Genome-wide comparison and in silico analysis of splicing factor SYF2/NTC31/p29 in eukaryotes: Special focus on vertebrates

文献类型： 外文期刊

第一作者： Huang, Bao-Xing

作者： Huang, Bao-Xing;Liu, Xiao-Rong;Chen, Yun-Sheng;Jia, Zi-Chang;Chen, Mo-Xian;Jia, Zi-Chang;Chen, Mo-Xian;Jia, Zi-Chang;Yang, Xue;Cheng, Chao-Lin;Zhang, Jianhua;Yang, Jing-Fang

作者机构：

关键词： alternative splicing; SYF2; expression profile; gene family; proteogenomics

期刊名称：FRONTIERS IN GENETICS （ 影响因子：4.772； 五年影响因子：4.933 ）

ISSN：

年卷期： 2022 年 13 卷

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收录情况： SCI

摘要： The gene SYF2-an RNA splicing factor-can interact with Cyclin D-type binding protein 1 (GICP) in many biological processes, including splicing regulation, cell cycle regulation, and DNA damage repair. In our previous study we performed genome-wide identification and functional analysis of SYF2 in plant species. The phylogenetic relationships and expression profiles of SYF2 have not been systematically studied in animals, however. To this end, the gene structure, genes, and protein conserved motifs of 102 SYF2 homologous genes from 91 different animal species were systematically analyzed, along with conserved splicing sites in 45 representative vertebrate species. A differential comparative analysis of expression patterns in humans and mice was made. Molecular bioinformatics analysis of SYF2 showed the gene was conserved and functional in different animal species. In addition, expression pattern analysis found that SYF2 was highly expressed in hematopoietic stem cells, T cells, and lymphoid progenitor cells; in ovary, lung, and spleen; and in other cells and organs. This suggests that changes in SYF2 expression may be associated with disease development in these cells, tissues, or organs. In conclusion, our study analyzes the SYF2 disease resistance genes of different animal species through bioinformatics, reveals the relationship between the SYF2 genotype and the occurrence of certain diseases, and provides a theoretical basis for follow-up study of the relationship between the SYF2 gene and animal diseases.

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