The Study Of Cell Death Essay Example
The Study Of Cell Death Essay Example

The Study Of Cell Death Essay Example

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  • Pages: 6 (1625 words)
  • Published: September 19, 2017
  • Type: Research Paper
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Cell death is an important process for living beings, which includes necrosis and apoptosis as two separate forms. These forms have distinct morphological features that are often used to distinguish between them.

Initially, necrotic cells undergo swelling and slight changes in chromatin. Subsequently, the atomic structure and compartments within the necrotic cells become disorganized, including chondriosome swelling and inner mitochondrial membrane shrinkage. In the later stage of cell death, cyto-architecture is disrupted, resulting in loss of chromatin and release of nuclease and lysosomal contents. This ultimately triggers an inflammatory response as the cytoplasmic membrane ruptures and releases cell contents. Monocytes and macrophages are then recruited to remove the necrotic cells from the site of cell death.

However, mortification is a pathological cell decease caused by external decease factors that is harmful to environing cells. Every single cell in mu


lticellular beings must work harmoniously with its neighboring cells, its specialized tissue, and the whole being. Inappropriate decease or proliferation of cells leads to the loss of tissue homeostasis. The physiological in-built self-destruction under familial control, programmed cell death, is polar to weave homeostasis and is a requirement for being endurance. A fresh signifier of cell decease exhibiting morphological difference from mortification was foremost discovered in craniate growth and named 'cell devolution' (Glucksmann, 1951). Subsequently, the definition of 'programmed cell decease' was prompted from descriptive work to experimental confirmation by Saunders & Fallon (1966).

The term "programmed cell death" was introduced to describe a new type of cell death discovered in animal embryogenesis, based on its morphological characteristics (Lockshin & Beaulaton, 1974). In 1972, Kerr et al. coined the term "apoptosis" to refer to this unique form of cell death

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that occurs in various physiological processes and development stages. Apoptotic cells undergo distinct morphological changes, separate from neighboring cells, and lose specific membrane structures.

Apoptosis is characterized by various cellular transformations such as shrinkage, blebbing, chromatin condensation, and compression of organelles. While the endoplasmic reticulum connects to the cell surface, the mitochondria remain unaffected. The last phase of apoptosis includes phagocytosis carried out by neighboring or scavenger cells. In addition to this method, cells can also be eliminated through macrophagy which can be categorized into type I (phagocytosis) or type II (autophagic cell death).

Autophagic cell death results in the creation of autophagosomes, which are dual membrane cysts filled with cytoplasm and organelles. These autophagosomes merge with lysosomes for degradation. The presence of autophagy or phagocytosis varies depending on the cell type and other processes. In contrast to necrosis, programmed cell death is characterized by the rapid disappearance of apoptotic cells without causing inflammation. Alterations on the surface of apoptotic cells allow for their recognition and removal before the plasma membrane ruptures, thereby preventing an inflammatory response (Savill, 1997).

In programmed cell death, DNA fragmentation is a distinguishing feature compared to necrosis. The genomic DNA is broken down into fragments ranging from 50kbp to 300kbp in an indiscriminate manner. Additionally, smaller DNA fragments at 180bp and 200bp are observed in apoptotic cells due to further cleavage. The degradation of DNA during necrosis results in a phenomenon known as 'DNA smearing' on agarose gel electrophoresis. Apoptosis is widely present in various aspects of animal development, physiological processes, and immune responses throughout the lifespan. During development, cells that are no longer needed or improperly differentiated are eliminated through programmed cell


The vanishing of a Xenopus tadpole's tail serves as a frequently referenced example of programmed cell death during embryogenesis. Additionally, damaged cells can be eliminated through this process. Animals have developed an innate apoptotic mechanism to halt virus proliferation in living organisms. This mechanism induces programmed cell death in both infected and neighboring cells, effectively preventing the spread of infection as a defense mechanism. However, viruses also produce programmed cell death inhibitors as a means to counteract this protection.

Abnormal programmed cell death, which occurs in conditions like Alzheimer's disease, can disrupt homeostasis. There are different experimental methods to distinguish programmed cell death from necrosis based on their morphological and biochemical characteristics. Apoptotic cell blebbing and chromatin condensation can be identified using microscopy and electron microscopy. Terminal deoxynucleotidyl transferase dUTP nick terminal labeling (TUNEL) is a technique that detects DNA fragmentation by labeling the open-OH group on the 3' end of nucleic acids.

Deoxyribonucleic acid laddering, cytochrome degree Celsius release, and the initiation of caspase activity are also commonly used indicators of programmed cell death.

Programmed cell death in plants

Programmed cell death in plants refers to apoptotic-like cell death that is tightly controlled by genes. Typical programmed cell death in animal cells must show the following characteristics: cell shrinkage, chromatin condensation, DNA fragmentation and laddering, activation of caspases, shedding of apoptotic bodies, and phagocytosis or autophagy. Except for the shedding of apoptotic bodies and phagocytosis, other apoptotic features can be detected in plant cells undergoing PCD.

For example, characteristics of PCD (Programmed Cell Death) include energid abjuration and cytol condensation after heat daze (Reape et al., 2008). In the context of PCD, similarities between plant and animal programmed cell

death have led to the application of several animal programmed cell death markers in plants. To illustrate this, cell death in liliopsid aleurone layer and endosperm, aging of petal, carpel tissue and leaves, or induced by different stimulations during anther development, are identified as PCD using DNA laddering (Danon et al.).

, 2000). TUNEL is the most commonly used method to detect apoptosis in animals and can also be used in the identification of plant programmed cell death (PCD). The activation of caspase-like activity is detected in plant PCD. There are specific characteristics present in plant PCD, such as the crescent nucleus, which are not found in animal programmed cell death. Plant PCD can occur during developmental processes as well as in response to abiotic or biotic stresses.

The passage discusses how plant cells have a natural immune response to pathogens, heat stress, and starvation. During development, plant cells undergo programmed cell death (PCD) which begins with swollen vacuoles. Then, the endoplasmic reticulum (ER) and other cell compartments are eliminated. Following this, the mitochondria and nucleus move from their original positions causing ruptures in both vacuolar and cytoplasmic membranes. However, certain cell types such as supportive cells, vessels, xylem and bast fibers, cork cells etc., do not experience any changes to their cell walls during PCD. This phenomenon results in the formation of specialized tissues with cell walls like vascular bundles.

On the contrary, cell walls in aerenchyma, endosperm, and aging mesophyll completely disappear after programmed cell death (PCD) (van Doorn; A; Woltering, 2005). Autophagy, which is a process of intracellular constituents turnover by lysosome and autophagosome, provides an alternative method of disposing cells that is different from

phagocytosis in animal programmed cell death. In plant PCD, phagocytosis does not occur due to the suppression of cell wall. The degradation of cellular organelles in plant PCD is likely due to the autophagy exerted by vacuole in most plant cells.

However, programmed cell death (PCD) of endosperms in cereals like barley, wheat, and rice involves exclusion from vacuole-mediated autophagy. The allergic response (HR) is an innate immune response in plants to defend against pathogen attacks. HR includes PCD in infected and neighboring cells, local secretion of anti-pathogen chemicals, and the activation of host resistance (Mur et al., 2008).

The susceptibility of host plants to pathogen is reduced by HR triggered by fungal toxin, bacteria, and viruses, which also helps them avoid further invasion. HR-mediated PCD occurs more quickly than in plant development. The initiation of HR-mediated PCD depends on the interaction between the products of "Resistance gene" (R gene) and pathogen avirulence gene (avr gene). Radical defense response also prevents infection spread through R-gene mediated PCD.

The mechanism of autophagy in the programmed cell death (PCD) triggered by HR is unknown. PCD, a prevalent occurrence during development, includes apoptosis which is crucial for development and tissue homeostasis in multicellular animals. The apoptotic machinery is conserved across species with similar factors and pathways involved. In Caenorhabditis elegans, a nematode, the apoptotic pathway accurately describes each individual cell's fate from fertilization to adulthood. Various genes regulate the 1090 cell births and 131 cell deaths experienced by C. elegans during its growth.

Homologues of the 13 cistrons with significant functional and structural similarity have been found in craniate organisms. This means that the apoptotic pathway observed in the roundworm is conserved

in more complex mammalian programmed cell death. For example, the anti-apoptotic cistron bcl-2 is the mammalian equivalent of ced-9, which can inhibit programmed cell death in C. elegans. Plant programmed cell death (PCD) that occurs in xylem development, pollen self-incompatibility, aging, or allergic reactions also exhibits similar morphological changes. However, the exact apoptotic pathway in plant PCD, which does not involve major animal components like caspase cascade, remains unknown.

Extrapolation and identification of apoptotic parallels in plants will enhance the understanding of programmed cell death (PCD) mechanisms in plants. Interestingly, yeast, a unicellular organism, can undergo a cell death process similar to apoptosis when chemically stimulated with substances such as H2O2, acetic acid, or sugar. This apoptotic-like cell death is also observed during yeast aging and reproduction. Several orthologues of apoptotic genes have been identified (Madeo et al.).

, 2004; Wissing et al., 2004; He et al., 2007). Apoptosis also occurs in crude monocellular protists Dictyostelium discoideum.

The process of chaff formation during starvation in the digestive system includes a cell death process that shows similarities to programmed cell death in animals in terms of morphology. It is suggested that programmed cell death evolves from primitive individual cell organisms and may result from a conflict between archaebacteria and protomitochondria (Blackstone; Kirkwood, 2003). In Dictyostelium, yeast, and plants, phagocytosis is not present in the final stage of programmed cell death, while autophagy has been shown to contribute to the disposal of dead cells (Levine; Klionsky, 2004; Hofius et al., 2009).

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