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Litopenaeus vannamei sirtuin 6 homolog (LvSIRT6) is involved in immune response by modulating hemocytes ROS production and apoptosis.
Fish & Shellfish Immunology ( IF 4.1 ) Pub Date : 2020-01-20 , DOI: 10.1016/j.fsi.2020.01.029
Junjie Nie 1 , Zhixue Yu 1 , Defu Yao 1 , Fan Wang 1 , Chunhua Zhu 2 , Kaihui Sun 3 , Jude Juventus Aweya 1 , Yueling Zhang 1
Affiliation  

The histone deacetylase, sirtuin 6 (SIRT6), plays an essential role in the regulation of oxidative stress, mitochondrial function and inflammation in mammals. However, the specific role of SIRT6 in invertebrate immunity has not been reported. Here, we characterized for the first time, a sirtuin 6 homolog in Litopenaeus vannamei (LvSIRT6), with full-length cDNA of 2919 bp and 1536 bp open reading frame (ORF) encoding a putative protein of 511 amino acids, which contains a typical SIR2 domain. Sequence and phylogenetic analysis revealed that LvSIRT6 shares a close evolutionary relationship with SIRT6 from invertebrates. Real-time quantitative PCR analysis of LvSIRT6 transcripts revealed that they were ubiquitously expressed in shrimp and induced in hepatopancreas and hemocytes upon challenge with Vibrio parahaemolyticus, Streptococcus iniae, lipopolysaccharide (LPS), and white spot syndrome virus (WSSV), suggesting the involvement of LvSIRT6 in shrimp immune response. Moreover, knockdown of LvSIRT6 decreased mitochondrial membrane potential and increased total ROS level in hemocytes, especially upon V. parahaemolyticus challenge. Depletion of LvSIRT6 also increased hemocytes apoptosis in terms of decreased expression of pro-survival LvBcl-2, but increased expression of pro-apoptotic LvBax and LvCytochrome C, coupled with high LvCaspase3/7 activity. Shrimp were rendered more susceptible to V. parahaemolyticus infection upon LvSIRT6 knockdown. Taken together, our present data suggest that LvSIRT6 plays an important role in shrimp immune response by modulating hemocytes ROS production and apoptosis during pathogen challenge.

中文翻译:

凡纳滨对虾sirtuin 6同源物(LvSIRT6)通过调节血细胞ROS的产生和凋亡参与免疫反应。

组蛋白脱乙酰基酶sirtuin 6(SIRT6)在调节哺乳动物的氧化应激,线粒体功能和炎症中起着至关重要的作用。但是,尚未报道SIRT6在无脊椎动物免疫中的特定作用。在这里,我们首次表征了南美白对虾中的沉默调节蛋白6同源物(LvSIRT6),全长cDNA为2919 bp,开放阅读框为1536 bp,编码一个推定的511个氨基酸的蛋白质,其中包含一个典型的SIR2域。序列和系统发育分析表明,LvSIRT6与来自无脊椎动物的SIRT6有着密切的进化关系。对LvSIRT6转录本的实时定量PCR分析显示,它们在虾中无处不在表达,并在溶血性弧菌,链球菌,海豚链球菌攻击后在肝胰腺和血细胞中被诱导。脂多糖(LPS)和白斑综合症病毒(WSSV),表明LvSIRT6参与虾的免疫反应。而且,LvSIRT6的敲低降低了血细胞中的线粒体膜电位并增加了总ROS水平,尤其是在溶血弧菌攻击后。LvSIRT6的耗竭还降低了生存前LvBcl-2的表达,但也增加了血细胞凋亡,但增加了促凋亡LvBax和LvCytochrome C的表达,并具有高LvCaspase3 / 7活性。击倒LvSIRT6后,虾更易感染副溶血性弧菌。两者合计,我们目前的数据表明LvSIRT6在病原体攻击过程中通过调节血细胞ROS的产生和凋亡在虾的免疫应答中起重要作用。提示LvSIRT6参与虾的免疫反应。而且,LvSIRT6的敲低降低了血细胞中的线粒体膜电位并增加了总ROS水平,尤其是在溶血弧菌攻击后。LvSIRT6的耗竭还降低了生存前LvBcl-2的表达,但也增加了血细胞凋亡,但增加了促凋亡LvBax和LvCytochrome C的表达,并具有高LvCaspase3 / 7活性。击倒LvSIRT6后,虾更易感染副溶血性弧菌。两者合计,我们目前的数据表明LvSIRT6在病原体攻击过程中通过调节血细胞ROS的产生和凋亡在虾的免疫应答中起重要作用。提示LvSIRT6参与虾的免疫反应。而且,LvSIRT6的敲低降低了血细胞中的线粒体膜电位并增加了总ROS水平,尤其是在溶血弧菌攻击后。LvSIRT6的耗竭还降低了生存前LvBcl-2的表达,但也增加了血细胞凋亡,但增加了促凋亡LvBax和LvCytochrome C的表达,并具有高LvCaspase3 / 7活性。击倒LvSIRT6后,虾更易感染副溶血性弧菌。两者合计,我们目前的数据表明LvSIRT6在病原体攻击过程中通过调节血细胞ROS的产生和凋亡在虾的免疫应答中起重要作用。击倒LvSIRT6会降低血细胞中的线粒体膜电位并增加总ROS水平,尤其是在溶血弧菌攻击后。LvSIRT6的耗竭还降低了生存前LvBcl-2的表达,但也增加了血细胞凋亡,但增加了促凋亡LvBax和LvCytochrome C的表达,并具有高LvCaspase3 / 7活性。击倒LvSIRT6后,虾更易感染副溶血性弧菌。两者合计,我们目前的数据表明LvSIRT6在病原体攻击过程中通过调节血细胞ROS的产生和凋亡在虾的免疫应答中起重要作用。击倒LvSIRT6会降低血细胞中的线粒体膜电位并增加总ROS水平,尤其是在溶血弧菌攻击后。LvSIRT6的耗竭还降低了生存前LvBcl-2的表达,但也增加了血细胞凋亡,但增加了促凋亡LvBax和LvCytochrome C的表达,并具有高LvCaspase3 / 7活性。击倒LvSIRT6后,虾更易感染副溶血性弧菌。两者合计,我们目前的数据表明LvSIRT6在病原体攻击过程中通过调节血细胞ROS的产生和凋亡在虾的免疫应答中起重要作用。LvSIRT6的耗竭还降低了生存前LvBcl-2的表达,但也增加了血细胞凋亡,但增加了促凋亡LvBax和LvCytochrome C的表达,并具有高LvCaspase3 / 7活性。击倒LvSIRT6后,虾更易感染副溶血性弧菌。两者合计,我们目前的数据表明LvSIRT6在病原体攻击过程中通过调节血细胞ROS的产生和凋亡在虾的免疫应答中起重要作用。LvSIRT6的耗竭还降低了生存前LvBcl-2的表达,但也增加了血细胞凋亡,但增加了促凋亡LvBax和LvCytochrome C的表达,并具有高LvCaspase3 / 7活性。击倒LvSIRT6后,虾更易感染副溶血性弧菌。两者合计,我们目前的数据表明LvSIRT6在病原体攻击过程中通过调节血细胞ROS的产生和凋亡在虾的免疫应答中起重要作用。
更新日期:2020-01-21
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