the most nutrient poor region with higher OC-to-nutrient ratios under coniferous than deciduous forest sites. This potentially caused the significantly enhanced OC-normalized DOC leaching rates under coniferous forests. However, in the two other study regions tree species had a significant effect on N and S leaching rates and the ratio of OC-to-nutrient leaching despite similar stoichiometry. Overall, our study suggests that increasing nutrient scarcity enhances microbial based CO2 and DOC production, possibly because of increased energy demand for enzyme production and to remove excess OC to reach and mobilize more nutrients, thereby allowing for high nutrient leaching rates despite small total stocks. Forest management affected OC-to-nutrient mineralization rates mostly via tree species selection, but observed differences were not obviously caused by soil stoichiometry but rather by other ecological differences between forest types.

Research on plastics in global ecosystems is rapidly evolving. Oceans have been the primary focus of studies to date, whereas rivers are generally considered little more than conduits of plastics to marine ecosystems. Within a watershed, however, plastics of all sizes are retained, transformed, and even extracted via freshwater use or litter cleanup. As such, plastic litter in terrestrial and freshwater ecosystems is an important but underappreciated component of global plastic pollution. To gain a holistic perspective, we developed a conceptual model that synthesizes all sources, fluxes, and fates for plastics in a watershed, including containment (ie disposed in landfill), non‐containment (ie persists as environmental pollution), mineralization, export to oceans, atmospheric interactions, and freshwater extraction. We used this model of the “plastic cycle” to illustrate which components have received the most scientific attention and to reveal overlooked pathways. Our main objective is for this framework to inform future research, offer a new perspective to adapt management across diverse waste governance scenarios, and improve global models of plastic litter.