Document Type : Original Paper
Authors
1
Department of Animal Science, Faculty of Agriculture, Yasouj University, Yasouj, Iran
2
Department of Agriculture, Payam Noor University, Tehran, Iran
3
Department of Biophysics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
10.22069/psj.2025.23331.2262
Abstract
Ascites syndrome is a multifactorial disease in poultry, associated with high mortality and significant economic losses. Genomic studies have identified UTS2B gene as a candidate gene associated with ascites syndrome in poultry. Therefore, this study employed an in-silico approach to explore the structural and functional characteristics of the UTS2B protein and its potential link to ascites. The amino-acid sequence of UTS2B protein was retrieved from the NCBI database and subjected to analyze through ProtParam, ProtScale, NetPhos, NetNGlyc, LocTree3, and SignalP tools to determine its sequence features and physicochemical properties. Secondary and tertiary structures were predicted using I-TASSER, AlphaFold, and trRosetta, with structural quality validated by PROCHECK (Ramachandran plot analysis) and ERRAT scores. Promoter analysis was performed using MEME Suite, TOMTOM, and GOMo to identify regulatory motifs. The UTS2B protein exhibited a theoretical isoelectric point of 5.67, an instability index of 42.33, and an average hydrophilicity coefficient of -0.199, indicating a hydrophilic and moderately unstable nature. It contains 17 phosphorylation sites and 4 N-glycosylation sites, suggesting post-translational modifications that impact extracellular activity in peptide signalling pathways. Secondary structure analysis revealed a predominance of alpha helices and random loops. Among the predicted 3D models, the trRosetta structure achieved the highest quality, with 92.4% of residues in favorable regions of the Ramachandran plot and an ERRAT score of 85.6. Protein network analysis indicated that UTS2B may interact with proteins involved in pathways associated with calcium ion binding and cellular stress responses, both of which play a critical role in the pathophysiology of ascites. Promoter analysis identified regulatory motifs potentially linked to ion transport and inflammation, providing further insights into gene regulation. The findings suggest that UTS2B may play a role in calcium ion signalling and peptide-mediated extracellular pathways, contributing to ascites syndrome. This study presented critical bioinformatics insights into the UTS2B protein, providing foundational knowledge for future research aimed at understanding its role in ascites syndrome.
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