scholarly journals The tale of caspase homologues and their evolutionary outlook: deciphering programmed cell death in cyanobacteria

2020 ◽  
Vol 71 (16) ◽  
pp. 4639-4657
Author(s):  
Samujjal Bhattacharjee ◽  
Arun Kumar Mishra
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Inclusive Fitness ◽  
Bioinformatic Analysis ◽  
Molecular Evidence ◽  
Ecological Significance ◽  
Comprehensive Description ◽  
Functional Roles ◽  
Novel Proteins ◽  
Functional Versatility

Abstract Programmed cell death (PCD), a genetically orchestrated mechanism of cellular demise, is paradoxically required to support life. As in lower eukaryotes and bacteria, PCD in cyanobacteria is poorly appreciated, despite recent biochemical and molecular evidence that supports its existence. Cyanobacterial PCD is an altruistic reaction to stressful conditions that significantly enhances genetic diversity and inclusive fitness of the population. Recent bioinformatic analysis has revealed an abundance of death-related proteases, i.e. orthocaspases (OCAs) and their mutated variants, in cyanobacteria, with the larger genomes of morphologically complex strains harbouring most of them. Sequence analysis has depicted crucial accessory domains along with the proteolytic p20-like sub-domain in OCAs, predicting their functional versatility. However, the cascades involved in sensing death signals, their transduction, and the downstream expression and activation of OCAs remain to be elucidated. Here, we provide a comprehensive description of the attempts to identify mechanisms of PCD and the existence and importance of OCAs based on in silico approaches. We also review the evolutionary and ecological significance of PCD in cyanobacteria. In the future, the analysis of cyanobacterial PCD will identify novel proteins that have varied functional roles in signalling cascades and also help in understanding the incipient mechanism of PCD morphotype(s) from where eukaryotic PCD might have originated.

scholarly journals Plant Mitophagy in Comparison to Mammals: What Is Still Missing?

2021 ◽  
Vol 22 (3) ◽  
pp. 1236
Author(s):  
Kaike Ren ◽  
Lanlan Feng ◽  
Shuangli Sun ◽  
Xiaohong Zhuang
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Dynamics ◽  
Plant Cells ◽  
Molecular Evidence ◽  
Double Membrane ◽  
Mitochondrial Homeostasis ◽  
A Cell ◽  
Mitochondrial Number

Mitochondrial homeostasis refers to the balance of mitochondrial number and quality in a cell. It is maintained by mitochondrial biogenesis, mitochondrial fusion/fission, and the clearance of unwanted/damaged mitochondria. Mitophagy represents a selective form of autophagy by sequestration of the potentially harmful mitochondrial materials into a double-membrane autophagosome, thus preventing the release of death inducers, which can trigger programmed cell death (PCD). Recent advances have also unveiled a close interconnection between mitophagy and mitochondrial dynamics, as well as PCD in both mammalian and plant cells. In this review, we will summarize and discuss recent findings on the interplay between mitophagy and mitochondrial dynamics, with a focus on the molecular evidence for mitophagy crosstalk with mitochondrial dynamics and PCD.

scholarly journals Iron Starvation and Culture Age Activate Metacaspases and Programmed Cell Death in the Marine Diatom Thalassiosira pseudonana

2007 ◽  
Vol 7 (2) ◽  
pp. 223-236 ◽  
Author(s):  
Kay D. Bidle ◽  
Sara J. Bender
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Plasma Membranes ◽  
Molecular Mechanisms ◽  
Short Circuit ◽  
Thalassiosira Pseudonana ◽  
Marine Diatom ◽  
Molecular Evidence ◽  
Iron Starvation ◽  
Gene And Protein Expression

ABSTRACT In the modern ocean, phytoplankton maintain extremely high primary production/biomass ratios, indicating that they bloom, die, and are replaced weekly. The molecular mechanisms regulating cellular mortality and turnover are largely unknown, even though they effectively short-circuit carbon export to the deep ocean and channel primary productivity to microbial food webs. Here, we present morphological, biochemical, and molecular evidence of caspase-mediated, autocatalytic programmed cell death (PCD) in the diatom Thalassiosira pseudonana in response to iron starvation. Transmission electron microscopy revealed internal degradation of nuclear, chloroplastic, and mitochondrial organelles, all while the plasma membranes remained intact. Cellular degradation was concomitant with dramatic decreases in photosynthetic efficiency, externalization of phosphatidylserine, and significantly elevated caspase-specific activity, with the addition of a broad-spectrum caspase inhibitor rescuing cells from death. A search of the T. pseudonana genome identified six distinct putative metacaspases containing a conserved caspase domain structure. Quantitative reverse transcription-PCR and Western blot analysis revealed differential gene and protein expression of T. pseudonana metacaspases, some of which correlated with physiological stress and caspase activity. Taken together with the recent discovery of the metacaspase-mediated viral infection of phytoplankton (K. D. Bidle, L. Haramaty, J. Barcelos-Ramos, and P. G. Falkowski, Proc. Natl. Acad. Sci. USA 104:6049-6054, 2007), our findings reveal a key role for metacaspases in the turnover of phytoplankton biomass in the oceans. Furthermore, given that Fe is required for photosynthetic electron transfer and is chronically limiting in a variety of oceanic systems, including high-nutrient low-chlorophyll regions, our findings provide a potential ecological context for PCD in these unicellular photoautotrophs.

scholarly journals Cytoplasmic and Nuclear Localizations Are Important for the Hypersensitive Response Conferred by Maize Autoactive Rp1-D21 Protein

2015 ◽  
Vol 28 (9) ◽  
pp. 1023-1031 ◽  
Author(s):  
Guan-Feng Wang ◽  
Peter J. Balint-Kurti
Keyword(s):  
Cell Death ◽  
Disease Resistance ◽  
Programmed Cell Death ◽  
Hypersensitive Response ◽  
Nicotiana Benthamiana ◽  
Coiled Coil ◽  
Intragenic Recombination ◽  
R Genes ◽  
Leucine Rich Repeat ◽  
Functional Roles

Disease resistance (R) genes have been isolated from many plant species. Most encode nucleotide binding leucine-rich repeat (NLR) proteins that trigger a rapid localized programmed cell death called the hypersensitive response (HR) upon pathogen recognition. Despite their structural similarities, different NLR are distributed in a range of subcellular locations, and analogous domains play diverse functional roles. The autoactive maize NLR gene Rp1-D21 derives from an intragenic recombination between two NLR genes, Rp1-D and Rp1-dp2, and confers a HR independent of the presence of a pathogen. Rp1-D21 and its N-terminal coiled coil (CC) domain (CCD21) confer autoactive HR when transiently expressed in Nicotiana benthamiana. Rp1-D21 was predominantly localized in cytoplasm with a small amount in the nucleus, while CCD21 was localized in both nucleus and cytoplasm. Targeting of Rp1-D21 or CCD21 predominantly to either the nucleus or the cytoplasm abolished HR-inducing activity. Coexpression of Rp1-D21 or CCD21 constructs confined, respectively, to the nucleus and cytoplasm did not rescue full activity, suggesting nucleocytoplasmic movement was important for HR induction. This work emphasizes the diverse structural and subcellular localization requirements for activity found among plant NLR R genes.

scholarly journals Evolutionary plasticity and functional versatility of CRISPR systems

PLoS Biology ◽  
2022 ◽  
Vol 20 (1) ◽  
pp. e3001481
Author(s):  
Eugene V. Koonin ◽  
Kira S. Makarova
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Defense Mechanisms ◽  
Biological Function ◽  
Cellular Functions ◽  
Target Dna ◽  
Major Route ◽  
Multiple Levels ◽  
Regulatory Functions ◽  
Functional Versatility

The principal biological function of bacterial and archaeal CRISPR systems is RNA-guided adaptive immunity against viruses and other mobile genetic elements (MGEs). These systems show remarkable evolutionary plasticity and functional versatility at multiple levels, including both the defense mechanisms that lead to direct, specific elimination of the target DNA or RNA and those that cause programmed cell death (PCD) or induction of dormancy. This flexibility is also evident in the recruitment of CRISPR systems for nondefense functions. Defective CRISPR systems or individual CRISPR components have been recruited by transposons for RNA-guided transposition, by plasmids for interplasmid competition, and by viruses for antidefense and interviral conflicts. Additionally, multiple highly derived CRISPR variants of yet unknown functions have been discovered. A major route of innovation in CRISPR evolution is the repurposing of diverged repeat variants encoded outside CRISPR arrays for various structural and regulatory functions. The evolutionary plasticity and functional versatility of CRISPR systems are striking manifestations of the ubiquitous interplay between defense and “normal” cellular functions.

scholarly journals Novel lncRNA-miRNA-mRNA Competing Endogenous RNA Triple Networks Associated Programmed Cell Death in Heart Failure

2021 ◽  
Vol 8 ◽  
Author(s):  
Yu Zheng ◽  
Yingjie Zhang ◽  
Xiu Zhang ◽  
Yini Dang ◽  
Yihui Cheng ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Regulatory Networks ◽  
Enrichment Analysis ◽  
Bioinformatic Analysis ◽  
Differentially Expressed ◽  
Regulatory Pathways ◽  
Regulatory Functions

Objective: Increasing evidence has uncovered the roles of lncRNA-miRNA-mRNA regulatory networks in cardiovascular diseases. However, the crosstalk between ceRNA networks and development of heart failure (HF) remains unclear. This study was to investigate the role of lncRNA-mediated ceRNA networks in the pathophysiological process of HF and its potential regulatory functions on programmed cell death.Methods: We firstly screened the GSE77399, GSE52601 and GSE57338 datasets in the NCBI GEO database for screening differentially expressed lncRNAs, miRNAs and mRNAs. lncRNA-miRNA-mRNA regulatory networks based on the ceRNA theory were subsequently constructed. GO and KEGG enrichment analysis was conducted to predict potential biological functions of mRNAs in ceRNA networks. Differentially expressed mRNAs were then interacted with programmed cell death related genes. lncRNA-mediated ceRNA regulatory pathways on programmed cell death were validated with qRT-PCR testing.Results: Based on our bioinformatic analysis, two lncRNAs, eight miRNAs and 65 mRNAs were extracted to construct two lncRNAs-mediated ceRNA networks in HF. Biological processes and pathways were enriched in extracellular matrix. Seven lncRNA-mediated ceRNA regulatory pathways on programmed cell death, GAS5/miR-345-5p/ADAMTS4, GAS5/miR-18b-5p/AQP3, GAS5/miR-18b-5p/SHISA3, GAS5/miR-18b-5p/C1orf105, GAS5/miR-18b-5p/PLIN2, GAS5/miR-185-5p/LPCAT3, and GAS5/miR-29b-3p/STAT3, were finally validated.Conclusions: Two novel ceRNA regulatory networks in HF were discovered based on our bioinformatic analysis. Based on the interaction and validation analysis, seven lncRNA GAS5-mediated ceRNA regulatory pathways were hypothesized to impact programmed cell death including seven for apoptosis, three for ferroptosis, and one for pyroptosis. Upon which, we provided novel insights and potential research plots for bridging ceRNA regulatory networks and programmed cell death in HF.

Programmed Cell Death Ligand 1 and Venous Thromboembolism in Patients with Primary Brain Tumors

2019 ◽  
Author(s):  
P. Seyed Mir ◽  
A.-S. Berghoff ◽  
M. Preusser ◽  
G. Ricken ◽  
J. Riedl ◽  
...  
Keyword(s):  
Cell Death ◽  
Venous Thromboembolism ◽  
Programmed Cell Death ◽  
Brain Tumors ◽  
Primary Brain Tumors

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

Dynamical analysis of the programmed cell death pathway

2007 ◽  
Author(s):  
Luciano Carotenuto ◽  
Vincenza Pace ◽  
Dina Bellizzi ◽  
Giovanna De Benedictis
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dynamical Analysis ◽  
Cell Death Pathway
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