This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ku, C. Y. Articles by Sanborn, B. M. Search for Related Content PubMed PubMed Citation Articles by Ku, C. Y. Articles by Sanborn, B. M.

Hormonal Regulation of Cytochrome Oxidase Subunit Messenger RNAs in Rat Sertoli Cells

Department of Biochemistry and Molecular Biology, University of Texas Medical School Houston, Texas 77030

Address requests for reprints to: Dr. B. M. Sanborn, Department of Biochemistry and Molecular Biology, University of Texas Medical School, P.O. Box 20708, Houston, Texas 77225.

Abstract

Using differential hybridization to screen a rat Sertoli cell cDNA library for hormonally regulated gene products, we isolated a clone, designated 13–10, which contained a 1.0-kilobase insert and hybridized to a 1.7-kilobase message in total testis, Sertoli cells, and peritubular cells. This mRNA was decreased relative to untreated control levels in total testicular RNA from hypophysectomized rats, but was increased by FSH treatment begun on the day of hypophysectomy. FSH caused a transient rise in 13–10 mRNA at 24 h in cultured Sertoli cells. There was no comparable rise in β-actin RNA or the RNA/DNA ratio at this time, suggesting that the effect on 13–10 was specific. Testosterone had no effect at any time interval studied. The 13–10 mRNA was not increased in peritubular cells treated in vitro with FSH or testosterone. Sequence analysis of 13–10 revealed more than 99% homology with a portion of the sequence of rat liver cytochrome oxidase subunit I (COX I). The clone included 58% of the open reading frame of COX I as well as that for the adjacent Ser-tRNA. COX I is a mitochondrial gene, and Southern analysis confirmed 13% homology with a portion of the sequence of rat liver cytochrome oxidase subunit I (COX I). The clone included 58% of the open 10 sequence in testicular mitochondrial DNA. In addition to FSH, forskolin and (Bu)₂cAMP also increased COX I steady state mRNA in Sertoli cells (3.8-, 4.1-, and 9.2-fold, respectively). (Bu)₂cAMP increased mRNA for other mitochondrial gene products, COX subunit II and 16S rRNA (6.9- and 5.4-fold, respectively), whereas the smaller effects elicited by forskolin and FSH were not statistically significant. The mRNA for COX Va, a cytochrome oxidase subunit encoded by a nuclear gene, was significantly stimulated by FSH, forskolin, and (Bu)₂cAMP (3.1-, 3.5-, and 8.1-fold, respectively). These data suggest that FSH, via cAMP, may regulate the transcription and/or stability of RNAs coding for cytochrome oxidase subunits and may, thus, play an important role in establishing and maintaining mitochondrial function in Sertoli cells.

FOOTNOTES

This work was supported by Grant HD-17795. Portions of this work were presented in preliminary form at the 72nd Annual Meeting of The Endocrine Society, Atlanta, GA, June 1990.

Received for publication May 8, 1991. Revision received August 2, 1991. Accepted for publication August 19, 1991.

This article has been cited by other articles:

				W. K. Sumanasekera, G. U. Sumanasekera, K. A. Mattingly, S. M. Dougherty, R. S. Keynton, and C. M. Klinge Estradiol and dihydrotestosterone regulate endothelial cell barrier function after hypergravity-induced alterations in MAPK activity Am J Physiol Cell Physiol, August 1, 2007; 293(2): C566 - C573. [Abstract] [Full Text] [PDF]

				N. Shirafuji, S. Takahashi, S. Matsuda, and S. Asano Mitochondrial Antisense RNA for Cytochrome C Oxidase (MARCO) Can Induce Morphologic Changes and Cell Death in Human Hematopoietic Cell Lines Blood, December 1, 1997; 90(11): 4567 - 4577. [Abstract] [Full Text] [PDF]