These findings provide the first comprehensive characterization of the BxATG family and offer insights into its potential roles in nematode development, stress adaptation, and pathogenicity.
Abstract
Autophagy-related genes (ATGs) are key regulators of cellular homeostasis and physiological processes and play important roles in nematode growth, development, and lifespan. In this study, we systematically identified 23
Bxatg
s in
Bursaphelenchus xylophilus
through genome-wide sequence alignment and comprehensive bioinformatics analyses. The predicted molecular weights of BxATGs ranged from 19.13 to 243.37 kDa, with theoretical isoelectric points ranging from 4.53 to 8.92. Secondary structure analysis indicated that
α
-helices (0.26%–76.64%) and random coils (18.17%–63.89%) were the predominant structural elements, whereas
β
-sheets (4.41%–48.41%) and
β
-turns (0.00%–18.25%) accounted for smaller proportions. Phylogenetic analysis classified the 23 BxATGs into four distinct subgroups, and conserved motif analysis revealed strong conservation of their core functional regions. Chromosomal mapping showed that BxATGs were distributed across all six chromosomes, with tandem duplication events on chromosome 1 potentially contributing to their evolutionary expansion. Predicted tertiary structures revealed diverse three-dimensional conformations, consistent with their functional diversification in autophagy regulation. Expression profiling across developmental stages revealed distinct stage-specific expression patterns. Notably,
Bxatg
7 exhibited consistently high expression throughout development, whereas other
Bxatgs
showed preferential upregulation during embryogenesis, larval development, or infection-related stages. These findings provide the first comprehensive characterization of the BxATG family and offer insights into its potential roles in nematode development, stress adaptation, and pathogenicity. This study also provides a foundation for functional validation of individual BxATGs and the development of targeted molecular strategies for controlling pine wilt disease.
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