Although iron has a major role in mitochondrial activity, the processes of iron transport, trafficking and homeostasis in plant mitochondria are mostly unknown. A first evidence of accumulation of the iron storage protein ferritin in plant mitochondria was recently shown but, up to now, the Arabidopsis ferritin gene encoding the mitochondrial isoform was not identified. According to computer analysis with four different programs (Target P, ChloroP, Mitoprot II, Predotar) predicting localization of protein in the different organelles, AtFer4 is the ferritin isoform with highest scores for localization in mitochondria. For this reason we therefore isolated and characterized two independent Arabidopsis atfer4 mutants knock out in the AtFer4 isoform, named atfer4-1 and atfer4-2. Analysis of atfer4-1 and atfer4-2 plant phenotypes was performed during seedling development, at mature plant stage and during senescence, in the aerial organs and in the roots: atfer4-1 and atfer4-2 mutant plants show no alteration of phenotype attributable to lack of AtFer4, at any stage or in any organ analysed, not even during senescence, which on the reverse is accelerated in atfer1 KO mutants. However, when grown in suspension cultures, atfer4 mutants show impaired growth and higher cell death. Purification of mitochondria from atfer4 suspension cultured cells allowed to show that ATFER4 is mitochondria-localized and that it accumulates in mitochondria regardless of exogenous iron treatment. Furthermore, at least another ferritin isoform, different from ATFER4, accumulates in mitochondria of iron-treated atfer4 and wt Col cells. Such accumulation at same levels in both atfer4 and wt Col mitochondria takes place, in atfer4 cells, under unexpected reduced accumulation of AtFer1, AtFer3 and AtFer2 transcripts. Interestingly, atfer4 mitochondria accumulate more iron than wt ones, both in control conditions or upon iron treatment. All these results indicate that ferritin targeting to mitochondria is a complex event involving constitutively ATFER4 and at least one other ferritin isoform under iron loading; also, they indicate that AtFer4 has a key role for the iron trafficking/homeostasis in mitochondria in conditions in which such organelles are the sole energy source, that is in suspension cultured cells.

THE ATFER4 FERRITIN IS A KEY COMPONENT FOR THE CONTROL OF THE IRON HOMEOSTASIS IN MITOCHONDRIA OF ARABIDOPSIS CELLS / I. Murgia, D. Tarantino, V. Vazzola, F. Casagrande, H.P. Braun, J. Heinemeyer, K. Ravet, F. Gaymard, C. Soave. ((Intervento presentato al convegno XIV International symposium on Iron nutrition and interaction in plants (ISINIP) tenutosi a Beijing, (China) nel 2008.

THE ATFER4 FERRITIN IS A KEY COMPONENT FOR THE CONTROL OF THE IRON HOMEOSTASIS IN MITOCHONDRIA OF ARABIDOPSIS CELLS.

I. Murgia
Primo
;
D. Tarantino
Secondo
;
C. Soave
Ultimo
2008

Abstract

Although iron has a major role in mitochondrial activity, the processes of iron transport, trafficking and homeostasis in plant mitochondria are mostly unknown. A first evidence of accumulation of the iron storage protein ferritin in plant mitochondria was recently shown but, up to now, the Arabidopsis ferritin gene encoding the mitochondrial isoform was not identified. According to computer analysis with four different programs (Target P, ChloroP, Mitoprot II, Predotar) predicting localization of protein in the different organelles, AtFer4 is the ferritin isoform with highest scores for localization in mitochondria. For this reason we therefore isolated and characterized two independent Arabidopsis atfer4 mutants knock out in the AtFer4 isoform, named atfer4-1 and atfer4-2. Analysis of atfer4-1 and atfer4-2 plant phenotypes was performed during seedling development, at mature plant stage and during senescence, in the aerial organs and in the roots: atfer4-1 and atfer4-2 mutant plants show no alteration of phenotype attributable to lack of AtFer4, at any stage or in any organ analysed, not even during senescence, which on the reverse is accelerated in atfer1 KO mutants. However, when grown in suspension cultures, atfer4 mutants show impaired growth and higher cell death. Purification of mitochondria from atfer4 suspension cultured cells allowed to show that ATFER4 is mitochondria-localized and that it accumulates in mitochondria regardless of exogenous iron treatment. Furthermore, at least another ferritin isoform, different from ATFER4, accumulates in mitochondria of iron-treated atfer4 and wt Col cells. Such accumulation at same levels in both atfer4 and wt Col mitochondria takes place, in atfer4 cells, under unexpected reduced accumulation of AtFer1, AtFer3 and AtFer2 transcripts. Interestingly, atfer4 mitochondria accumulate more iron than wt ones, both in control conditions or upon iron treatment. All these results indicate that ferritin targeting to mitochondria is a complex event involving constitutively ATFER4 and at least one other ferritin isoform under iron loading; also, they indicate that AtFer4 has a key role for the iron trafficking/homeostasis in mitochondria in conditions in which such organelles are the sole energy source, that is in suspension cultured cells.
2008
Settore BIO/04 - Fisiologia Vegetale
Settore AGR/13 - Chimica Agraria
Settore BIO/11 - Biologia Molecolare
THE ATFER4 FERRITIN IS A KEY COMPONENT FOR THE CONTROL OF THE IRON HOMEOSTASIS IN MITOCHONDRIA OF ARABIDOPSIS CELLS / I. Murgia, D. Tarantino, V. Vazzola, F. Casagrande, H.P. Braun, J. Heinemeyer, K. Ravet, F. Gaymard, C. Soave. ((Intervento presentato al convegno XIV International symposium on Iron nutrition and interaction in plants (ISINIP) tenutosi a Beijing, (China) nel 2008.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/211453
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