The first suicides: a legacy inherited by parasitic protozoans from prokaryote ancestors

Taylor-Brown, Emilie; Hurd, Hilary

doi:10.1186/1756-3305-6-108

Cited by 31 publications

(18 citation statements)

References 112 publications

(153 reference statements)

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“…We propose that high‐density environments induce a unique death phenotype in P. falciparum , which has apoptotic‐like features. This is consistent with other studies describing Plasmodium sexual commitment and density‐dependent death in various microorganisms, where both sexual commitment and cell death are distinct developmental decisions undertaken as a response to varying external conditions . In particular, the global transcriptional changes observed meet one of the criteria for a density‐sensing system like quorum sensing in yeast.…”

Section: Discussionsupporting

confidence: 90%

A high parasite density environment induces transcriptional changes and cell death in Plasmodium falciparum blood stages

et al. 2018

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Transient regulation of Plasmodium numbers below the density that induces fever has been observed in chronic malaria infections in humans. This species transcending control cannot be explained by immunity alone. Using an in vitro system we have observed density dependent regulation of malaria population size as a mechanism to possibly explain these in vivo observations. Specifically, Plasmodium falciparum blood stages from a high but not low‐density environment exhibited unique phenotypic changes during the late trophozoite (LT) and schizont stages of the intraerythrocytic cycle. These included in order of appearance: failure of schizonts to mature and merozoites to replicate, apoptotic‐like morphological changes including shrinking, loss of mitochondrial membrane potential, and blebbing with eventual release of aberrant parasites from infected erythrocytes. This unique death phenotype was triggered in a stage‐specific manner by sensing of a high‐density culture environment. Conditions of glucose starvation, nutrient depletion, and high lactate could not induce the phenotype. A high‐density culture environment induced rapid global changes in the parasite transcriptome including differential expression of genes involved in cell remodeling, clonal antigenic variation, metabolism, and cell death pathways including an apoptosis‐associated metacaspase gene. This transcriptional profile was also characterized by concomitant expression of asexual and sexual stage‐specific genes. The data show strong evidence to support our hypothesis that density sensing exists in P. falciparum. They indicate that an apoptotic‐like mechanism may play a role in P. falciparum density regulation, which, as in yeast, has features quite distinguishable from mammalian apoptosis. Database Gene expression data are available in the GEO databases under the accession number http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE91188.

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Section: Discussionsupporting

confidence: 90%

A high parasite density environment induces transcriptional changes and cell death in Plasmodium falciparum blood stages

et al. 2018

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“…Later, more apoptotic mechanisms were discovered, some of which occurred in non-animal eukaryotes or bacteria. Programmed cell death induced by mitochondria is now believed to occur in a broad range of eukaryotic organisms [37].…”

Section: Phylogenetic Analyzesmentioning

confidence: 99%

Apoptosis: its origin, history, maintenance and the medical implications for cancer and aging

2016

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Programmed cell death is a basic cellular mechanism. Apoptotic-like programmed cell death (called apoptosis in animals) occurs in both unicellular and multicellular eukaryotes, and some apoptotic mechanisms are observed in bacteria. Endosymbiosis between mitochondria and eukaryotic cells took place early in the eukaryotic evolution, and some of the apoptotic-like mechanisms of mitochondria that were retained after this event now serve as parts of the eukaryotic apoptotic machinery. Apoptotic mechanisms have several functions in unicellular organisms: they include kin-selected altruistic suicide that controls population size, sharing common goods, and responding to viral infection. Apoptotic factors also have non-apoptotic functions. Apoptosis is involved in the cellular aging of eukaryotes, including humans. In addition, apoptosis is a key part of the innate tumor-suppression mechanism. Several anticancer drugs induce apoptosis, because apoptotic mechanisms are inactivated during oncogenesis. Because of the ancient history of apoptosis, I hypothesize that there is a deep relationship between mitochondrial metabolism, its role in aerobic versus anaerobic respiration, and the connection between apoptosis and cancer. Whereas normal cells rely primarily on oxidative mitochondrial respiration, most cancer cells use anaerobic metabolism. According to the Warburg hypothesis, the remodeling of the metabolism is one of the processes that leads to cancer. Recent studies indicate that anaerobic, non-mitochondrial respiration is particularly active in embryonic cells, stem cells, and aggressive stem-like cancer cells. Mitochondrial respiration is particularly active during the pathological aging of human cells in neurodegenerative diseases. According to the reversed Warburg hypothesis formulated by Demetrius, pathological aging is induced by mitochondrial respiration. Here, I advance the hypothesis that the stimulation of mitochondrial metabolism leads to pathological aging.

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“…AIF is suggested to be a caspase‐independent apoptosis‐inducing factor (Cande et al ., ). Also, AIF is highly conserved between human and mouse and a significant homology with oxidorductases from all eukaryotic and prokaryotic kingdoms has been identified (Liang et al ., ; Taylor‐Brown and Hurd, ). Altogether, AIF has been regarded as the key to the conserved caspase‐independent pathway of cell death (Candé et al ., ; Cabon et al ., ).…”

Section: Introductionmentioning

confidence: 99%

Role of Aif1 in regulation of cell death under environmental stress in Candida albicans

Zhang

Wang

et al. 2016

Yeast

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Apoptosis-inducing factor (AIF) is a conserved flavoprotein localized in the mitochondria, inducing apoptosis after translocation into the nucleus. However, its role in the important fungal pathogen, Candida albicans, remains to be investigated. In this study, we find that the C. albicans AIF protein Aif1, similar to its homologues in other organisms, is localized at the mitochondria and translocated into the nucleus under apoptosis-inducing conditions. Moreover, deletion of AIF1 causes attenuated apoptosis in this pathogen under apoptosis-inducing conditions, such as the treatment of 2 mm H2 O2 , 10 mm acetic acid or 0.08 mg/l caspofungin, and its overexpression enhances this process. Interestingly, treatment with high levels of these agents leads to reversed sensitivity of aif1Δ/Δ and the overexpression strain AIF1ov. In addition, the virulence of C. albicans is not affected by deletion or overexpression of AIF1. Hence, C. albicans Aif1, as a mitochondria-localized protein, plays a dual role in the regulation of cell death under different concentrations of the stress-caused agents. Copyright © 2016 John Wiley & Sons, Ltd.

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The first suicides: a legacy inherited by parasitic protozoans from prokaryote ancestors

Cited by 31 publications

References 112 publications

A high parasite density environment induces transcriptional changes and cell death in Plasmodium falciparum blood stages

A high parasite density environment induces transcriptional changes and cell death in Plasmodium falciparum blood stages

Apoptosis: its origin, history, maintenance and the medical implications for cancer and aging

Role of Aif1 in regulation of cell death under environmental stress in Candida albicans

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