State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Ningbo University, PR China.
State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Ningbo University, PR China.
Fish Shellfish Immunol. 2023 Jul;138:108855. doi: 10.1016/j.fsi.2023.108855. Epub 2023 May 29.
CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) belongs to the C/EBP family of transcription factors that has been proven to regulate apoptosis in many vertebrate species. However, the functional role of CHOP in invertebrates is largely unknown. In this paper, the open reading frame of CHOP was cloned and characterized in the sea cucumber Apostichopus japonicus (AjCHOP). The deuced amino acid of AjCHOP shared a conserved RTP801_C domain from 63 to 171 aa. Phylogenetic analysis indicated that AjCHOP clustered with CHOPs from Lytechinus variegatus and Strongylocentrotus purpuratus. To confirm the immune function of AjCHOP, the time-course expression profiles of AjCHOP were investigated, and the findings revealed AjCHOP was significantly induced in coelomocytes at mRNA and protein levels after Vibro splendidus challenge. Furthermore, knockdown of AjCHOP in coelomocyes by siRNA transfection significantly decreased the apoptosis level induced by V. splendidus. Mechanically, AjCHOP-mediated apoptosis was dependent on the activation of p38-MAPK pathway but not JNK/ERK-MAPK. Overall, our results supported that V. splendidus triggers apoptosis among the coelomocytes, whereas AjCHOP mediates through the p38-MAPK pathway in A. japonicus.
CCAAT/增强子结合蛋白（C/EBP）同源蛋白（CHOP）属于 C/EBP 转录因子家族，已被证明在许多脊椎动物物种中调节细胞凋亡。然而，CHOP 在无脊椎动物中的功能作用在很大程度上是未知的。在本文中，克隆并鉴定了海参（Apostichopus japonicus）（AjCHOP）中的 CHOP 开放阅读框。AjCHOP 的推导氨基酸在 63 到 171 个氨基酸处共享一个保守的 RTP801_C 结构域。系统发育分析表明，AjCHOP 与 Lytechinus variegatus 和 Strongylocentrotus purpuratus 的 CHOPs 聚类在一起。为了确认 AjCHOP 的免疫功能，研究了 AjCHOP 的时间表达谱，结果表明在 Vibro splendidus 刺激后，腔细胞中的 AjCHOP 在 mRNA 和蛋白质水平上均显著诱导。此外，通过 siRNA 转染在腔细胞中敲低 AjCHOP 显著降低了 V. splendidus 诱导的细胞凋亡水平。在机制上，AjCHOP 介导的细胞凋亡依赖于 p38-MAPK 途径的激活，而不依赖于 JNK/ERK-MAPK。总的来说，我们的结果支持 V. splendidus 触发腔细胞中的细胞凋亡，而 AjCHOP 在 A. japonicus 中通过 p38-MAPK 途径介导。
