CRESSENT: a bioinformatics toolkit to explore and improve ssDNA virus annotation ssDNA viruses are important components of diverse ecosystems; however, it remains challenging to systematically identify and classify them. This is partly due to their broad host range and resulting genomic diversity, structure and rapid evolutionary rates. In addition, distinguishing genuine ssDNA genomes from contaminating sequences in metagenomic datasets (e.g. from commercial kits) has been an unresolved issue for years. Here, we present CRESSENT (CRESS-DNA Extended aNnotation Toolkit), a comprehensive and modular bioinformatic pipeline focused on ssDNA virus ‘genome-to-analysis’ and annotation. The pipeline integrates multiple functionalities organized into several modules: sequence dereplication, decontamination, phylogenetic analysis, motif discovery, stem-loop structure prediction and recombination detection. Each module can be used independently or in combination with others, allowing researchers to customize their analysis workflow. With this tool, researchers can comprehensively and systematically include ssDNA viruses in their viromics workflows and facilitate comparative genomic studies, which are often limited to dsDNA viruses, therefore leaving behind a crucial component of the microbiome community under study. Benchmarking analyses demonstrated that CRESSENT efficiently processes ssDNA virus datasets of varying scales, completing small family-level analyses within minutes and moderate comparative genomics studies within hours using standard computing resources. Its modular, parallelized design ensures scalability and low memory usage, making it accessible to research groups with diverse computational capacities.

🔬 New #ssDNA virus annotation toolkit CRESSENT accelerates #viromics & ecosystem virus discovery with modular, scalable analyses for decontamination, structuring & phylogeny. 🧬💻#Virology #Bioinformatics #Metagenomics
📄 https://doi.org/10.1099/mgen.0.001632
👤 EVBC member: Matthew Sullivan

RAD51 protects abasic sites to prevent replication fork breakage Hanthi et al. found that RAD51 recognizes and binds to abasic sites. Together with BRCA2, RAD51 prevents the accumulation of abasic site-induced replicative DNA gaps (caused by DNA methylation, oxidat...

Excited to share my first co-first author paper! We uncovered a conserved role for RAD51/BRCA2 in protecting abasic sites at replication forks from MRE11 cleavage.
#ssDNA gaps, #DNMT1, #POLθ, #Cryo-EM of #RAD51 bound to AP sites, and much more! Check it out!

Interesting article: the mammal-associated #ssDNA virus zoo is growing! Plasma virome of cattle ... revealed diverse small circular ssDNA viral genomes #virologyj