A prototype of the mammalian sulfotransferase 1 (SULT1) family in Xenopus laevis: Characterization of a biased usage of SULT1 genes located in the S-subgenome
A prototype of the mammalian sulfotransferase 1 (SULT1) family in Xenopus laevis: Characterization of a biased usage of SULT1 genes located in the S-subgenome
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DOI：
10.1016/j.gene.2022.146495
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发表时间：
2022-04-29
期刊：
影响因子：
3.5
通讯作者：
Yamauchi，Kiyoshi
中科院分区：
文献类型：
--
作者：
Sato，Kosuke;Ishihara，Akinori;Yamauchi，Kiyoshi
使用克隆的X对先前针对Xenopus基因组数据库进行的BLAST搜索。通过对LAEVISCytosolic磺基转移酶1（SULT 1）cDNA序列的分析，揭示了该基因家族的十几个成员的存在。其中，11个基因在X染色体上是同源基因，包括5组、4对和1个三联体。由S亚基因组和L亚基因组组成的laevisallotetraploid基因组（在一组内具有≥83%的同一性）。系统发育分析和同线性分析表明，四足动物的SULT 1基因与X.其中4个与哺乳动物SULT 1基因亚家族相关，2个为变温脊椎动物和两栖动物特异的SULT 1基因亚家族。5套同源重组SULT 1基因被定位为一个基因簇，并显示S-亚基因组偏向的基因表达模式。组蛋白H3在赖氨酸9和H4处的乙酰化水平在S亚基因组上的同源染色体SULT 1基因中也高于L亚基因组上的组蛋白H3，然而，组蛋白H3在赖氨酸9处的甲基化水平和DNA甲基化水平与其转录水平无关。总之，组蛋白修饰，如乙酰化可能是一个关键因素，控制的S-亚基因组偏向表达的同源异型SULT 1基因。
BLAST searches previously carried out againstXenopusgenome databases, using the clonedX. laeviscytosolic sulfotransferase 1 (SULT1) cDNA sequence, revealed the presence of more than a dozen members of this gene family. Among them, 11 genes composed of five sets, four pairs and a triplet, were homeologous genes in theX. laevisallotetraploid genome consisting of S- and L-subgenomes (≥83% identity within a set). Phylogenetic and synteny analyses of tetrapod SULT1 genes demonstrated thatX. laevispossessed six subfamilies, four of which were related to mammalian SULT1 gene subfamilies, while two were ectothermic vertebrate-specific and amphibian-specific SULT1 gene subfamilies. Five sets of homeologous SULT1 genes were located as a gene cluster, and showed S-subgenome-biased gene expression patterns. Acetylation levels of histone H3 at lysine 9 and H4 were also higher in the homeologous SULT1 genes on the S-subgenome than those on the L-subgenome, however, methylation levels of histone H3 at lysine 9 and DNA methylation levels showed no correlation with their transcript levels. In conclusion, histone modifications such as acetylation may be a key factor that controls the S-subgenome-biased expression of the homeologous SULT1 genes.