Activation of Cysteine Proteases in Cowpea Plants during the Hypersensitive Response—A Form of Programmed Cell Death

1998 ◽  
Vol 245 (2) ◽  
pp. 389-399 ◽  
Author(s):  
Icy D'Silva ◽  
Guy G. Poirier ◽  
Michèle C. Heath
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Hypersensitive Response ◽  
Cysteine Proteases

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 Caspases in Cell Death, Inflammation, and Pyroptosis

2020 ◽  
Vol 38 (1) ◽  
pp. 567-595 ◽  
Author(s):  
Sannula Kesavardhana ◽  
R.K. Subbarao Malireddi ◽  
Thirumala-Devi Kanneganti
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Responses ◽  
Cross Talk ◽  
Cysteine Proteases ◽  
Proteolytic Processing ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
New Research ◽  
Multicellular Organisms

Caspases are a family of conserved cysteine proteases that play key roles in programmed cell death and inflammation. In multicellular organisms, caspases are activated via macromolecular signaling complexes that bring inactive procaspases together and promote their proximity-induced autoactivation and proteolytic processing. Activation of caspases ultimately results in programmed execution of cell death, and the nature of this cell death is determined by the specific caspases involved. Pioneering new research has unraveled distinct roles and cross talk of caspases in the regulation of programmed cell death, inflammation, and innate immune responses. In-depth understanding of these mechanisms is essential to foster the development of precise therapeutic targets to treat autoinflammatory disorders, infectious diseases, and cancer. This review focuses on mechanisms governing caspase activation and programmed cell death with special emphasis on the recent progress in caspase cross talk and caspase-driven gasdermin D–induced pyroptosis.

Pathogen-induced programmed cell death in tobacco

1997 ◽  
Vol 110 (11) ◽  
pp. 1333-1344 ◽  
Author(s):  
R. Mittler ◽  
L. Simon ◽  
E. Lam
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Tobacco Mosaic Virus ◽  
Chloroplast Dna ◽  
Mosaic Virus ◽  
Hypersensitive Response ◽  
Nuclear Periphery ◽  
Death Process ◽  
Tobacco Plants ◽  
Systemic Spread

Sacrificing an infected cell or cells in order to prevent systemic spread of a pathogen appears to be a conserved strategy in both plants and animals. We studied some of the morphological and biochemical events that accompany programmed cell death during the hypersensitive response of tobacco plants infected with tobacco mosaic virus. Certain aspects of this cell death process appeared to be similar to those that take place during apoptosis in animal cells. These included condensation and vacuolization of the cytoplasm and cleavage of nuclear DNA to 50 kb fragments. In contrast, internucleosomal fragmentation, condensation of chromatin at the nuclear periphery and apoptotic bodies were not observed in tobacco plants during tobacco mosaic virus-induced hypersensitive response. A unique aspect of programmed cell death during the hypersensitive response of tobacco to tobacco mosaic virus involved an increase in the amount of monomeric chloroplast DNA. Morphological changes to the chloroplast and cytosol of tobacco cells and increase in monomeric chloroplast DNA occurred prior to gross changes in nuclear morphology and significant chromatin cleavage. Our findings suggest that certain aspects of programmed cell death may have been conserved during the evolution of plants and animals.

Papain-like cysteine proteases are involved in programmed cell death in plants under heavy metal stress

2020 ◽  
Vol 174 ◽  
pp. 104041 ◽  
Author(s):  
Klaudia Sychta ◽  
Ewa Dubas ◽  
Kenji Yamada ◽  
Aneta Słomka ◽  
Monika Krzewska ◽  
...  
Keyword(s):  
Heavy Metal ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Heavy Metal Stress ◽  
Cysteine Proteases ◽  
Metal Stress

scholarly journals Hematopoietic Factor Erythropoietin Fosters Neuroprotection through Novel Signal Transduction Cascades

2002 ◽  
Vol 22 (5) ◽  
pp. 503-514 ◽  
Author(s):  
Zhao Zhong Chong ◽  
Jing-Qiong Kang ◽  
Kenneth Maiese
Keyword(s):  
Signal Transduction ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanisms ◽  
Cysteine Proteases ◽  
Cellular Membrane ◽  
Nuclear Factor Κb ◽  
Erythropoietin Receptor ◽  
Signal Transduction Pathways ◽  
Tyrosine Kinase 2

In addition to promoting the survival, proliferation, and differentiation of immature erythroid cells, erythropoietin and the erythropoietin receptor have recently been shown to modulate cellular signal transduction pathways that extend beyond the erythropoietic function of erythropoietin. In particular, erythropoietin has been linked to the prevention of programmed cell death in neuronal systems. Although this work is intriguing, the underlying molecular mechanisms that serve to mediate neuroprotection by erythropoietin are not well understood. Further analysis illustrates that erythropoietin modulates two distinct components of programmed cell death that involve the degradation of DNA and the externalization of cellular membrane phosphatidylserine residues. Initiation of the cascades that modulate protection by erythropoietin and its receptor may begin with the activation of the Janus tyrosine kinase 2 protein. Subsequent downstream mechanisms appear to lead to the activation of multiple signal transduction pathways that include transcription factor STAT5 (signal transducers and activators of transcription), Bcl-2, protein kinase B, cysteine proteases, mitogen-activated protein kinases, proteintyrosine phosphatases, and nuclear factor-κB. New knowledge of the cellular pathways regulated by erythropoietin in neuronal environments will potentially solidify the development and initiation of therapeutic strategies against nervous system disorders.

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