Although iron has a major role in mitochondrial activity, the processes of iron transport, trafficking and homeostasis in plant mitochondria are still mostly unknown. Ferritins are iron-storage proteins which, in plant cells, are localized in chloroplast but can also be localized in mitochondria. We characterized two independent Arabidopsis mutants, KO in the AtFer4 ferritin isoform. When grown in suspension cultures, atfer4 mutants show higher cell death and higher O2 consumption rates. Mitochondria of atfer4 cells are larger size and possess higher total iron content than wt ones, both in control conditions or upon treatment with iron excess. A more pronounced accumulation of a still unidentified ferritin(s) is observed in mitochondria of iron-treated atfer4 cells, when compared to wt ones. These results indicate that AtFer4 has a role for the iron trafficking/homeostasis in mitochondria in conditions in which such organelles are the sole energy source. Friedreich ataxia (FRDA), an autosomal recessive neurological dysfunction that severely impairs motor coordination in humans, is caused by a deficiency in frataxin, a nuclear-encoded mitochondrial protein. Although several groups have shown in the past that frataxin is involved in the assembly, regulation and repair of the [Fe-S] cluster, as well as in the homeostasis of mitochondrial iron, its primary role is still matter of debate. We have shown that the Arabidopsis frataxin homolog, named AtFH, is expressed mainly in flowers and developing embryos and that it encodes an essential protein, since the knocking out of AtFH gene causes arrest of Arabidopsis embryo development at the globular stage. To overcome experimental constraints due to embryo lethality of AtFH KO, we are currently producing Arabidopsis transgenic lines, by inducible RNA-interference, in which microRNA can switch off AtFH frataxin transcript accumulation upon treatment with either ethanol or dexametasone.

Ferritins and frataxin take part in the iron homeostasis and trafficking in Arabidopsis mitochondria / I.;.T.D.;.V.V.;.S.C. Murgia, D. Tarantino, V. Vazzola, C. Soave. ((Intervento presentato al convegno Plant ROS 2009 -A SFRR Plant Oxygen Group meeting on reactive oxygen and nitrogen species tenutosi a Helsinki, Finland nel 2009.

Ferritins and frataxin take part in the iron homeostasis and trafficking in Arabidopsis mitochondria

I.;.T.D.;.V.V.;.S.C. Murgia;D. Tarantino;C. Soave
2009

Abstract

Although iron has a major role in mitochondrial activity, the processes of iron transport, trafficking and homeostasis in plant mitochondria are still mostly unknown. Ferritins are iron-storage proteins which, in plant cells, are localized in chloroplast but can also be localized in mitochondria. We characterized two independent Arabidopsis mutants, KO in the AtFer4 ferritin isoform. When grown in suspension cultures, atfer4 mutants show higher cell death and higher O2 consumption rates. Mitochondria of atfer4 cells are larger size and possess higher total iron content than wt ones, both in control conditions or upon treatment with iron excess. A more pronounced accumulation of a still unidentified ferritin(s) is observed in mitochondria of iron-treated atfer4 cells, when compared to wt ones. These results indicate that AtFer4 has a role for the iron trafficking/homeostasis in mitochondria in conditions in which such organelles are the sole energy source. Friedreich ataxia (FRDA), an autosomal recessive neurological dysfunction that severely impairs motor coordination in humans, is caused by a deficiency in frataxin, a nuclear-encoded mitochondrial protein. Although several groups have shown in the past that frataxin is involved in the assembly, regulation and repair of the [Fe-S] cluster, as well as in the homeostasis of mitochondrial iron, its primary role is still matter of debate. We have shown that the Arabidopsis frataxin homolog, named AtFH, is expressed mainly in flowers and developing embryos and that it encodes an essential protein, since the knocking out of AtFH gene causes arrest of Arabidopsis embryo development at the globular stage. To overcome experimental constraints due to embryo lethality of AtFH KO, we are currently producing Arabidopsis transgenic lines, by inducible RNA-interference, in which microRNA can switch off AtFH frataxin transcript accumulation upon treatment with either ethanol or dexametasone.
lug-2009
Settore BIO/04 - Fisiologia Vegetale
Settore AGR/13 - Chimica Agraria
Settore BIO/11 - Biologia Molecolare
Ferritins and frataxin take part in the iron homeostasis and trafficking in Arabidopsis mitochondria / I.;.T.D.;.V.V.;.S.C. Murgia, D. Tarantino, V. Vazzola, C. Soave. ((Intervento presentato al convegno Plant ROS 2009 -A SFRR Plant Oxygen Group meeting on reactive oxygen and nitrogen species tenutosi a Helsinki, Finland nel 2009.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/211641
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