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Hartke, T.

Publications and source records attributed to Hartke, T..

2 recordsLinked to original sources

annoSnake: a Snakemake workflow for taxonomic and functional annotation of metagenomes and metagenome-assembled genomes (MAGs)

Omic technologies revolutionised research in microbiomics and helped decipher the complex community structure of gut microbiota, each comprising hundreds of species of bacteria, archaea, and protists. Even as sequencing costs decrease, understanding these communities remains a challenge. Here, we introduce annoSnake, a Snakemake workflow that facilitates taxonomic and functional annotation of metagenomes and metagenomic-assembled genomes (MAGs). This user-friendly and highly flexible workflow integrates state-of-the-art software packages, taking raw sequencing reads, assembling them into contigs, assigning taxonomies and annotating them using various popular protein databases. The workflow handles paired-end as well as interleaved read data, and provides publication-ready figures and tables for downstream analysis. annoSnake, as all Snakemake workflows, is highly scalable, reproducible, and portable, enabling execution across diverse high-performance computing environments with remarkable efficiency.

bioinformatics↗

Enhanced Sodium Channel Inactivation by Temperature and FHF2 Deficiency Blocks Heat Nociception

Transient voltage-gated sodium currents are essential for the initiation and conduction of action potentials in neurons and cardiomyocytes. The amplitude and duration of sodium currents are tuned by intracellular fibroblast growth factor homologous factors (FHFs/iFGFs) that associate with the cytoplasmic tails of voltage-gated sodium channels (Navs), and genetic ablation of Fhf genes disturbs neurological and cardiac functions. Among reported phenotypes, Fhf2null mice undergo lethal hyperthermia-induced cardiac conduction block attributable to the combined effects of FHF2 deficiency and elevated temperature on the cardiac sodium channel (Nav1.5) inactivation rate. Fhf2null mice also display a lack of heat nociception, while retaining other somatosensory capabilities. Here, we use electrophysiological and computational methods to show that the heat nociception deficit can be explained by the combined effects of elevated temperature and FHF2 deficiency on the fast inactivation gating of Nav1.7 and tetrodotoxin-resistant sodium channels expressed in dorsal root ganglion C fibers. Hence, neurological and cardiac heat-associated deficits in Fhf2null mice derive from shared impacts of FHF deficiency and temperature towards Nav inactivation gating kinetics in distinct tissues.

neuroscience↗