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Cells
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Programmed Cell Death Regulation in Plants
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Programmed Cell Death Regulation in Plants

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Plant, Algae and Fungi Cell Biology".

Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 27842

Special Issue Editors

Prof. Dr. Stanislaw Karpinski

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Guest Editor
Institute of Biology, Department of Plant Genetics, Breeding and Biotechnology, Warsaw University of Life Sciences, Nowoursynowska 159, 02-767 Warszawa, Poland
Interests: cell death; hormonal and reactive oxygen species signaling; retrograde signaling and regulation of photosynthesis; systemic stress and defence responses; transcription factors and gene expression; nonphotochemical quenching; plant physiology and molecular biology
Special Issues, Collections and Topics in MDPI journals
Dr. Weronika Czarnocka

E-Mail Website
Guest Editor
Warsaw University of Life Sciences, Institute of Biology, Department of Plant Genetics, Breeding and Biotechnology, Nowoursynowska 159, 02-767 Warszawa, Poland
Interests: plant physiology and molecular biology; transcription factors and gene expression; cell death; hormonal and reactive oxygen species signaling; legume–rhizobia symbiosis; root nodule development

Special Issue Information

Dear Colleagues,

Programmed cell death (PCD) is the ultimate end of the cell cycle which is genetically regulated and controlled. PCD regulation attracts tremendous research efforts. In plants, PCD mechanism and regulation is very similar to PCD in animals. However, in plant cells, which are able to photosynthesize, a specific molecular mechanism of PCD has evolved and is controlled by the nonphotochemical quenching (NPQ) of excess light energy and chloroplast retrograde signaling. Exciting new data shed new light on the molecular and physiological details of PCD regulation and its signaling cascades, which are dependent on photorespiration, hormonal, reactive oxygen species (ROS), and electrical intra- and intercellular signaling. These processes involve a broad variety of proteins, such as transcriptional regulators, kinases, phosphatases, calcium channels, phototropins, and ROS metabolizing enzymes. Moreover, it becomes evident that PCD regulation in plants depends on excess light energy dissipation as heat and manifests itself in foliar temperature changes, and simultaneous induction of defense and acclimation responses. Therefore, PCD regulators in plants have been successfully used in biotechnological improvement of crops and woody plants, in order to enhance growth, yield, and improve cell wall chemical composition, stress tolerance, and disease resistance.

This Special Issue aims at presenting new discoveries in the field of PCD and at summarizing the current knowledge of the role of PCD regulators in cellular metabolism, plant physiology, and retrograde signaling-related cross-tolerance phenomena in plants.

We look forward to your contributions.

Prof. Dr. Stanislaw Karpinski
Dr Weronika Czarnocka
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cell death
  • reactive oxygen species (ROS) and hormonal signaling
  • gene expression regulation
  • crosstolerance
  • nonphotochemical quenching
  • temperature regulation

Published Papers (6 papers)

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Research

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12 pages, 2279 KiB  
Communication
Salicylic Acid Accumulation Controlled by LSD1 Is Essential in Triggering Cell Death in Response to Abiotic Stress
by Maciej Jerzy Bernacki, Anna Rusaczonek, Weronika Czarnocka and Stanisław Karpiński
Cells 2021, 10(4), 962; https://doi.org/10.3390/cells10040962 - 20 Apr 2021
Cited by 14 | Viewed by 3408
Abstract
Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. [...] Read more.
Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. LESION SIMULATING DISEASE 1 (LSD1) is one of the best-known cell death regulators in Arabidopsis thaliana. The lsd1 mutant, lacking functional LSD1 protein, accumulates SA and is conditionally susceptible to many biotic and abiotic stresses. In order to get more insight into the role of LSD1-dependent regulation of SA accumulation during cell death, we crossed the lsd1 with the sid2 mutant, caring mutation in ISOCHORISMATE SYNTHASE 1(ICS1) gene and having deregulated SA synthesis, and with plants expressing the bacterial nahG gene and thus decomposing SA to catechol. In response to UV A+B irradiation, the lsd1 mutant exhibited clear cell death phenotype, which was reversed in lsd1/sid2 and lsd1/NahG plants. The expression of PR-genes and the H2O2 content in UV-treated lsd1 were significantly higher when compared with the wild type. In contrast, lsd1/sid2 and lsd1/NahG plants demonstrated comparability with the wild-type level of PR-genes expression and H2O2. Our results demonstrate that SA accumulation is crucial for triggering cell death in lsd1, while the reduction of excessive SA accumulation may lead to a greater tolerance toward abiotic stress. Full article
(This article belongs to the Special Issue Programmed Cell Death Regulation in Plants)
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24 pages, 3336 KiB  
Article
Phototropin 1 and 2 Influence Photosynthesis, UV-C Induced Photooxidative Stress Responses, and Cell Death
by Anna Rusaczonek, Weronika Czarnocka, Patrick Willems, Marzena Sujkowska-Rybkowska, Frank Van Breusegem and Stanisław Karpiński
Cells 2021, 10(2), 200; https://doi.org/10.3390/cells10020200 - 20 Jan 2021
Cited by 9 | Viewed by 3814
Abstract
Phototropins are plasma membrane-associated photoreceptors of blue light and UV-A/B radiation. The Arabidopsis thaliana genome encodes two phototropins, PHOT1 and PHOT2, that mediate phototropism, chloroplast positioning, and stomatal opening. They are well characterized in terms of photomorphogenetic processes, but so far, little [...] Read more.
Phototropins are plasma membrane-associated photoreceptors of blue light and UV-A/B radiation. The Arabidopsis thaliana genome encodes two phototropins, PHOT1 and PHOT2, that mediate phototropism, chloroplast positioning, and stomatal opening. They are well characterized in terms of photomorphogenetic processes, but so far, little was known about their involvement in photosynthesis, oxidative stress responses, and cell death. By analyzing phot1, phot2 single, and phot1phot2 double mutants, we demonstrated that both phototropins influence the photochemical and non-photochemical reactions, photosynthetic pigments composition, stomata conductance, and water-use efficiency. After oxidative stress caused by UV-C treatment, phot1 and phot2 single and double mutants showed a significantly reduced accumulation of H2O2 and more efficient photosynthetic electron transport compared to the wild type. However, all phot mutants exhibited higher levels of cell death four days after UV-C treatment, as well as deregulated gene expression. Taken together, our results reveal that on the one hand, both phot1 and phot2 contribute to the inhibition of UV-C-induced foliar cell death, but on the other hand, they also contribute to the maintenance of foliar H2O2 levels and optimal intensity of photochemical reactions and non-photochemical quenching after an exposure to UV-C stress. Our data indicate a novel role for phototropins in the condition-dependent optimization of photosynthesis, growth, and water-use efficiency as well as oxidative stress and cell death response after UV-C exposure. Full article
(This article belongs to the Special Issue Programmed Cell Death Regulation in Plants)
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19 pages, 3892 KiB  
Article
EDS1-Dependent Cell Death and the Antioxidant System in Arabidopsis Leaves is Deregulated by the Mammalian Bax
by Maciej Jerzy Bernacki, Weronika Czarnocka, Magdalena Zaborowska, Elżbieta Różańska, Mateusz Labudda, Anna Rusaczonek, Damian Witoń and Stanisław Karpiński
Cells 2020, 9(11), 2454; https://doi.org/10.3390/cells9112454 - 10 Nov 2020
Cited by 3 | Viewed by 3181
Abstract
Cell death is the ultimate end of a cell cycle that occurs in all living organisms during development or responses to biotic and abiotic stresses. In the course of evolution, plants and animals evolve various molecular mechanisms to regulate cell death; however, some [...] Read more.
Cell death is the ultimate end of a cell cycle that occurs in all living organisms during development or responses to biotic and abiotic stresses. In the course of evolution, plants and animals evolve various molecular mechanisms to regulate cell death; however, some of them are conserved among both these kingdoms. It was found that mammalian proapoptotic BCL-2 associated X (Bax) protein, when expressed in plants, induces cell death, similar to hypersensitive response (HR). It was also shown that changes in the expression level of genes encoding proteins involved in stress response or oxidative status regulation mitigate Bax-induced plant cell death. In our study, we focused on the evolutional compatibility of animal and plant cell death molecular mechanisms. Therefore, we studied the deregulation of reactive oxygen species burst and HR-like propagation in Arabidopsis thaliana expressing mammalian Bax. We were able to diminish Bax-induced oxidative stress and HR progression through the genetic cross with plants mutated in ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1), which is a plant-positive HR regulator. Plants expressing the mouse Bax gene in eds1-1 null mutant background demonstrated less pronounced cell death and exhibited higher antioxidant system efficiency compared to Bax-expressing plants. Moreover, eds1/Bax plants did not show HR marker genes induction, as in the case of the Bax-expressing line. The present study indicates some common molecular features between animal and plant cell death regulation and can be useful to better understand the evolution of cell death mechanisms in plants and animals. Full article
(This article belongs to the Special Issue Programmed Cell Death Regulation in Plants)
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16 pages, 5802 KiB  
Article
FMO1 Is Involved in Excess Light Stress-Induced Signal Transduction and Cell Death Signaling
by Weronika Czarnocka, Yosef Fichman, Maciej Bernacki, Elżbieta Różańska, Izabela Sańko-Sawczenko, Ron Mittler and Stanisław Karpiński
Cells 2020, 9(10), 2163; https://doi.org/10.3390/cells9102163 - 24 Sep 2020
Cited by 15 | Viewed by 4562
Abstract
Because of their sessile nature, plants evolved integrated defense and acclimation mechanisms to simultaneously cope with adverse biotic and abiotic conditions. Among these are systemic acquired resistance (SAR) and systemic acquired acclimation (SAA). Growing evidence suggests that SAR and SAA activate similar cellular [...] Read more.
Because of their sessile nature, plants evolved integrated defense and acclimation mechanisms to simultaneously cope with adverse biotic and abiotic conditions. Among these are systemic acquired resistance (SAR) and systemic acquired acclimation (SAA). Growing evidence suggests that SAR and SAA activate similar cellular mechanisms and employ common signaling pathways for the induction of acclimatory and defense responses. It is therefore possible to consider these processes together, rather than separately, as a common systemic acquired acclimation and resistance (SAAR) mechanism. Arabidopsis thaliana flavin-dependent monooxygenase 1 (FMO1) was previously described as a regulator of plant resistance in response to pathogens as an important component of SAR. In the current study, we investigated its role in SAA, induced by a partial exposure of Arabidopsis rosette to local excess light stress. We demonstrate here that FMO1 expression is induced in leaves directly exposed to excess light stress as well as in systemic leaves remaining in low light. We also show that FMO1 is required for the systemic induction of ASCORBATE PEROXIDASE 2 (APX2) and ZINC-FINGER OF ARABIDOPSIS 10 (ZAT10) expression and spread of the reactive oxygen species (ROS) systemic signal in response to a local application of excess light treatment. Additionally, our results demonstrate that FMO1 is involved in the regulation of excess light-triggered systemic cell death, which is under control of LESION SIMULATING DISEASE 1 (LSD1). Our study indicates therefore that FMO1 plays an important role in triggering SAA response, supporting the hypothesis that SAA and SAR are tightly connected and use the same signaling pathways. Full article
(This article belongs to the Special Issue Programmed Cell Death Regulation in Plants)
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Review

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20 pages, 1620 KiB  
Review
Calcium Signaling in Plant Programmed Cell Death
by Huimin Ren, Xiaohong Zhao, Wenjie Li, Jamshaid Hussain, Guoning Qi and Shenkui Liu
Cells 2021, 10(5), 1089; https://doi.org/10.3390/cells10051089 - 02 May 2021
Cited by 40 | Viewed by 6009
Abstract
Programmed cell death (PCD) is a process intended for the maintenance of cellular homeostasis by eliminating old, damaged, or unwanted cells. In plants, PCD takes place during developmental processes and in response to biotic and abiotic stresses. In contrast to the field of [...] Read more.
Programmed cell death (PCD) is a process intended for the maintenance of cellular homeostasis by eliminating old, damaged, or unwanted cells. In plants, PCD takes place during developmental processes and in response to biotic and abiotic stresses. In contrast to the field of animal studies, PCD is not well understood in plants. Calcium (Ca2+) is a universal cell signaling entity and regulates numerous physiological activities across all the kingdoms of life. The cytosolic increase in Ca2+ is a prerequisite for the induction of PCD in plants. Although over the past years, we have witnessed significant progress in understanding the role of Ca2+ in the regulation of PCD, it is still unclear how the upstream stress perception leads to the Ca2+ elevation and how the signal is further propagated to result in the onset of PCD. In this review article, we discuss recent advancements in the field, and compare the role of Ca2+ signaling in PCD in biotic and abiotic stresses. Moreover, we discuss the upstream and downstream components of Ca2+ signaling and its crosstalk with other signaling pathways in PCD. The review is expected to provide new insights into the role of Ca2+ signaling in PCD and to identify gaps for future research efforts. Full article
(This article belongs to the Special Issue Programmed Cell Death Regulation in Plants)
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20 pages, 5798 KiB  
Review
Insights into Plant Programmed Cell Death Induced by Heavy Metals—Discovering a Terra Incognita
by Klaudia Sychta, Aneta Słomka and Elżbieta Kuta
Cells 2021, 10(1), 65; https://doi.org/10.3390/cells10010065 - 04 Jan 2021
Cited by 50 | Viewed by 5664
Abstract
Programmed cell death (PCD) is a process that plays a fundamental role in plant development and responses to biotic and abiotic stresses. Knowledge of plant PCD mechanisms is still very scarce and is incomparable to the large number of studies on PCD mechanisms [...] Read more.
Programmed cell death (PCD) is a process that plays a fundamental role in plant development and responses to biotic and abiotic stresses. Knowledge of plant PCD mechanisms is still very scarce and is incomparable to the large number of studies on PCD mechanisms in animals. Quick and accurate assays, e.g., the TUNEL assay, comet assay, and analysis of caspase-like enzyme activity, enable the differentiation of PCD from necrosis. Two main types of plant PCD, developmental (dPCD) regulated by internal factors, and environmental (ePCD) induced by external stimuli, are distinguished based on the differences in the expression of the conserved PCD-inducing genes. Abiotic stress factors, including heavy metals, induce necrosis or ePCD. Heavy metals induce PCD by triggering oxidative stress via reactive oxygen species (ROS) overproduction. ROS that are mainly produced by mitochondria modulate phytotoxicity mechanisms induced by heavy metals. Complex crosstalk between ROS, hormones (ethylene), nitric oxide (NO), and calcium ions evokes PCD, with proteases with caspase-like activity executing PCD in plant cells exposed to heavy metals. This pathway leads to very similar cytological hallmarks of heavy metal induced PCD to PCD induced by other abiotic factors. The forms, hallmarks, mechanisms, and genetic regulation of plant ePCD induced by abiotic stress are reviewed here in detail, with an emphasis on plant cell culture as a suitable model for PCD studies. The similarities and differences between plant and animal PCD are also discussed. Full article
(This article belongs to the Special Issue Programmed Cell Death Regulation in Plants)
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