Senescence‐associated superoxide dismutase influences mitochondrial gene expression in budding tunicates. (16th May 2013)

• Record Type: Journal Article
• Authors: Kawamura, Kaz; Sunanaga, Takeshi
• Is Part Of: Development growth and differentiation. Volume 55:Number 5(2013)
• Page Start: 606
• Page End: 614
• Publication Date: 2013-05-16
• Subjects: Embryology -- Periodicals; Developmental biology -- Periodicals; Growth -- Periodicals; 574.3
• DOI: 10.1111/dgd.12065
• Languages: English
• ISSNs: 0012-1592

Abstract

<abstract abstract-type="main" id="dgd12065-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>A recent study has shown that in the budding tunicate <italic>Polyandrocarpa misakiensis</italic>, 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 of <italic>cytochrome c oxidase</italic> subunit 1 (<italic>COX1</italic>) in aged zooids. By RT‐PCR and <italic>in situ</italic> hybridization, <italic>Cu/Zn‐SOD</italic> (<italic>SOD1</italic>) 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 of <italic>SOD1</italic> was similar to that of <italic>COX1</italic>. In contrast to <italic>SOD1</italic>, <italic> Mn‐SOD</italic> (<italic>SOD2</italic>) was expressed constitutively in both somatic and germline tissues of buds, juvenile zooids, and senescent adult zooids. Knockdown of <italic>SOD1</italic> by RNAi diminished the gene activity of not only <italic>SOD1</italic> but also of <italic>COX1</italic>. The resultant zooids had transient deficiencies in growth and budding, and they recovered from these deficiencies approximately 1 month later. Our results indicate that in <italic>P</italic>. <italic>misakiensis</italic>, <italic> SOD1</italic> is a senescence‐associated nuclear gene and that the experimental decline in <italic>SOD1</italic> gene expression accompanies the attenuation of MRC gene activity. Although it is uncertain how <italic>SOD1</italic> is downregulated during tunicate senescence, the decreased <italic>SOD1</italic> activity could be one of the main causes of MRC gene attenuation during normal senescence.</p> </abstract>