Zhao Yaofeng, Pan-Hammarström Qiang, Zhao Zhihui, Hammarström Lennart
Division of Clinical Immunology, Department of Laboratory Medicine, Karolinska Institute at Huddinge Hospital, SE-141 86 Stockholm, Sweden.
Dev Comp Immunol. 2005;29(1):61-71. doi: 10.1016/j.dci.2004.05.005.
In the present study, we report the identification of the activation-induced cytidine deaminase (AID) encoding gene in frog, dog and chimpanzee, where both somatic hypermutation and class switch recombination (CSR) occurs and in zebrafish and fugu, species lacking CSR. The cDNA sequence of the zebrafish AID reported here suggests both N and C ends of the previously predicted protein sequence are incorrect. A comparison of AID sequences among mammals, birds, amphibians and fish revealed conserved aa residues which may be essential for AID activity, although the cytidine deaminase active motif in the latter is nine amino acids longer. Furthermore, an aa deletion, and extensive substitutions in the C terminal end of AID from bony fish indicate that the molecule may not yet have developed a capacity to recruit the specific cofactor(s) needed to initiate CSR.
在本研究中,我们报告了在青蛙、狗和黑猩猩中激活诱导的胞苷脱氨酶(AID)编码基因的鉴定结果,在这些物种中发生了体细胞高频突变和类别转换重组(CSR),而在缺乏CSR的斑马鱼和河豚中也进行了鉴定。这里报道的斑马鱼AID的cDNA序列表明,先前预测的蛋白质序列的N端和C端都是不正确的。对哺乳动物、鸟类、两栖动物和鱼类的AID序列进行比较,发现了保守的氨基酸残基,这些残基可能对AID活性至关重要,尽管后者的胞苷脱氨酶活性基序长九个氨基酸。此外,硬骨鱼AID的C末端存在氨基酸缺失和广泛的替换,这表明该分子可能尚未发展出招募启动CSR所需特定辅助因子的能力。