This work was supported by the FCT project PTDC/BIA-BCM/69448/200

Alves, Sara Cristina Sequeira

Camougrand, Nadine

Chaves, S. R.

Coutinho, Clara Pereira

Coutinho, O. P.

Côrte-Real, Manuela

Gerós, H.

Manon, Stéphen

Marques, Carolina

Preto, Ana

Rodrigues, Andreia

Salin, Bénédict

Silva, Rui

Sousa, Maria João

Universidade do Minho: RepositoriUM

 Vacuole-mitochondrial crosstalk during apoptosis induced by acetic acid in yeast   Chaves S1, Pereira C1#, Marques C1, Rodrigues A1,3, Salin B2, Alves S1, Silva R1, Gerós H3, Coutinho OP1, Preto A1, Camougrand N2, Manon S2, Sousa MJ1 and Côrte-Real M1  1CBMA (Centre of Molecular and Environmental Biology)/Department of Biology, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal. 2CNRS and Université de Bordeaux 2, UMR5095, Bordeaux, France. 3CITAB (Centro de Investigação e de Tecnologias Agro-Ambientais e Biológicas), Vila Real, Portugal. #Actual address: Laboratório de Microbiologia, Faculdade de Farmácia, Universidade do Porto.  We have previously shown that acetic acid activates a mitochondria-dependent death process in Saccharomyces cerevisiae and that the ADP/ATP carrier (AAC) is required for mitochondrial outer membrane permeabilization and cytochrome c release. Mitochondrial fragmentation and degradation have also been shown in response to this death stimulus. We showed that vacuolar protease Pep4p is released from the vacuole into the cytosol in response to acetic acid treatment. Furthermore using yeast genetic approaches we found that the Pep4p and AAC proteins have a role in mitochondrial degradation. Depletion and overexpression of Pep4p, an orthologue of human cathepsin D, delays and enhances mitochondrial degradation, respectively. Moreover, AAC-deficient cells also show a decrease in mitochondrial degradation in response to acetic acid and are not defective in Pep4p release. Therefore, AAC proteins seem to affect mitochondrial degradation at a step subsequent to Pep4p release, possibly triggering degradation through their involvement in mitochondrial permeabilization. Since autophagy is not active in cells undergoing acetic acid-induced apoptosis, vacuolar membrane permeabilization associated with the release of Pep4p may act as an alternative mitochondrial degradation process. In the present communication, I will cover our recent studies with isolated vacuoles towards the understanding of the role of this organelle in acetic acid induced apoptosis. The validation in mammalian cell lines of the hypothesis postulated with the yeast model will be also discussed.  This work was supported by the FCT project PTDC/BIA-BCM/69448/2006.  

Vacuole-mitochondrial crosstalk during apoptosis induced by acetic acid in yeast

Vacuole-mitochondrial crosstalk during apoptosis induced by acetic acid in yeast

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Universidade do Minho: RepositoriUM