Senescence-associated superoxide dismutase influences mitochondrial gene expression in budding tunicates.
Senescence-associated superoxide dismutase influences mitochondrial gene expression in budding tunicates.
复制标题
衰老相关的超氧化物歧化酶影响出芽被囊类动物的线粒体基因表达。
DOI：
10.1111/dgd.12065
复制
发表时间：
2013
影响因子：
2.5
通讯作者：
T.
中科院分区：
文献类型：
--
作者：
Kawamura;K. and Sunanaga;T.
最近的一项研究表明，在萌发的鳞片多雄果中，线粒体呼吸链(MRC)在衰老过程中显著减弱了基因的活性。在这项研究中，我们研究了超氧化物歧化酶(SOD)可能参与了老年带状动物细胞色素c氧化亚单位1(COX1)基因表达的减弱。RT-PCR和原位杂交发现，铜/锌-超氧化物歧化酶(SOD1)在芽体和幼体的大部分细胞和组织中都有表达，但在衰老的成体组织中表达明显减少，幼年卵母细胞胞质染色较深的性腺组织除外。SOD1的这种表达模式与COX1相似。与SOD1不同的是，在芽体、幼体和衰老的成体组织中，Mn-SOD(SOD2)在体细胞和胚系组织中都有结构性表达。被RNAi敲除的SOD1不仅降低了SOD1的基因活性，也降低了COX1的基因活性。由此产生的动物园在生长和萌芽方面存在暂时性缺陷，大约一个月后它们就从这些缺陷中恢复过来。我们的结果表明，在水曲柳中，SOD1是一个与衰老相关的核基因，并且SOD1基因表达的实验性下降伴随着MRC基因活性的下降。尽管目前还不清楚SOD1在被囊体衰老过程中如何下调，但SOD1活性降低可能是正常衰老过程中MRC基因衰减的主要原因之一。
A recent study has shown that in the budding tunicatePolyandrocarpa misakiensis, the mitochondrial respiratory chain (MRC) dramatically attenuates the gene activity during senescence. In this study, we examined the possible involvement of superoxide dismutase (SOD) in the attenuation of gene expression ofcytochrome c oxidasesubunit 1 (COX1) in aged zooids. By RT‐PCR andin situhybridization,Cu/Zn‐SOD(SOD1) was found to be expressed in most cells and tissues of buds and juvenile zooids but showed a conspicuous decline in senescent adult zooids, except in the gonad tissue in which the cytoplasm of juvenile oocytes was stained heavily. This expression pattern ofSOD1was similar to that ofCOX1. In contrast toSOD1,Mn‐SOD(SOD2) was expressed constitutively in both somatic and germline tissues of buds, juvenile zooids, and senescent adult zooids. Knockdown ofSOD1by RNAi diminished the gene activity of not onlySOD1but also ofCOX1. The resultant zooids had transient deficiencies in growth and budding, and they recovered from these deficiencies approximately 1 month later. Our results indicate that inP.misakiensis,SOD1is a senescence‐associated nuclear gene and that the experimental decline inSOD1gene expression accompanies the attenuation of MRC gene activity. Although it is uncertain howSOD1is downregulated during tunicate senescence, the decreasedSOD1activity could be one of the main causes of MRC gene attenuation during normal senescence.