scholarly journals ‘Bacterial Programmed Cell Death’: cellular altruism or genetic selfism?

2020 ◽  
Vol 367 (16) ◽  
Author(s):  
Bhaskar Chandra Mohan Ramisetty ◽  
Pavithra Anantharaman Sudhakari
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Free Living ◽  
Selfish Genes ◽  
A Cell ◽  
Unicellular Organisms ◽  
Multicellular Organisms ◽  
Restriction Modification ◽  
Restriction Modification Systems ◽  
Selection Of

ABSTRACT Cell-dependent propagation of the ‘self’ is the driver of all species, organisms and even genes. Conceivably, elimination of these entities is caused by cellular death. Then, how can genes that cause the death of the same cell evolve? Programmed cell death (PCD) is the gene-dependent self-inflicted death. In multicellular organisms, PCD of a cell confers fitness to the surviving rest of the organism, which thereby allows the selection of genes responsible for PCD. However, PCD in free-living bacteria is intriguing; the death of the cell is the death of the organism. How can such PCD genes be selected in unicellular organisms? The bacterial PCD in a population is proposed to confer fitness to the surviving kin in the form of sporulation, nutrition, infection-containment and matrix materials. While the cell-centred view leading to propositions of ‘altruism’ is enticing, the gene-centred view of ‘selfism’ is neglected. In this opinion piece, we reconceptualize the PCD propositions as genetic selfism (death due to loss/mutation of selfish genes) rather than cellular altruism (death for the conferment of fitness to kin). Within the scope and the available evidence, we opine that some of the PCD-like observations in bacteria seem to be the manifestation of genetic selfism by Restriction–Modification systems and Toxin–Antitoxin systems.

scholarly journals Stress Management in Cyst-Forming Free-Living Protists: Programmed Cell Death and/or Encystment

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Naveed Ahmed Khan ◽  
Junaid Iqbal ◽  
Ruqaiyyah Siddiqui
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Stress Management ◽  
Environmental Conditions ◽  
Free Living ◽  
Cyst Form ◽  
The Face ◽  
A Cell ◽  
Cellular Machinery ◽  
Harsh Conditions

In the face of harsh conditions and given a choice, a cell may (i) undergo programmed cell death, (ii) transform into a cancer cell, or (iii) enclose itself into a cyst form. In metazoans, the available evidence suggests that cellular machinery exists only to execute or avoid programmed cell death, while the ability to form a cyst was either lost or never developed. For cyst-forming free-living protists, here we pose the question whether the ability to encyst was gained at the expense of the programmed cell death or both functions coexist to counter unfavorable environmental conditions with mutually exclusive phenotypes.

scholarly journals “Programmed Cell Death: A Process of Death for Survival” – How Far Terminology Pertinent for Cell Death in Unicellular Organisms

2018 ◽  
Vol 11 ◽  
pp. 117906601879025 ◽  
Author(s):  
Shiv Shanker Pandey ◽  
Samer Singh ◽  
Chandramani Pathak ◽  
Budhi Sagar Tiwari
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Normal Growth ◽  
Death Process ◽  
Target Cells ◽  
Dna Ladder ◽  
Cell Death Process ◽  
Unicellular Organisms ◽  
Multicellular Organisms ◽  
Dna Nicks

Programmed cell death (PCD) is genetically regulated phenomenon of selective elimination of target cells that are either under pathological conditions or unwanted for organism’s normal growth and development due to other reasons. The process although being genetically controlled is physiological in nature that renders some hallmarks like blebs in the cell membrane, lobe formation in nuclear membrane, DNA nicks resulting to DNA ladder of 200 bp, and downstream activation of caspases. Moreover, as the process refers to the death of “targeted cell”, the term is exclusively suitable for multicellular organisms. Number of reports advocate similar type of cell death process in unicellular organisms. As cell death in unicellular organisms is also reflected by the signature of PCD obtained in metazoans, such cell death has been grouped under the broad category of PCD. It is pertinent to mention that by definition a unicellular organism is made of a single cell wherein it carries out all of its life processes. Using the term “Programmed Cell Death” with a preset “survival strategy of the organism” for unicellular organisms looks misnomer. Therefore, this correspondence argues and requests recommendation committee on cell death to revisit for the nomenclature of the cell death process in the unicellular organisms.

Programmed cell death in African trypanosomes

Parasitology ◽  
2006 ◽  
Vol 132 (S1) ◽  
pp. S7-S18 ◽  
Author(s):  
S. C. WELBURN ◽  
E. MACLEOD ◽  
K. FIGARELLA ◽  
M. DUZENSKO
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Growth And Development ◽  
Parasitic Protozoa ◽  
African Trypanosomes ◽  
Cell Death Pathway ◽  
A Cell ◽  
Multicellular Organisms

Until recently it had generally been assumed that apoptosis and other forms of programmed cell death evolved during evolution of the metazoans to regulate growth and development in these multicellular organisms. However, recent research is adding strength to the original phenotypic observations described almost a decade ago which indicated that some parasitic protozoa may have evolved a cell death pathway analogous to the process described as apoptosis in metazoa. Here we explore the implications of a programmed cell death pathway in the African tsetse-transmitted trypanosomes.

Freezing

2017 ◽  
Author(s):  
Andrew Clarke
Keyword(s):  
Thermal Hysteresis ◽  
Higher Plants ◽  
Terrestrial Environment ◽  
Cold Temperatures ◽  
Cellular Dehydration ◽  
A Cell ◽  
Unicellular Organisms ◽  
Cell Cytosol ◽  
Freezing Temperatures ◽  
Multicellular Organisms

Freezing is a widespread ecological challenge, affecting organisms in over half the terrestrial environment as well as both polar seas. With very few exceptions, if a cell freezes internally, it dies. Polar teleost fish in shallow waters avoid freezing by synthesising a range of protein or glycoprotein antifreezes. Terrestrial organisms are faced with a far greater thermal challenge, and exhibit a more complex array of responses. Unicellular organisms survive freezing temperatures by preventing ice nucleating within the cytosol, and tolerating the cellular dehydration and membrane disruption that follows from ice forming in the external environment. Multicellular organisms survive freezing temperatures by manipulating the composition of the extracellular body fluids. Terrestrial organisms may freeze at high subzero temperatures, often promoted by ice nucleating proteins, and small molecular mass cryoprotectants (often sugars and polyols) moderate the osmotic stress on cells. A range of chaperone proteins (dehydrins, LEA proteins) help maintain the integrity of membranes and macromolecules. Thermal hysteresis (antifreeze) proteins prevent damaging recrystallisation of ice. In some cases arthropods and higher plants prevent freezing in their extracellular fluids and survive by supercooling. Vitrification of extracellular water, or of the cell cytosol, may be a more widespread response to very cold temperatures than recognised to date.

scholarly journals Macrophage Autophagy and Oxidative Stress: An Ultrastructural and Immunoelectron Microscopical Study

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Ida Perrotta ◽  
Valentina Carito ◽  
Emilio Russo ◽  
Sandro Tripepi ◽  
Saveria Aquila ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Defense Mechanisms ◽  
Ultrastructural Localization ◽  
Microscopical Study ◽  
Beclin 1 ◽  
Cell Organelles ◽  
A Cell ◽  
First Time

The word autophagy broadly refers to the cellular catabolic processes that lead to the removal of damaged cytosolic proteins or cell organelles through lysosomes. Although autophagy is often observed during programmed cell death, it may also serve as a cell survival mechanism. Accumulation of reactive oxygen species within tissues and cells induces various defense mechanisms or programmed cell death. It has been shown that, besides inducing apoptosis, oxidative stress can also induce autophagy. To date, however, the regulation of autophagy in response to oxidative stress remains largely elusive and poorly understood. Therefore, the present study was designed to examine the ratio between oxidative stress and autophagy in macrophages after oxidant exposure (AAPH) and to investigate the ultrastructural localization of beclin-1, a protein essential for autophagy, under basal and stressful conditions. Our data provide evidence that oxidative stress induces autophagy in macrophages. We demonstrate, for the first time by immunoelectron microscopy, the subcellular localization of beclin-1 in autophagic cells.

scholarly journals TaMCA4, a Novel Wheat Metacaspase Gene Functions in Programmed Cell Death Induced by the Fungal Pathogen Puccinia striiformis f. sp. tritici

2012 ◽  
Vol 25 (6) ◽  
pp. 755-764 ◽  
Author(s):  
Xiaodong Wang ◽  
Xiaojie Wang ◽  
Hao Feng ◽  
Chunlei Tang ◽  
Pengfei Bai ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Fungal Pathogen ◽  
Puccinia Striiformis ◽  
Transcript Level ◽  
Structural Features ◽  
Virus Induced Gene Silencing ◽  
Wheat Leaves ◽  
Multicellular Organisms ◽  
Bax Gene

Programmed cell death (PCD) is a physiological process to remove redundant or harmful cells, for the development of multicellular organisms, or for restricting the spread of pathogens (hypersensitive response). Metacaspases are cysteine-dependent proteases which play an essential role in PCD. Triticum aestivum metacaspase 4 (TaMCA4) is a type II metacaspase gene cloned from ‘Suwon11’ wheat, with typical structural features such as peptidase C14 caspase domain and a long linker sequence between the two subunits. Transient expression of TaMCA4 in tobacco leaves failed to induce PCD directly but enhanced cell death triggered by a mouse Bax gene or a candidate effector gene from Puccinia striiformis f. sp. tritici. Enhancement of PCD was also observed in wheat leaves co-bombarded with TaMCA4. When challenged with the avirulent race of P. striiformis f. sp. tritici, the expression level of TaMCA4 in wheat leaves was sharply upregulated, whereas the transcript level was not significantly induced by the virulent race. Moreover, knocking down TaMCA4 expression by virus-induced gene silencing enhanced the susceptibility of Suwon11 to the avirulent race of P. striiformis f. sp. tritici and reduced the necrotic area at infection sites.

scholarly journals T-2 mycotoxin induced apoptosis in broiler’s liver tissue

2018 ◽  
Vol 27 (1) ◽  
pp. 9-16
Author(s):  
Piret Hussar ◽  
Tõnu Järveots ◽  
Lazo Pendovski ◽  
Katerina Blagoevska ◽  
Trpe Ristoski ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Liver Tissue ◽  
Immunohistochemical Staining ◽  
Mammalian Cells ◽  
Gallus Domesticus ◽  
Gallus Gallus Domesticus ◽  
Histopathological Changes ◽  
Induced Apoptosis ◽  
Multicellular Organisms

Apoptosis is a process of programmed cell death that occurs in multicellular organisms. As T-2 toxin is known to induce apoptosis in mammalian cells, the aim of the present experiment was to study the toxic effect of T-2 on chicken liver tissue using apoptosis-related antibodies p21 and p53 which are involved in the p53/p21-mediated apoptotic signalling pathway. The experiment was conducted on fourteen 40-day-old broilers (Gallus gallus domesticus) who were divided into control and T-2 toxin groups. For the T-2 toxin group, T-2 toxin (Sigma, Germany) was dissolved in water and given per os for three consecutive days. The material of the liver was taken 24 hours after the last application. The specimens were fixed with 10% formalin and embedded into paraffin; slices 5 μm in thickness were cut followed by immunohistochemical staining with polyclonal primary antibodies p21 and p53 (Abcam, UK) according to the manufacturer’s guidelines (IHC kit, Abcam, UK). Strong expression of p21 and p53 found in hepatocytes, endotheliocytes and around blood vessels together with large tissue destructions in T-2 toxin group birds’ liver indicates apoptosis and histopathological changes in liver tissue during T-2 mycotoxicosis.

scholarly journals Long-term depression: a cell biological view

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130138 ◽  
Author(s):  
Morgan Sheng ◽  
Ali Ertürk
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dendritic Spines ◽  
Crucial Role ◽  
Molecular Mechanisms ◽  
Signalling Pathways ◽  
Long Term Depression ◽  
A Cell ◽  
Biological Programme

Recent studies of the molecular mechanisms of long-term depression (LTD) suggest a crucial role for the signalling pathways of apoptosis (programmed cell death) in the weakening and elimination of synapses and dendritic spines. With this backdrop, we suggest that LTD can be considered as the electrophysiological aspect of a larger cell biological programme of synapse involution, which uses localized apoptotic mechanisms to sculpt synapses and circuits without causing cell death.

scholarly journals Role of Ced-3/ICE-family proteases in staurosporine-induced programmed cell death.

1996 ◽  
Vol 133 (5) ◽  
pp. 1041-1051 ◽  
Author(s):  
M D Jacobsen ◽  
M Weil ◽  
M C Raff
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mammalian Cell ◽  
Mammalian Cells ◽  
Apoptotic Cell ◽  
Interleukin 1 ◽  
Cell Types ◽  
Cysteine Proteases ◽  
A Cell ◽  
Bona Fide

In the accompanying paper by Weil et al. (1996) we show that staurosporine (STS), in the presence of cycloheximide (CHX) to inhibit protein synthesis, induces apoptotic cell death in a large variety of nucleated mammalian cell types, suggesting that all nucleated mammalian cells constitutively express all of the proteins required to undergo programmed cell death (PCD). The reliability of that conclusion depends on the evidence that STS-induced, and (STS + CHS)-induced, cell deaths are bona fide examples of PCD. There is rapidly accumulating evidence that some members of the Ced-3/Interleukin-1 beta converting enzyme (ICE) family of cysteine proteases are part of the basic machinery of PCD. Here we show that Z-Val-Ala-Asp-fluoromethylketone (zVAD-fmk), a cell-permeable, irreversible, tripeptide inhibitor of some of these proteases, suppresses STS-induced and (STS + CHX)-induced cell death in a wide variety of mammalian cell types, including anucleate cytoplasts, providing strong evidence that these are all bona fide examples of PCD. We show that the Ced-3/ICE family member CPP32 becomes activated in STS-induced PCD, and that Bcl-2 inhibits this activation. Most important, we show that, in some cells at least, one or more CPP32-family members, but not ICE itself, is required for STS-induced PCD. Finally, we show that zVAD-fmk suppresses PCD in the interdigital webs in developing mouse paws and blocks the removal of web tissue during digit development, suggesting that this inhibition will be a useful tool for investigating the roles of PCD in various developmental processes.

scholarly journals A cell fitness selection model for neuronal survival during development

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Yiqiao Wang ◽  
Haohao Wu ◽  
Paula Fontanet ◽  
Simone Codeluppi ◽  
Natalia Akkuratova ◽  
...  
Keyword(s):  
Cell Death ◽  
Sensory Neurons ◽  
Neural Circuits ◽  
Survival Outcome ◽  
Molecular Signatures ◽  
Molecular Features ◽  
Functional Maturation ◽  
A Cell ◽  
Developmental Cell Death ◽  
Selection Of

Abstract Developmental cell death plays an important role in the construction of functional neural circuits. In vertebrates, the canonical view proposes a selection of the surviving neurons through stochastic competition for target-derived neurotrophic signals, implying an equal potential for neurons to compete. Here we show an alternative cell fitness selection of neurons that is defined by a specific neuronal heterogeneity code. Proprioceptive sensory neurons that will undergo cell death and those that will survive exhibit different molecular signatures that are regulated by retinoic acid and transcription factors, and are independent of the target and neurotrophins. These molecular features are genetically encoded, representing two distinct subgroups of neurons with contrasted functional maturation states and survival outcome. Thus, in this model, a heterogeneous code of intrinsic cell fitness in neighboring neurons provides differential competitive advantage resulting in the selection of cells with higher capacity to survive and functionally integrate into neural networks.

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