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Bright, K.

Publications and source records attributed to Bright, K..

2 recordsLinked to original sources

Metagenomic Insights Into Microbial Controls of Carbon Cycling in Alpine Soils

Alpine riparian zones span topographic gradients from wet soils on the plain near streams to drier soils on adjacent slopes. These differences in soil moisture are generally associated with shifts in soil redox state from anoxic on the plain to oxic on the slope. In anoxic plain soils, soil organic carbon (SOC) may accumulate due to thermodynamic constraints on microbial activity. Here, we used shotgun metagenomics to examine how microbial diversity and functional potential varies across differing redox conditions on plain and slope soils in two catchments in the Swiss Alps. We complemented these analyses with soil physicochemical characteristics and information on the chemical composition of organic matter. Plain soils had higher SOC stocks and higher relative abundance of phenol compounds relative to slope soils, consistent with SOC preservation and preferential mineralisation of easily degradable organic compounds under anoxic conditions. Microbial communities in plain soils further exhibited greater taxonomic and functional diversity, including an increased potential for anaerobic respiration pathways. Genes for nitrate, iron, and sulfate reduction were linked to Chloroflexota, Acidobacteria, and Desulfobacterota phyla, respectively. Based on NMDS correlations, electron accepting capacity, calcium content, and pH shaped microbial community composition. Slope soils, by contrast, supported less diverse microbial communities, determined mainly by electron donating capacity and clay content. Our work demonstrates how soil redox conditions and microbial functional potential shape carbon cycling across landscape positions in alpine riparean zones. This mechanistic understanding is critical to anticipate changes in carbon cycling in alpine ecosystems in a changing climate.

microbiology↗

The zinc-finger protein POGZ associates with Polycomb repressive complex 1 to regulate bone morphogenetic protein signaling during neuronal differentiation

Polycomb Repressive Complex 1 (PRC1) is a family of epigenetic regulators critical for mammalian development. Elucidating PRC1 composition and function across cell types and developmental stages is key to understanding the epigenetic regulation of cell fate determination. In this study, we discovered POGZ, a prominent Autism Spectrum Disorder (ASD) risk factor, as a novel component of PRC1.6, forming the PRC1.6-POGZ complex. Functional assays revealed that POGZ elicits transcriptional repression that is dependent on RING1B expression. Analysis of publicly available ChIP-Seq data showed that POGZ highly colocalizes with RING1B and HP1{gamma}, two PRC1.6 components, at genes involved in multiple aspects of transcriptional regulation in the embryonic mouse cortex. Although Pogz knockout (KO) does not compromise stem cell pluripotency, Pogz ablation in neuronal progenitor cells (NPCs) led to widespread transcriptomic dysregulation with failed activation of key neuronal genes. Finally, we demonstrated that PRC1.6-POGZ regulates neuronal differentiation by repressing the bone morphogenetic protein (BMP) signaling pathway. These findings reveal a mechanism by which PRC1 and POGZ coordinate transcriptional regulation during neuronal differentiation, which offers insights into how disruptions in this pathway may contribute to neurodevelopmental disorders such as ASD.

biochemistry↗