scholarly journals Translation machinery reprogramming in programmed cell death in Saccharomyces cerevisiae

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Francesco Monticolo ◽  
Emanuela Palomba ◽  
Maria Luisa Chiusano

AbstractProgrammed cell death involves complex molecular pathways in both eukaryotes and prokaryotes. In Escherichia coli, the toxin–antitoxin system (TA-system) has been described as a programmed cell death pathway in which mRNA and ribosome organizations are modified, favoring the production of specific death-related proteins, but also of a minor portion of survival proteins, determining the destiny of the cell population. In the eukaryote Saccharomyces cerevisiae, the ribosome was shown to change its stoichiometry in terms of ribosomal protein content during stress response, affecting the relative proportion between ohnologs, i.e., the couple of paralogs derived by a whole genome duplication event. Here, we confirm the differential expression of ribosomal proteins in yeast also during programmed cell death induced by acetic acid, and we highlight that also in this case pairs of ohnologs are involved. We also show that there are different trends in cytosolic and mitochondrial ribosomal proteins gene expression during the process. Moreover, we show that the exposure to acetic acid induces the differential expression of further genes coding for products related to translation processes and to rRNA post-transcriptional maturation, involving mRNA decapping, affecting translation accuracy, and snoRNA synthesis. Our results suggest that the reprogramming of the overall translation apparatus, including the cytosolic ribosome reorganization, are relevant events in yeast programmed cell death induced by acetic acid.

Mitochondrion ◽  
2011 ◽  
Vol 11 (6) ◽  
pp. 987-991 ◽  
Author(s):  
Nicoletta Guaragnella ◽  
Salvatore Passarella ◽  
Ersilia Marra ◽  
Sergio Giannattasio

Gene ◽  
2005 ◽  
Vol 354 ◽  
pp. 93-98 ◽  
Author(s):  
Sergio Giannattasio ◽  
Nicoletta Guaragnella ◽  
Manuela Corte-Real ◽  
Salvatore Passarella ◽  
Ersilia Marra

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Jingjin Hu ◽  
Yachen Dong ◽  
Wei Wang ◽  
Wei Zhang ◽  
Hanghang Lou ◽  
...  

Abstract Background Programmed cell death (PCD) induced by acetic acid, the main by-product released during cellulosic hydrolysis, cast a cloud over lignocellulosic biofuel fermented by Saccharomyces cerevisiae and became a burning problem. Atg22p, an ignored integral membrane protein located in vacuole belongs to autophagy-related genes family; prior study recently reported that it is required for autophagic degradation and efflux of amino acids from vacuole to cytoplasm. It may alleviate the intracellular starvation of nutrition caused by Ac and increase cell tolerance. Therefore, we investigate the role of atg22 in cell death process induced by Ac in which attempt is made to discover new perspectives for better understanding of the mechanisms behind tolerance and more robust industrial strain construction. Results In this study, we compared cell growth, physiological changes in the absence and presence of Atg22p under Ac exposure conditions. It is observed that disruption and overexpression of Atg22p delays and enhances acetic acid-induced PCD, respectively. The deletion of Atg22p in S. cerevisiae maintains cell wall integrity, and protects cytomembrane integrity, fluidity and permeability upon Ac stress by changing cytomembrane phospholipids, sterols and fatty acids. More interestingly, atg22 deletion increases intracellular amino acids to aid yeast cells for tackling amino acid starvation and intracellular acidification. Further, atg22 deletion upregulates series of stress response genes expression such as heat shock protein family, cell wall integrity and autophagy. Conclusions The findings show that Atg22p possessed the new function related to cell resistance to Ac. This may help us have a deeper understanding of PCD induced by Ac and provide a new strategy to improve Ac resistance in designing industrial yeast strains for bioethanol production during lignocellulosic biofuel fermentation.


FEBS Letters ◽  
2010 ◽  
Vol 584 (16) ◽  
pp. 3655-3660 ◽  
Author(s):  
Nicoletta Guaragnella ◽  
Salvatore Passarella ◽  
Ersilia Marra ◽  
Sergio Giannattasio

BMC Genomics ◽  
2013 ◽  
Vol 14 (1) ◽  
pp. 838 ◽  
Author(s):  
Marlene Sousa ◽  
Ana Duarte ◽  
Tânia R Fernandes ◽  
Susana R Chaves ◽  
Andreia Pacheco ◽  
...  

Microbiology ◽  
2001 ◽  
Vol 147 (9) ◽  
pp. 2409-2415 ◽  
Author(s):  
Paula Ludovico ◽  
Maria João Sousa ◽  
Manuel T Silva ◽  
Cecı́lia Leão ◽  
Manuela Côrte-Real

2002 ◽  
Vol 13 (8) ◽  
pp. 2598-2606 ◽  
Author(s):  
Paula Ludovico ◽  
Fernando Rodrigues ◽  
Agostinho Almeida ◽  
Manuel T. Silva ◽  
Antoni Barrientos ◽  
...  

Evidence is presented that mitochondria are implicated in the previously described programmed cell death (PCD) process induced by acetic acid in Saccharomyces cerevisiae. In yeast cells undergoing a PCD process induced by acetic acid, translocation of cytochrome c (CytC) to the cytosol and reactive oxygen species production, two events known to be proapoptotic in mammals, were observed. Associated with these events, reduction in oxygen consumption and in mitochondrial membrane potential was found. Enzymatic assays showed that the activity of complexbc 1 was normal, whereas that of cytochrome c oxidase (COX) was strongly decreased. This decrease is in accordance with the observed reduction in the amounts of COX II subunit and of cytochromesa+a 3 . The acetic acid-induced PCD process was found to be independent of oxidative phosphorylation because it was not inhibited by oligomycin treatment. The inability ofS. cerevisiae mutant strains (lacking mitochondrial DNA, heme lyase, or ATPase) to undergo acetic acid-induced PCD and in the ATPase mutant (knockout in ATP10) the absence of CytC release provides further evidence that the process is mediated by a mitochondria-dependent apoptotic pathway. The understanding of the involvement of a mitochondria-dependent apoptotic pathway inS. cerevisiae PCD process will be most useful in the further elucidation of an ancestral pathway common to PCD in metazoans.


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