scholarly journals Golgi anti-apoptotic proteins are evolutionarily conserved ion channels that regulate cell death in plants

2019 ◽  
Author(s):  
Maija Sierla ◽  
David L. Prole ◽  
Nuno Saraiva ◽  
Guia Carrara ◽  
Natalia Dinischiotu ◽  
...  
Keyword(s):  
Cell Death ◽  
Ion Channels ◽  
Programmed Cell Death ◽  
Stress Responses ◽  
Fluorescent Protein ◽  
Yellow Fluorescent Protein ◽  
Lesion Mimic ◽  
Evolutionarily Conserved ◽  
Apoptotic Proteins ◽  
Regulate Cell Death

ABSTRACTProgrammed cell death regulates developmental and stress responses in eukaryotes. Golgi anti-apoptotic proteins (GAAPs) are evolutionarily conserved cell death regulators. Human and viral GAAPs inhibit apoptosis and modulate intracellular Ca2+fluxes, and viral GAAPs form cation-selective channels. Although most mammalian cell death regulators are not conserved at the sequence level in plants, the GAAP gene family shows expansion, with five paralogues (AtGAAP1-5) in the Arabidopsis genome. We pursued molecular and physiological characterization of AtGAAPs making use of the advanced knowledge of their human and viral counterparts. Structural modeling of AtGAAPs predicted the presence of a channel-like pore, and electrophysiological recordings from purified AtGAAP3 reconstituted into lipid bilayers confirmed that plant GAAPs can function as ion channels. AtGAAP1 and AtGAAP4 localized exclusively to the Golgi within the plant cell, while AtGAAP2, AtGAAP3 and AtGAAP5 also showed tonoplastic localization. Gene expression analysis revealed differential spatial expression and abundance of transcript forAtGAAPparalogues in Arabidopsis tissues. We demonstrate that AtGAAP1-5 inhibit Bax-induced cell death in yeast. However, overexpression of AtGAAP1 induces cell death inNicotiana benthamianaleaves and lesion mimic phenotype in Arabidopsis. We propose that AtGAAPs function as Golgi-localized ion channels that regulate cell death by affecting ionic homeostasis within the cell.HighlightArabidopsis Golgi anti-apoptotic proteins (GAAPs) share functional conservation with their human and viral counterparts in cell death regulation and ion channel activityAbbreviationsAtGAAP,Arabidopsis thalianaGAAP; BI-1, Bax inhibitor-1; CFP, cyan fluorescent protein; CMLV, camelpox virus; ER, Endoplasmic reticulum; GAAP, Golgi anti-apoptotic protein; GFP, green fluorescent protein; hGAAP, human GAAP; LFG, Lifeguard; LMM, lesion mimic mutant; PCD, programmed cell death; TMBIM, transmembrane Bax inhibitor-1 motif-containing; TMDs, transmembrane domains; vGAAP, viral GAAP; YFP, yellow fluorescent protein

scholarly journals SPL36 Encodes a Receptor-like Protein Kinase that Regulates Programmed Cell Death and Defense Responses in Rice

Rice ◽  
2021 ◽  
Vol 14 (1) ◽  
Author(s):  
R. A. O. Yuchun ◽  
J. I. A. O. Ran ◽  
W. A. N. G. Sheng ◽  
W. U. Xianmei ◽  
Y. E. Hanfei ◽  
...  
Keyword(s):  
Cell Death ◽  
Salt Stress ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Stress Responses ◽  
Defense Responses ◽  
Base Substitution ◽  
Wild Type ◽  
Salt Stress Response ◽  
Lesion Mimic

AbstractLesion mimic mutants spontaneously produce disease spots in the absence of biotic or abiotic stresses. Analyzing lesion mimic mutants’ sheds light on the mechanisms underlying programmed cell death and defense-related responses in plants. Here, we isolated and characterized the rice (Oryza sativa) spotted leaf 36 (spl36) mutant, which was identified from an ethyl methanesulfonate-mutagenized japonica cultivar Yundao population. spl36 displayed spontaneous cell death and enhanced resistance to rice bacterial pathogens. Gene expression analysis suggested that spl36 functions in the disease response by upregulating the expression of defense-related genes. Physiological and biochemical experiments indicated that more cell death occurred in spl36 than the wild type and that plant growth and development were affected in this mutant. We isolated SPL36 by map-based cloning. A single base substitution was detected in spl36, which results in a cysteine-to-arginine substitution in SPL36. SPL36 is predicted to encode a receptor-like protein kinase containing leucine-rich domains that may be involved in stress responses in rice. spl36 was more sensitive to salt stress than the wild type, suggesting that SPL36 also negatively regulates the salt-stress response. These findings suggest that SPL36 regulates the disease resistance response in rice by affecting the expression of defense- and stress-related genes.

scholarly journals Harpin Inactivates Mitochondria in Arabidopsis Suspension Cells

2004 ◽  
Vol 17 (2) ◽  
pp. 131-139 ◽  
Author(s):  
Maren Krause ◽  
Jörg Durner
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Pseudomonas Syringae ◽  
Stress Responses ◽  
Time Course ◽  
Defense Responses ◽  
Ros Generation ◽  
Suspension Cells ◽  
Mitochondrial Functions ◽  
Arabidopsis Cells

Harpin is a well-known proteinaceous bacterial elicitor that can induce an oxidative burst and programmed cell death in various host plants. Given the demonstrated roles of mitochondria in animal apoptosis, we investigated the effect of harpin from Pseudomonas syringae on mitochondrial functions in Arabidopsis suspension cells in detail. Fluorescence microscopy in conjunction with double-staining for reactive oxygen species (ROS) and mitochondria suggested co-localization of mitochondria and ROS generation. Plant defense responses or cell death after pathogen attack have been suggested to be regulated by the concerted action of ROS and nitric oxide (NO). However, although Arabidopsis cells respond to harpin treatment with NO generation, time course analyses suggest that NO generation is not involved in initial responses but, rather, is a consequence of cellular decay. Among the fast responses we observed was a decrease of the mitochondrial membrane potential Δψm and, possibly as a direct consequence, of ATP production. Furthermore, treatment of Arabidopsis cells with harpin protein induced a rapid cytochrome C release from mitochondria into the cytosol, which is regarded as a hallmark of programmed cell death or apoptosis. Northern and DNA array analyses showed strong induction of protecting or scavenging systems such as alternative oxidase and small heat shock proteins, components that are known to be associated with cellular stress responses. In sum, the presented data suggest that harpin inactivates mitochondria in Arabidopsis cells.

Proteomics Analysis of Rice Lesion Mimic Mutant (spl1) Reveals Tightly Localized Probenazole-Induced Protein (PBZ1) in Cells Undergoing Programmed Cell Death

2008 ◽  
Vol 7 (4) ◽  
pp. 1750-1760 ◽  
Author(s):  
Sun Tae Kim ◽  
Sang Gon Kim ◽  
Young Hyun Kang ◽  
Yiming Wang ◽  
Jae-Yean Kim ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Proteomics Analysis ◽  
Lesion Mimic ◽  
Lesion Mimic Mutant ◽  
In Cells

Emerging Role of Mitophagy in Inflammatory Diseases: Cellular and Molecular Episodes

2020 ◽  
Vol 26 (4) ◽  
pp. 485-491 ◽  
Author(s):  
Mohamed Adil A.A. ◽  
Shabnam Ameenudeen ◽  
Ashok Kumar ◽  
S. Hemalatha ◽  
Neesar Ahmed ◽  
...  
Keyword(s):  
Quality Control ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Inflammatory Diseases ◽  
Mitochondrial Quality Control ◽  
Mitochondrial Injury ◽  
Cellular Events ◽  
Evolutionarily Conserved

Mitochondria are the crucial regulators for the major source of ATP for different cellular events. Due to damage episodes, mitochondria have been established for a plethora ofalarming signals of stress that lead to cellular deterioration, thereby causing programmed cell death. Defects in mitochondria play a key role in arbitrating pathophysiological machinery with recent evince delineating a constructive role in mitophagy mediated mitochondrial injury. Mitophagy has been known for the eradication of damaged mitochondria via the autophagy process. Mitophagy has been investigated as an evolutionarily conserved mechanism for mitochondrial quality control and homeostasis. Impaired mitophagy has been critically linked with the pathogenesis of inflammatory diseases. Nevertheless, the exact mechanism is not quite revealed, and it is still debatable. The purpose of this review was to investigate the possible role of mitophagy and its associated mechanism in inflammation-mediated diseases at both the cellular and molecular levels.

BH3-only proteins — evolutionarily conserved proapoptotic Bcl-2 family members essential for initiating programmed cell death

2002 ◽  
Vol 115 (8) ◽  
pp. 1567-1574 ◽  
Author(s):  
Philippe Bouillet ◽  
Andreas Strasser
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Family Members ◽  
Protein Family ◽  
Cell Stress ◽  
Protective Function ◽  
Evolutionarily Conserved ◽  
Apoptotic Cascade

The BH3-only members of the Bcl-2 protein family are essential initiators of programmed cell death and are required for apoptosis induced by cytotoxic stimuli. These proteins have evolved to recognise distinct forms of cell stress. In response, they unleash the apoptotic cascade by inactivating the protective function of the pro-survival members of the Bcl-2 family and by activating the Bax/Bax-like pro-apoptotic family members.

Tudor staphylococcal nuclease is an evolutionarily conserved component of the programmed cell death degradome

2009 ◽  
Vol 11 (11) ◽  
pp. 1347-1354 ◽  
Author(s):  
Jens F. Sundström ◽  
Alena Vaculova ◽  
Andrei P. Smertenko ◽  
Eugene I. Savenkov ◽  
Anna Golovko ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Staphylococcal Nuclease ◽  
Evolutionarily Conserved
Sign in / Sign up

Export Citation Format

Share Document