http://www.cnr.it/ontology/cnr/individuo/prodotto/ID254757
Yeast growth in raffinose results in resistance to acetic-acid induced programmed cell death mostly due to the activation of the mitochondrial retrograde pathway. (Articolo in rivista)
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- Yeast growth in raffinose results in resistance to acetic-acid induced programmed cell death mostly due to the activation of the mitochondrial retrograde pathway. (Articolo in rivista) (literal)
- Anno
- 2013-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.bbamcr.2013.07.017 (literal)
- Alternative label
Guaragnella N, Zdralevi? M, Lattanzio P, Marzulli D, Pracheil T, Liu Z, Passarella S, Marra E, Giannattasio S. (2013)
Yeast growth in raffinose results in resistance to acetic-acid induced programmed cell death mostly due to the activation of the mitochondrial retrograde pathway.
in Biochimica et biophysica acta. Molecular cell research
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Guaragnella N, Zdralevi? M, Lattanzio P, Marzulli D, Pracheil T, Liu Z, Passarella S, Marra E, Giannattasio S. (literal)
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- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- CNR, Istituto di Biomembrane e Bioenergetica, Via Amendola 165/a, 70126 Bari, Italy
Department of Biological Sciences, University of New Orleans, 2000 Lakeshore Drive, New Orleans, LA 70148, USA
Dipartimento di Medicina e Scienze per la Salute, Università del Molise, Via de Sanctis, 86100 Campobasso, Italy (literal)
- Titolo
- Yeast growth in raffinose results in resistance to acetic-acid induced programmed cell death mostly due to the activation of the mitochondrial retrograde pathway. (literal)
- Abstract
- In order to investigate whether and how a modification of mitochondrialmetabolism can affect yeast sensitivity
to programmed cell death (PCD) induced by acetic acid (AA-PCD), yeast cells were grown on raffinose, as a sole carbon source, which, differently from glucose, favours mitochondrial respiration. We found that, differently from glucose-grown cells, raffinose-grown cells were mostly resistant to AA-PCD and that this was due to the activation of mitochondrial retrograde (RTG) response, which increased with time, as revealed by the upregulation
of the peroxisomal isoform of citrate synthase and isocitrate dehydrogenase isoform 1, RTG pathway
target genes. Accordingly, the deletion of RTG2 and RTG3, a positive regulator and a transcription factor of the RTG pathway, resulted in AA-PCD, as shown by TUNEL assay. Neither deletion in raffinose-grown cells of HAP4,
encoding the positive regulatory subunit of the Hap2,3,4,5 complex nor constitutive activation of the RTG pathway in glucose-grown cells due to deletion of MKS1, a negative regulator of RTG pathway, had effect on yeast AA-PCD. The RTG pathway was found to be activated in yeast cells containing mitochondria, in which membrane potential wasmeasured, capable to consume oxygen in amanner stimulated by the uncoupler CCCP and inhibited by the respiratory chain inhibitor antimycin A. AA-PCD resistance in raffinose-grown cells occurs with a decrease in both ROS production and cytochrome c release as compared to glucose-grown cells en route to AA-PCD. (literal)
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