The prohibitin family of mitochondrial proteins regulate replicative lifespan

P. J. Coates, D. J. Jamieson, K. Smart, A. R. Prescott, P. A. Hall

    Research output: Contribution to journalArticle

    154 Citations (Scopus)

    Abstract

    Cellular senescence is determined by multiple factors, including the genetic regulation of metabolism and responses to endogenous and exogenous stresses [1-4]. Recent studies implicate a limited number of gene products in elongating lifespan in yeast and Caenorhabditis elegans [2-4]; these include the C, elegans gene cik-1, a central regulator of metabolism [5], and yeast RAS2, which controls the response to ultraviolet irradiation and other stresses [3]. Another gene postulated to effect senescence is PHB1, the yeast homologue of prohibitin [3], a rodent gene initially identified as a potential regulator of growth arrest and tumour suppressor [6-8]. Highly conserved prohibitin homologues have been identified in mammals [9], Drosophila [10], C. elegans [9], plants [11] and yeast. A second mammalian gene, encoding BAP37, a protein with sequence similarity to prohibitin, is thought to be involved in lymphocyte function [9]. Here, we show that the nuclear-encoded mammalian prohibitin and BAP37 proteins are present in mitochondria, are co-expressed, and interact physically with each other. Deletion of the Saccharomyces cerevisiae homologues, PHB1 and PHB2, results in a decreased replicative lifespan and a defect in mitochondrial membrane potential. Our observations highlight the relationship between the metabolic efficiency of cells and the ageing process, and provide evidence for its evolutionary conservation.
    Original languageEnglish
    Pages (from-to)607-610
    Number of pages4
    JournalCurrent Biology
    Volume7
    Issue number8
    DOIs
    Publication statusPublished - 1997

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    Mitochondrial Proteins
    Yeast
    Genes
    Yeasts
    yeasts
    Cell Aging
    Caenorhabditis elegans
    genes
    Metabolism
    proteins
    Mitochondria
    Gene encoding
    Mammals
    metabolism
    Lymphocytes
    Mitochondrial Membrane Potential
    membrane potential
    growth regulators
    Drosophila
    Saccharomyces cerevisiae

    Cite this

    Coates, P. J. ; Jamieson, D. J. ; Smart, K. ; Prescott, A. R. ; Hall, P. A. / The prohibitin family of mitochondrial proteins regulate replicative lifespan. In: Current Biology. 1997 ; Vol. 7, No. 8. pp. 607-610.
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    abstract = "Cellular senescence is determined by multiple factors, including the genetic regulation of metabolism and responses to endogenous and exogenous stresses [1-4]. Recent studies implicate a limited number of gene products in elongating lifespan in yeast and Caenorhabditis elegans [2-4]; these include the C, elegans gene cik-1, a central regulator of metabolism [5], and yeast RAS2, which controls the response to ultraviolet irradiation and other stresses [3]. Another gene postulated to effect senescence is PHB1, the yeast homologue of prohibitin [3], a rodent gene initially identified as a potential regulator of growth arrest and tumour suppressor [6-8]. Highly conserved prohibitin homologues have been identified in mammals [9], Drosophila [10], C. elegans [9], plants [11] and yeast. A second mammalian gene, encoding BAP37, a protein with sequence similarity to prohibitin, is thought to be involved in lymphocyte function [9]. Here, we show that the nuclear-encoded mammalian prohibitin and BAP37 proteins are present in mitochondria, are co-expressed, and interact physically with each other. Deletion of the Saccharomyces cerevisiae homologues, PHB1 and PHB2, results in a decreased replicative lifespan and a defect in mitochondrial membrane potential. Our observations highlight the relationship between the metabolic efficiency of cells and the ageing process, and provide evidence for its evolutionary conservation.",
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    The prohibitin family of mitochondrial proteins regulate replicative lifespan. / Coates, P. J.; Jamieson, D. J.; Smart, K.; Prescott, A. R.; Hall, P. A.

    In: Current Biology, Vol. 7, No. 8, 1997, p. 607-610.

    Research output: Contribution to journalArticle

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