Background: Discontinuous transcription allows coronaviruses to efficiently replicate and transmit within host cells, enhancing their adaptability and survival. Assembling viral transcripts is crucial for virology research and the development of antiviral strategies. However, traditional transcript assembly methods primarily designed for variable alternative splicing events in eukaryotes are not suitable for the viral transcript assembly problem. The current algorithms designed for assembling viral transcripts often struggle with low accuracy in determining the transcript boundaries. There is an urgent need to develop a highly accurate viral transcript assembly algorithm.
Results: In this work, we propose Cov-trans, a reference-based transcript assembler specifically tailored for the discontinuous transcription of coronaviruses. Cov-trans first identifies canonical transcripts based on discontinuous transcription mechanisms, start and stop codons, as well as reads alignment information. Subsequently, it formulates the assembly of non-canonical transcripts as a path extraction problem, and introduces a mixed integer linear programming to recover these non-canonical transcripts.
Conclusion: Experimental results show that Cov-trans outperforms other assemblers in both accuracy and recall, with a notable strength in accurately identifying the boundaries of transcripts. Cov-trans is freely available at https://github.com/computer-Bioinfo/Cov-trans.git .
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684287 | PMC |
PLoS One
January 2025
Département des Sciences Naturelles, Institut des Sciences de la Forêt Tempérée (ISFORT), Université du Québec en Outaouais (UQO), Ripon, Canada.
Forests face an escalating threat from the increasing frequency of extreme drought events driven by climate change. To address this challenge, it is crucial to understand how widely distributed species of economic or ecological importance may respond to drought stress. In this study, we examined the transcriptome of white spruce (Picea glauca (Moench) Voss) to identify key genes and metabolic pathways involved in the species' response to water stress.
View Article and Find Full Text PDFClin Rev Allergy Immunol
December 2024
Department of Dermatology, Second Affiliated Hospital, Zhejiang University School of Medicine, 88 Jiefang Road, Hangzhou, 310009, People's Republic of China.
The switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complexes (also referred to as BAF complexes) are composed of multiple subunits, which regulate the nucleosome translocation and chromatin accessibility. In recent years, significant advancements have been made in understanding mutated genes encoding subunits of the SWI/SNF complexes in cancer biology. Nevertheless, the role of SWI/SNF complexes in immune response and inflammatory diseases continues to attract significant attention.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Amsterdam UMC, Amsterdam, Netherlands.
Background: The TMEM106B protein is critical for proper functioning of the endolysomal system, which is utilised by all cells to traffic and degrade molecular cargo. Genome-wide association studies identified a haplotype in the TMEM106B gene that is associated with increased risk for Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), and frontotemporal lobar degeneration with TAR DNA binding protein inclusions (FTLD-TDP). However, the causal variant that drives the association has thus far remained elusive.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Genomics of Neurodegenerative Diseases and Aging, Human Genetics, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, Netherlands.
Background: Genome-Wide Association Studies (GWAS) have identified 86 SNPs associated with Alzheimer's disease (AD). GWAS-SNPs are markers of genetic variation in linkage disequilibrium (LD), which may drive the association with AD. One major class of genetic variation are Structural Variants (SVs), which can regulate transcription and translation of nearby genes.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Columbia University Medical Center, New York, NY, USA.
Background: The ubiquitin-proteasome system (UPS) is the primary protein degrading mechanism in eukaryotes, and is essential for cellular homeostasis. Dysregulation of the UPS has been linked to neurodegeneration through two hallmarks, pathogenic protein aggregation and aberrant proteostasis. However, the molecular changes that alter proteasome functioning in AD are poorly understood.
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