scholarly journals Cork cells in cork oak periderms undergo programmed cell death and proanthocyanidin deposition

2021 ◽  
Author(s):  
Vera Inácio ◽  
Carolina Lobato ◽  
José Graça ◽  
Leonor Morais-Cecílio
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Programmed Cell Death ◽  
Secondary Growth ◽  
Cork Oak ◽  
Comprehensive Overview ◽  
Highly Active ◽  
Transmission Electron ◽  
Traumatic Wound ◽  
The Impact

Abstract Vascular plants with secondary growth develop a periderm mostly composed of dead suberized cork cells to face environmental hostile conditions. Cork oak has a highly active and long-living phellogen forming a remarkably thick periderm that is periodically debarked for industrial purposes. This wounding originates the quick formation of a new traumatic periderm, making cork oak an exceptional model to study the first periderm differentiation during normal development in young sprigs and traumatic (wound) periderm formation after debarking. Here, we studied the poorly known first periderm differentiation steps that involve cell wall suberization, polyphenolic accumulation and programmed cell death (PCD) by combining transmission electron microscopy, histochemical and molecular methods in periderms from young sprigs. These processes were further compared with traumatic periderms formed after wounding using molecular and histochemical techniques, such as the polyphenolic accumulation. In the first periderms from young sprigs, four distinct differentiation stages were defined according to the presence of PCD morphological features. First young and traumatic periderms showed an upregulation of genes related to suberin biosynthesis, proanthocyanidins biosynthesis and transport, autophagy, and PCD. Traumatic periderms revealed an overall upregulation of these genes, likely resulting from ontogeny differences and distinct phellogen origin associated with a faster metabolism, highlighting the impact of wounding on phellogen activity after debarking. First periderms from young sprigs showed gradual accumulation of proanthocyanidins in the vacuoles throughout PCD stages until total filled lumens, whereas in traumatic periderms, these compounds were found cell wall linked in already empty cells. This work enabled a comprehensive overview of the cork cells differentiation processes contributing to deepening the knowledge of the fundamental ontogenic program of this protective tissue, which is also a unique forest product, constituting the basis of a sustainable and profitable industry.

scholarly journals Deletion of Atg22 gene contributes to reduce programmed cell death induced by acetic acid stress in Saccharomyces cerevisiae

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Jingjin Hu ◽  
Yachen Dong ◽  
Wei Wang ◽  
Wei Zhang ◽  
Hanghang Lou ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Amino Acids ◽  
Cell Death ◽  
Cell Wall ◽  
Acetic Acid ◽  
Programmed Cell Death ◽  
Cell Wall Integrity ◽  
Yeast Cells ◽  
Death Process ◽  
Lignocellulosic Biofuel

Abstract Background Programmed cell death (PCD) induced by acetic acid, the main by-product released during cellulosic hydrolysis, cast a cloud over lignocellulosic biofuel fermented by Saccharomyces cerevisiae and became a burning problem. Atg22p, an ignored integral membrane protein located in vacuole belongs to autophagy-related genes family; prior study recently reported that it is required for autophagic degradation and efflux of amino acids from vacuole to cytoplasm. It may alleviate the intracellular starvation of nutrition caused by Ac and increase cell tolerance. Therefore, we investigate the role of atg22 in cell death process induced by Ac in which attempt is made to discover new perspectives for better understanding of the mechanisms behind tolerance and more robust industrial strain construction. Results In this study, we compared cell growth, physiological changes in the absence and presence of Atg22p under Ac exposure conditions. It is observed that disruption and overexpression of Atg22p delays and enhances acetic acid-induced PCD, respectively. The deletion of Atg22p in S. cerevisiae maintains cell wall integrity, and protects cytomembrane integrity, fluidity and permeability upon Ac stress by changing cytomembrane phospholipids, sterols and fatty acids. More interestingly, atg22 deletion increases intracellular amino acids to aid yeast cells for tackling amino acid starvation and intracellular acidification. Further, atg22 deletion upregulates series of stress response genes expression such as heat shock protein family, cell wall integrity and autophagy. Conclusions The findings show that Atg22p possessed the new function related to cell resistance to Ac. This may help us have a deeper understanding of PCD induced by Ac and provide a new strategy to improve Ac resistance in designing industrial yeast strains for bioethanol production during lignocellulosic biofuel fermentation.

scholarly journals Association between PD-1 and PD-L1 Polymorphisms and the Risk of Cancer: A Meta-Analysis of Case-Control Studies

Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1150 ◽  
Author(s):  
Mohammad Hashemi ◽  
Shima Karami ◽  
Sahel Sarabandi ◽  
Abdolkarim Moazeni-Roodi ◽  
Andrzej Małecki ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Risk ◽  
Programmed Cell Death ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Case Control ◽  
Case Control Studies ◽  
Programmed Cell Death 1 ◽  
Risk Of Cancer ◽  
The Impact

A number of case-control studies regarding the association of the polymorphisms in the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) genes with the risk of cancer have yielded inconsistent findings. Therefore, we have conducted a comprehensive, updated meta-analysis study to identify the impact of PD-1 and PD-L1 polymorphisms on overall cancer susceptibility. The findings revealed that PD-1 rs2227981 and rs11568821 polymorphisms significantly decreased the overall cancer risk (Odds Ratio (OR) = 0.82, 95% CI = 0.68–0.99, p = 0.04, TT vs. CT+CC; OR = 0.79, 95% CI = 0.67–0.94, p = 0.006, AG vs. GG, and OR = 0.82, 95% CI = 0.70–0.96, p = 0.020, AG+AA vs. GG, respectively), while PD-1 rs7421861 polymorphism significantly increased the risk of developing cancer (OR = 1.16, 95% CI = 1.02–1.33, p = 0.03, CT vs. TT). The PD-L1 rs4143815 variant significantly decreased the risk of cancer in homozygous (OR = 0.62, 95% CI = 0.41–0.94, p = 0.02), dominant (OR = 0.70, 95% CI = 0.50–0.97, p = 0.03), recessive (OR = 0.76, 95% CI = 0.60–0.96, p = 0.02), and allele (OR = 0.78, 95% CI = 0.63–0.96, p = 0.02) genetic models. No significant association between rs2227982, rs36084323, rs10204525, and rs2890658 polymorphisms and overall cancer risk has been found. In conclusions, the results of this meta-analysis have revealed an association between PD-1 rs2227981, rs11568821, rs7421861, as well as PD-L1 rs4143815 polymorphisms and overall cancer susceptibility.

scholarly journals Evaluation of Metaxylem Vessel Histogenesis and the Occurrence of Vessel Collapse during Early Development in Primary Roots of Zea mays ssp. mexicana: A Result of Premature Programmed Cell Death?

Plants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 374
Author(s):  
Susumu Saito ◽  
Teruo Niki ◽  
Daniel K. Gladish
Keyword(s):  
Cell Death ◽  
Zea Mays ◽  
Programmed Cell Death ◽  
Primary Root ◽  
Cell Types ◽  
Root Apical Meristem ◽  
Root Tips ◽  
Primary Roots ◽  
Transmission Electron ◽  
Vessel Elements

Root apical meristem histological organization in Zea mays has been carefully studied previously. Classical histology describes its system as having a “closed organization” and a development of xylem that conforms to predictable rules. Among the first cell types to begin differentiation are late-maturing metaxylem (LMX) vessels. As part of a larger study comparing domestic maize root development to a wild subspecies of Z. mays (teosinte), we encountered a metaxylem development abnormality in a small percentage of our specimens that begged further study, as it interrupted normal maturation of LMX. Primary root tips of young seedlings of Zea mays ssp. mexicana were fixed, embedded in appropriate resins, and sectioned for light and transmission electron microscopy. Longitudinal and serial transverse sections were analyzed using computer imaging to determine the position and timing of key xylem developmental events. We observed a severe abnormality of LMX development among 3.5% of the 227 mexicana seedlings we screened. All LMX vessel elements in these abnormal roots collapsed and probably became non-functional shortly after differentiation began. Cytoplasm and nucleoplasm in the abnormal LMX elements became condensed and subdivided into irregularly-shaped “macrovesicles” as their cell walls collapsed inward. We propose that these seedlings possibly suffered from a mutation that affected the timing of the programmed cell death (PCD) that is required to produce functional xylem vessels, such that autolysis of the cytoplasm was prematurely executed, i.e., prior to the development and lignification of secondary walls.

scholarly journals Cell wall degradation and modification during programmed cell death in lace plant, Aponogeton madagascariensis (Aponogetonaceae)

2007 ◽  
Vol 94 (7) ◽  
pp. 1116-1128 ◽  
Author(s):  
Arunika H. L. A. N. Gunawardena ◽  
John S. Greenwood ◽  
Nancy G. Dengler
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Programmed Cell Death ◽  
Cell Wall Degradation

Characterization of programmed cell death in the endosperm cells of tomato seed: two distinct death programs

2006 ◽  
Vol 84 (5) ◽  
pp. 791-804 ◽  
Author(s):  
Allan G. DeBono ◽  
John S. Greenwood
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Gibberellic Acid ◽  
Genomic Dna ◽  
Electrophoretic Analysis ◽  
Tomato Seed ◽  
Solanum Lycopersicum L ◽  
Transmission Electron ◽  
Micropylar Endosperm

Programmed cell death (PCD) is a requisite, genetically controlled process in plants resulting in the death of particular cells and tissues and the recycling of the cellular constituents back to the organism. PCD in the lateral and micropylar endosperm cells during and following germination of tomato ( Solanum lycopersicum L.) seeds was characterized by transmission electron microscopy, by terminal d-UTP nick-end labelling of nuclei, and agarose gel electrophoretic analysis of genomic DNA. Postgerminative cells of lateral and micropylar endosperm displayed morphologies and terminal d-UTP nick-end labelling positive nuclei consistent with PCD. PCD was not detected in the lateral endosperm in the absence of the embryo. The embryo’s effect on promoting lateral endosperm PCD could be substituted with gibberellic acid at 50 μmol/L. Micropylar endosperm cells undergo PCD irrespective of incubation with or without the embryo; gibberellic acid only hastens the onset of PCD morphology. Precursor protease vesicles, novel endoplasmic reticulum derived organelles considered markers of PCD, were observed in postgerminative lateral and micropylar endosperm cells. Internucleosomal laddering was not detected in endospermic DNA. These results suggest that a late postimbibition gibberellic acid linked mechanism promotes PCD in the lateral endosperm, whereas the promotion of PCD in the micropylar endosperm occurs early in, or prior to, imbibition.

Prognostic Impact of Programmed Cell Death-1-Positive Cells on Follicular Lymphoma Patients Might Diminish in the Rituximab Era

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2645-2645
Author(s):  
Hiroyuki Takahashi ◽  
Naoto Tomita ◽  
Seiji Sakata ◽  
Chizuko Hashimoto ◽  
Rika Ohshima ◽  
...  
Keyword(s):  
Cell Death ◽  
Prognostic Factors ◽  
T Cell ◽  
Prognostic Factor ◽  
Programmed Cell Death ◽  
Follicular Lymphoma ◽  
Prognostic Impact ◽  
High Tendency ◽  
Programmed Cell Death 1 ◽  
The Impact

Abstract Abstract 2645 Background Programmed cell death-1 (PD-1) is involved in one of the inhibitory pathways of the B7-cluster of differentiation (CD) 28 family; this pathway is known to be involved in the attenuation of T cell responses and promotion of T cell tolerance. PD-1 is known to negatively regulate T cell receptor-mediated proliferation and cytokine production, lead to alternation in the tumor microenvironment. Carreas et al. (J Clin Oncol. 2009; 27: 1470–1476) examined 100 follicular lymphoma (FL) patients and reported better prognosis in the group that had high levels of PD-1-positive cells. In contrast, in the study performed by Richendollar et al. (Human Pathol. 2011; 42: 552–557), which involved 91 FL patients, high levels of PD-1-positive cells were found to have a poor prognostic impact. Although these studies have shown that high levels of PD-1-positive cells in FL patients influence their prognosis, both studies included patients treated without rituximab, and the prognostic impact of PD-1 positivity in the rituximab-era (R-era) has not yet been elucidated. Materials and methods We retrospectively analyzed data for 91 FL patients uniformly treated by standard rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) therapy in 5 institutions between 2001 and 2009. The median age of the entire cohort was 58 years (range, 34–85 years), and 46 (51%) of the patients were men. We also collected and examined biopsy specimens for diagnosis with respect to PD-1 positivity. The PD-1-positive cells were counted using computer analysis at the Cancer Institute, Japanese Foundation for Cancer Research. Results The FL grade on diagnosis was grade 1 for 34 (37%) patients, grade 2 for 41 (45%) patients, and grade 3 for 16 (18%) patients. The median positivity for PD-1 staining was 16.0% (range, 0.01–51.9%) and was significantly higher in the high beta-2 microglobulin (B2M; at least 3) group (P = 0.009); the men had a high tendency for PD-1 positivity (P = 0.08). After a median follow-up of 29.1 months, the 3-year progression-free survival (PFS) and overall survival (OS) were 61.1% and 88.6%, respectively. Stage 4 FL at diagnosis (P = 0.02) and bone marrow involvement (P = 0.05) resulted in worse PFS, and an Eastern Cooperative Oncology Group (ECOG) performance status of 2–4 (P = 0.04), high Follicular Lymphoma International Prognostic Index (FLIPI; P = 0.02), B symptoms (P = 0.04), and high B2M levels (P = 0.005) worsened OS. Multivariate analysis showed that age over 60 years (P = 0.04) and high B2M levels (P = 0.07) were prognostic factors for PFS. PD-1 positivity was not found to be a prognostic factor with respect to both PFS and OS. Because the addition of rituximab to therapy regimens has altered the clinical course and prognosis of FL, some new prognostic factors have been proposed, and the impact of known prognostic factors has been changing. Rituximab might also have changed the prognosis of FL patients with high levels of PD-1-positive cells. Conclusion High levels of PD-1-positive cells were not found to be a prognostic factor in this study, indicating that the prognostic impact of PD-1 positivity might be eliminated in the R-era. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Processes controlling programmed cell death of root velamen radicum in an epiphytic orchid

2020 ◽  
Vol 126 (2) ◽  
pp. 261-275
Author(s):  
Jia-Wei Li ◽  
Shi-Bao Zhang ◽  
Hui-Peng Xi ◽  
Corey J A Bradshaw ◽  
Jiao-Lin Zhang
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Programmed Cell Death ◽  
Secondary Cell Wall ◽  
Primary Root ◽  
Cysteine Proteases ◽  
Wall Thickening ◽  
Related Factors ◽  
Epiphytic Orchid ◽  
Cell Autolysis

Abstract Background and Aims Development of the velamen radicum on the outer surface of the root epidermis is an important characteristic for water uptake and retention in some plant families, particularly epiphytic orchids, for survival under water-limited environments. Velamen radicum cells derive from the primary root meristem; however, following this development, velamen radicum cells die by incompletely understood processes of programmed cell death (PCD). Methods We combined the use of transmission electron microscopy, X-ray micro-tomography and transcriptome methods to characterize the major anatomical and molecular changes that occur during the development and death of velamen radicum cells of Cymbidium tracyanum, a typical epiphytic orchid, to determine how PCD occurs. Key Results Typical changes of PCD in anatomy and gene expression were observed in the development of velamen radicum cells. During the initiation of PCD, we found that both cell and vacuole size increased, and several genes involved in brassinosteroid and ethylene pathways were upregulated. In the stage of secondary cell wall formation, significant anatomical changes included DNA degradation, cytoplasm thinning, organelle decrease, vacuole rupture and cell wall thickening. Changes were found in the expression of genes related to the biosynthesis of cellulose and lignin, which are instrumental in the formation of secondary cell walls, and are regulated by cytoskeleton-related factors and phenylalanine ammonia-lyase. In the final stage of PCD, cell autolysis was terminated from the outside to the inside of the velamen radicum. The regulation of genes related to autophagy, vacuolar processing enzyme, cysteine proteases and metacaspase was involved in the final execution of cell death and autolysis. Conclusions Our results showed that the development of the root velamen radicum in an epiphytic orchid was controlled by the process of PCD, which included initiation of PCD, followed by formation of the secondary cell wall, and execution of autolysis following cell death.

scholarly journals The Cell Wall Sensors Mtl1, Wsc1, and Mid2 Are Required for Stress-Induced Nuclear to Cytoplasmic Translocation of Cyclin C and Programmed Cell Death in Yeast

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Chunyan Jin ◽  
Andrey V. Parshin ◽  
Ira Daly ◽  
Randy Strich ◽  
Katrina F. Cooper
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cell Wall ◽  
Programmed Cell Death ◽  
Map Kinase ◽  
Genetic Interaction ◽  
Negative Regulator ◽  
Cell Wall Integrity ◽  
Surprising Result ◽  
Cyclin C

Mtl1 is a member of a cell wall sensor family that monitors cell wall integrity in budding yeast. In response to cell wall stress, Mtl1 activates the cell wall integrity (CWI) MAP kinase pathway which transmits this signal to the nucleus to effect changes in gene expression. One target of the CWI MAP kinase is cyclin C, a negative regulator of stress response genes. CWI activation results in cyclin C relocalization from the nucleus to the cytoplasm where it stimulates programmed cell death (PCD) before it is destroyed. This report demonstrates that under low oxidative stress conditions, a combination of membrane sensors, Mtl1 and either Wsc1 or Mid2, are required jointly to transmit the oxidative stress signal to initiate cyclin C destruction. However, when exposed to elevated oxidative stress, additional pathways independent of these three sensor proteins are activated to destroy cyclin C. In addition,N-glycosylation is important for Mtl1 function as mutating the receptor residue (Asn42) or an enzyme required for synthesis ofN-acetylglucosamine (Gfa1) reduces sensor activity. Finally, combininggfa1-1with the cyclin C null allele induces a severe synthetic growth defect. This surprising result reveals a previously unknown genetic interaction between cyclin C and plasma membrane integrity.

scholarly journals Rhinovirus and Cell Death

Viruses ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 629
Author(s):  
Shannic-Le Kerr ◽  
Cynthia Mathew ◽  
Reena Ghildyal
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Respiratory Tract ◽  
English Language ◽  
Severe Disease ◽  
Future Research ◽  
Upper Respiratory Tract ◽  
Cell Death Pathways ◽  
Tract Infections ◽  
The Impact

Rhinoviruses (RVs) are the etiological agents of upper respiratory tract infections, particularly the common cold. Infections in the lower respiratory tract is shown to cause severe disease and exacerbations in asthma and COPD patients. Viruses being obligate parasites, hijack host cell pathways such as programmed cell death to suppress host antiviral responses and prolong viral replication and propagation. RVs are non-enveloped positive sense RNA viruses with a lifecycle fully contained within the cytoplasm. Despite decades of study, the details of how RVs exit the infected cell are still unclear. There are some diverse studies that suggest a possible role for programmed cell death. In this review, we aimed to consolidate current literature on the impact of RVs on cell death to inform future research on the topic. We searched peer reviewed English language literature in the past 21 years for studies on the interaction with and modulation of cell death pathways by RVs, placing it in the context of the broader knowledge of these interconnected pathways from other systems. Our review strongly suggests a role for necroptosis and/or autophagy in RV release, with the caveat that all the literature is based on RV-A and RV-B strains, with no studies to date examining the interaction of RV-C strains with cell death pathways.

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