Estrogen-Mediated Regulation of Mitochondrial Gene Expression
Estrogens, in particular 17β-estradiol, are well-known regulators of essential cellular functions; however, discrepancies remain over the mechanisms by which they act on mitochondria. Here we propose a novel mechanism for the direct regulation of mitochondrial gene expression by estrogen under metab...
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| Published in | Molecular endocrinology (Baltimore, Md.) Vol. 29; no. 1; pp. 14 - 27 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Endocrine Society
01.01.2015
Oxford University Press |
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| Abstract | Estrogens, in particular 17β-estradiol, are well-known regulators of essential cellular functions; however, discrepancies remain over the mechanisms by which they act on mitochondria. Here we propose a novel mechanism for the direct regulation of mitochondrial gene expression by estrogen under metabolic stress. We show that in serum-depleted medium, estrogen stimulates a rapid relocation of estrogen receptor-α to mitochondria, in which it elicits a cellular response, resulting in an increase in mitochondrial RNA abundance. Mitochondrial RNA levels are regulated through the association of estrogen receptor-α with 17β-hydroxysteroid dehydrogenase 10, a multifunctional protein involved in steroid metabolism that is also a core subunit of the mitochondrial ribonuclease P complex responsible for the cleavage of mitochondrial polycistronic transcripts. Processing of mitochondrial transcripts affects mitochondrial gene expression by controlling the levels of mature RNAs available for translation. This work provides the first mechanism linking RNA processing and estrogen activation in mitochondrial gene expression and underscores the coordinated response between the nucleus and mitochondria in response to stress. |
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| AbstractList | Estrogens, in particular 17β-estradiol, are well-known regulators of essential cellular functions; however, discrepancies remain over the mechanisms by which they act on mitochondria. Here we propose a novel mechanism for the direct regulation of mitochondrial gene expression by estrogen under metabolic stress. We show that in serum-depleted medium, estrogen stimulates a rapid relocation of estrogen receptor-α to mitochondria, in which it elicits a cellular response, resulting in an increase in mitochondrial RNA abundance. Mitochondrial RNA levels are regulated through the association of estrogen receptor-α with 17β-hydroxysteroid dehydrogenase 10, a multifunctional protein involved in steroid metabolism that is also a core subunit of the mitochondrial ribonuclease P complex responsible for the cleavage of mitochondrial polycistronic transcripts. Processing of mitochondrial transcripts affects mitochondrial gene expression by controlling the levels of mature RNAs available for translation. This work provides the first mechanism linking RNA processing and estrogen activation in mitochondrial gene expression and underscores the coordinated response between the nucleus and mitochondria in response to stress. Abstract Estrogens, in particular 17β-estradiol, are well-known regulators of essential cellular functions; however, discrepancies remain over the mechanisms by which they act on mitochondria. Here we propose a novel mechanism for the direct regulation of mitochondrial gene expression by estrogen under metabolic stress. We show that in serum-depleted medium, estrogen stimulates a rapid relocation of estrogen receptor-α to mitochondria, in which it elicits a cellular response, resulting in an increase in mitochondrial RNA abundance. Mitochondrial RNA levels are regulated through the association of estrogen receptor-α with 17β-hydroxysteroid dehydrogenase 10, a multifunctional protein involved in steroid metabolism that is also a core subunit of the mitochondrial ribonuclease P complex responsible for the cleavage of mitochondrial polycistronic transcripts. Processing of mitochondrial transcripts affects mitochondrial gene expression by controlling the levels of mature RNAs available for translation. This work provides the first mechanism linking RNA processing and estrogen activation in mitochondrial gene expression and underscores the coordinated response between the nucleus and mitochondria in response to stress. |
| Author | Filipovska, Aleksandra Davies, Stefan M. K Shearwood, Anne-Marie J Rackham, Oliver Chia, Tiongsun Lopez Sanchez, Maria I. G |
| Author_xml | – sequence: 1 givenname: Maria I. G surname: Lopez Sanchez fullname: Lopez Sanchez, Maria I. G – sequence: 2 givenname: Anne-Marie J surname: Shearwood fullname: Shearwood, Anne-Marie J – sequence: 3 givenname: Tiongsun surname: Chia fullname: Chia, Tiongsun – sequence: 4 givenname: Stefan M. K surname: Davies fullname: Davies, Stefan M. K – sequence: 5 givenname: Oliver surname: Rackham fullname: Rackham, Oliver – sequence: 6 givenname: Aleksandra surname: Filipovska fullname: Filipovska, Aleksandra email: aleksandra.filipovska@uwa.edu.au |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25375021$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2015 by the Endocrine Society Copyright © 2015 by the Endocrine Society 2015 |
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| Notes | This work was supported by fellowships and project grants (to A.F and O.R.) from the National Health and Medical Research Council (Grants APP1058442, APP1045677, APP1041582, APP1023460, and APP1005030) and the Australian Research Council (Grants FT0991008, FT0991113, and DP140104111). ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
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| Snippet | Estrogens, in particular 17β-estradiol, are well-known regulators of essential cellular functions; however, discrepancies remain over the mechanisms by which... Abstract Estrogens, in particular 17β-estradiol, are well-known regulators of essential cellular functions; however, discrepancies remain over the mechanisms... |
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| SubjectTerms | 3-Hydroxyacyl CoA Dehydrogenases - biosynthesis 3-Hydroxyacyl CoA Dehydrogenases - genetics 3-Hydroxyacyl CoA Dehydrogenases - metabolism Cell Line, Tumor Estradiol - metabolism Estrogen Receptor alpha - biosynthesis Estrogen Receptor alpha - genetics Estrogen Receptor alpha - metabolism Estrogens - metabolism Gene Expression Regulation - genetics Genes, Mitochondrial - genetics Humans MCF-7 Cells Mitochondria - enzymology Mitochondria - genetics Mitochondria - metabolism Original Research RNA Interference RNA, Small Interfering |
| Title | Estrogen-Mediated Regulation of Mitochondrial Gene Expression |
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