Programmed cell death: genes involved in signaling, regulation, and execution in plants and animals

Botany ◽  
2015 ◽  
Vol 93 (4) ◽  
pp. 193-210 ◽  
Author(s):  
Gaolathe Rantong ◽  
Arunika H.L.A.N. Gunawardena
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Morphological Characteristics ◽  
Special Focus ◽  
Apoptotic Pathway ◽  
Signaling Regulation ◽  
Whole Plant ◽  
Cell Death Genes ◽  
Death Genes ◽  
Multicellular Organisms

Programmed cell death (PCD) is a suicide mechanism adopted by multicellular organisms that is essential for development and resistance to different forms of stress. In plants, PCD is involved from embryogenesis to death of the whole plant. PCD is genetically regulated and the molecular pathways involved in different forms of this process in animals are relatively more understood than in plants. At the morphological level, apoptosis, one of the forms of PCD in animals, and plant PCD have some similarities such as cell shrinkage, shrinkage of the nucleus, and DNA fragmentation. Because morphological characteristics are a product of the genetically encoded PCD mechanism, it is of interest to figure out how much of the apoptotic pathway is shared with plant PCD in terms of the genes involved. Evidence of some level of similarities has been gathered in the last decade, supporting conservation during signaling, regulation, and execution of apoptosis and plant PCD. A continued search into the genomes of plants has provided insights about homologues of apoptosis genes present in plants, and functional analysis provides evidence about which genes are carrying out similar roles during apoptosis and plant PCD. This review is aimed at updating on the progress of plant PCD mechanism research and highlighting some of the similarities and differences between plant and mammalian PCD mechanisms, with special focus on the commonalities.

scholarly journals Expression Analysis of Programmed Cell Death Genes in Porcine Parthenogenesis

2015 ◽  
Vol 30 (3) ◽  
pp. 239-248
Author(s):  
Jong-Yoon Son ◽  
Sang-Hwan Kim ◽  
Duk-Won Jung ◽  
Chun-Yeol Ryu ◽  
Jong-Taek Yoon
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Expression Analysis ◽  
Cell Death Genes ◽  
Death Genes

scholarly journals Network Analysis Identifies Drug Targets and Small Molecules to Modulate Apoptosis Resistant Cancers

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 851
Author(s):  
Samreen Fathima ◽  
Swati Sinha ◽  
Sainitin Donakonda
Keyword(s):  
Cell Death ◽  
Small Molecules ◽  
Drug Targets ◽  
Apoptotic Cell ◽  
Colon Adenocarcinoma ◽  
Interaction Networks ◽  
Small Cell Lung ◽  
Protein Protein Interaction ◽  
Cell Death Genes ◽  
Death Genes

Programed cell death or apoptosis fails to induce cell death in many recalcitrant cancers. Thus, there is an emerging need to activate the alternate cell death pathways in such cancers. In this study, we analyzed the apoptosis-resistant colon adenocarcinoma, glioblastoma multiforme, and small cell lung cancers transcriptome profiles. We extracted clusters of non-apoptotic cell death genes from each cancer to understand functional networks affected by these genes and their role in the induction of cell death when apoptosis fails. We identified transcription factors regulating cell death genes and protein–protein interaction networks to understand their role in regulating cell death mechanisms. Topological analysis of networks yielded FANCD2 (ferroptosis, negative regulator, down), NCOA4 (ferroptosis, up), IKBKB (alkaliptosis, down), and RHOA (entotic cell death, down) as potential drug targets in colon adenocarcinoma, glioblastoma multiforme, small cell lung cancer phenotypes respectively. We also assessed the miRNA association with the drug targets. We identified tumor growth-related interacting partners based on the pathway information of drug-target interaction networks. The protein–protein interaction binding site between the drug targets and their interacting proteins provided an opportunity to identify small molecules that can modulate the activity of functional cell death interactions in each cancer. Overall, our systematic screening of non-apoptotic cell death-related genes uncovered targets helpful for cancer therapy.

scholarly journals 1779 Cell Death Genes are Induced Immediately after Hypoxia-Reoxygenation (HR) in the Newborn Mouse Lung

2012 ◽  
Vol 97 (Suppl 2) ◽  
pp. A503-A503
Author(s):  
E. Wollen ◽  
A. Rognlien ◽  
M. Atneosen-Asegg ◽  
M. Wright ◽  
M. Bjoras ◽  
...  
Keyword(s):  
Cell Death ◽  
Mouse Lung ◽  
Newborn Mouse ◽  
Cell Death Genes ◽  
Death Genes ◽  
Hypoxia Reoxygenation

Interleukin-1α-converting enzyme (ICE) and related cell death genes ICErel-II and ICErel-III map to the same PAC clone at band 11q22.2-22.3

1997 ◽  
Vol 8 (8) ◽  
pp. 611-613 ◽  
Author(s):  
Jamal Nasir ◽  
Jane L. Theilmann ◽  
John P. Vaillancourt ◽  
Neil A. Munday ◽  
Ambereen Ali ◽  
...  
Keyword(s):  
Cell Death ◽  
Converting Enzyme ◽  
Related Cell ◽  
Interleukin 1Α ◽  
Cell Death Genes ◽  
Death Genes

scholarly journals A new method to detect apoptosis in paraffin sections: in situ end-labeling of fragmented DNA.

1993 ◽  
Vol 41 (1) ◽  
pp. 7-12 ◽  
Author(s):  
J H Wijsman ◽  
R R Jonker ◽  
R Keijzer ◽  
C J van de Velde ◽  
C J Cornelisse ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Staining Method ◽  
Morphological Characteristics ◽  
Image Cytometry ◽  
Apoptotic Cells ◽  
Dna Breaks ◽  
Paraffin Sections ◽  
Tissue Sections

Apoptosis (programmed cell death) can be difficult to detect in routine histological sections. Since extensive DNA fragmentation is an important characteristic of this process, visualization of DNA breaks could greatly facilitate the identification of apoptotic cells. We describe a new staining method for formalin-fixed, paraffin-embedded tissue sections that involves an in situ end-labeling (ISEL) procedure. After protease treatment to permeate the tissue sections, biotinylated nucleotides are in situ incorporated into DNA breaks by polymerase and subsequently stained with DAB via peroxidase-conjugated avidin. Staining of cells with the morphological characteristics of apoptosis was demonstrated in tissues known to exhibit programmed cell death, i.e., prostate and uterus after castration, tumors, lymph node follicles, and embryos. Apoptotic cells could be discriminated morphologically from areas of labeled necrotic cells, in which DNA degradation also occurs. Because apoptosis is relatively easily recognized in H&E-stained sections of involuting prostates of castrated rats, we used this model system to validate the ISEL method for the quantification of apoptotic cells. A high correlation was found between the fractions of ISEL-labeled cells and the fractions of apoptotic cells that were morphologically determined in adjacent sections. We conclude that ISEL is a useful technique for quantification of apoptosis in paraffin sections, especially for those tissues in which morphological determination is difficult. Furthermore, this new staining method enables the use of automated image cytometry for evaluating apoptosis.

Sign in / Sign up

Export Citation Format

Share Document