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Senescence‐associated superoxide dismutase influences mitochondrial gene expression in budding tunicates
Author(s) -
Kawamura Kaz,
Sunanaga Takeshi
Publication year - 2013
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1111/dgd.12065
Subject(s) - biology , sod1 , sod2 , superoxide dismutase , microbiology and biotechnology , zooid , senescence , budding , gene expression , gene knockdown , genetics , gene , anatomy , oxidative stress , endocrinology
A recent study has shown that in the budding tunicate Polyandrocarpa 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 of cytochrome c oxidase subunit 1 ( COX 1 ) in aged zooids. By RT ‐ PCR and in situ hybridization, Cu/Zn‐ SOD ( SOD 1 ) 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 SOD 1 was similar to that of COX 1 . In contrast to SOD 1 , Mn‐ SOD ( SOD 2 ) was expressed constitutively in both somatic and germline tissues of buds, juvenile zooids, and senescent adult zooids. Knockdown of SOD 1 by RNA i diminished the gene activity of not only SOD 1 but also of COX 1 . 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 P . misakiensis , SOD 1 is a senescence‐associated nuclear gene and that the experimental decline in SOD 1 gene expression accompanies the attenuation of MRC gene activity. Although it is uncertain how SOD 1 is downregulated during tunicate senescence, the decreased SOD 1 activity could be one of the main causes of MRC gene attenuation during normal senescence.