Introduction
Programmed Cell Death, also referred to as cellular suicide or apoptosis is the death of a cell from its own intracellular mechanism. This particular term was first used by Williams and Lockshin back in 1964 while referring to tissue development in insects. The word apoptosis comes from the Greek word apoptosis, which translates to "falling off" like leaves from a tree. It occurs through a biological process that is vital in the individual's life cycle. Like during the formation of an embryo's toes and fingers, the differentiation of the same is as a result of the apoptosis process by the cells between the fingers and the toes. It is a very important process in the cells development process. For there to be balance within an organism, the body must control both cell division and cell death. In most cases, the activation of cellular suicide occurs when the cell is no longer in need.
There are two types of cell deaths apoptosis, which is also known as Type I cell-death and autophagy, also known as Type II cell death. However, for the purposes of this study, the main focus will be on Type I cell-death. Apoptosis is a process that mainly takes place in multicellular organisms. It is triggered by biochemical reactions that involve cell change, otherwise known as morphological changes and eventually cell death. Most of these changes include shrinking of the cell, blebbing, chromatic condensation, chromosomal DNA fragmentation and nuclear fragmentation. On one side is the death of cells from a developmental point of view which involves inducing a positive signal for the cell to commit suicide while from the homeostatic point, the absence of vital survival factors tiger suicide.
There are various processes that lead to programmed cell death. Some of these processes follow a defined path of apoptosis while others take a more generalized path that leads to deletion. Both of these processes are synthetically and genetically motivated. True apoptosis is genetically mediated. Research indicates that the process of apoptosis and mitosis are linked in such a way that they provide balance in the organism and ensure its survival depending on the internal signals that are appropriate for either survival or growth. Factors that promote the death of a cell are referred to as atrophic factors. In most cases, most of these factors are as a result of natural forces, whereas, agents of chemical or mechanical stress or lysis of the cell are not considered to be atrophic factors.
Programmed Cell Death in Plants
According to Reape et al. (2008), programmed cell death in plants is an essential component in the defence and development mechanisms. In the defence process, it acts as a response mechanism in the restriction of the spread of pathogens. It also plays a vital role in the proper development and growth of the larger multicellular body plan. It is also important to note that apoptosis is controlled as compared to necrosis. This means that the process in both plants and animals is systematic. One such example is cellular destruction through apoptosis which is activated by caspases which are a family of cysteine proteases. There is a need for the caspases to be activated for the entire process to commence and the extrinsic death receptors or the intrinsic pathway is responsible for this step. The main organelles that take part in this process are the mitochondria as well as the release of the cytochrome c.
Presence of cytochrome c triggers the assembly of the apoptosome, which is a caspase-activating complex located in the cytoplasm. According to various studies, most regulators in the programmed cell death process promote or inhibit the loss of mitochondrial integrity. Necrosis is different from apoptosis in that it is defined as the uncontrolled death by cells as a result of stress which makes it difficult for the cell to trigger the apoptotic pathway. It is also different from apoptosis in that it causes cell swell instead of shrinkage as the defining feature in the morphological change. This is a result of a mechanism to regulate the rate of osmosis that leads to ion and water flooding in the cell (Lennon et al., 1991).
Programmed cell death is the facet for many developmental programs like the start of the plant's life cycle, development and formation of wood otherwise referred to as xylogenesis, and the end of the plant's life cycle also known as senescence. The process is also behind many cases of cell deaths that are witnessed in plants. Ultimately, this has led to confusion in the world of plant science. More research must be done to determine the differences between the different cell death types. Some researchers have gone on to test the level at which apoptosis is activated in plants. Researchers were able to establish programmed cell death results in the withdrawal of the cytoplasm in the presence of stressful conditions. Initially, it was through that in the presence of high levels of stress, and the cell collapsed on its own.
The process of apoptosis in plants leads to the formation of apoptotic bodies that are as a result of breaking up of the cell. Phagocytes then engulf these bodies. Recent studies indicate that even in the absence of evidence for classical caspases commonly found in the Arabidopsis genome, there are caspase-like molecules in the plant a feature that is supported by the caspase substrates that were cleaved during the programmed cell death process in plants. Further evidence suggests that DNA and other genes associated with apoptosis are also found in the programmed cell death in plants. Researchers have identified some plant cell deaths that resemble apoptosis but are also different from apoptosis in plants.
For this reason, Danon et al. (2000), suggests that morphologically distinct types of PCD should be referred to as apoptotic-like PCD (AL-PCD). Autophagy is also an example of programmed cell death that is also induced in the Arabidopsis suspension cultures as a result of carbon starvation. In most cases, the process is slow as seen when the plant is deprived of sucrose, but the viability of the cells is not altered with the first 24 hours of this deprivation.
There exists a significant difference between apoptosis and necrosis in both plant and animals. In plant culture, the main difference between the two is dependent on the severity of the stress. In an experiment carried out by some researchers, it was found out that cells undergo apoptosis-like programmed cell death in the presence of moderate stress like heat and those that are subjected to higher levels of stress die as a result of necrosis. One morphological difference during the apoptosis-like programmed cell death is the condensation of the protoplast towards the inner section of the cell and away from the cell wall.
Another distinguishing factor is the DNA cleavage. The apoptosis-like programmed cell death is different from programmed cell death in that PCD-activated nucleases cleave the DNA at linker sites that are located in the nucleosomes and in the end, the DNA is divided into fragments that are multimers in nature. These fragments are approximately made up of 180 base pairs, and when they are separated using electrophoresis in agarose gel, they run as a ladder pattern.
Unlike in animals, little is known about the components that initiate and sustain the process of programmed cell death in plants. This makes it challenging to track all the events that trigger processes like apoptosis-like programmed cell death and the death of that particular cell. Some researchers, however, have synchronously used biotic and abiotic stresses to initiate apoptosis-like programmed cell death as well as monitor the key events that eventually lead to cell death. One similarity between apoptosis-like programmed cell death and animal apoptosis is the release of the apoptogenic proteins from the mitochondria. Cytochrome c is also released from the mitochondria when exposed to heat stress. Cytochrome c relocation also takes part in the pollen tubes when the plant is trying to prevent self-fertilization as a result of self-incompatibility induction.
Programmed Cell Death in Animals and how it compares to that of the plant
The cell death system in animals is different from that in plants. It is divided into three categories, namely, Type I or apoptosis, Type II or autophagy cell death, and Type III or necrosis (Lockshin and Zakeri, 2004). Autophagy is different from apoptosis and necrosis in that it involves a self-eating mechanism that includes cytoplasmic materials that are degraded in the lysosomal activities in the cell. The main feature in this process is the formation of autophagic vacuoles, the dilation of the endoplasmic reticulum and the mitochondria as well as the enlargement of the Golgi apparatus. In that case, autophagy is mainly used to refer to the fatal destruction of cells.
Programmed cell death is involved in hypersensitive responses, like in the case of pathogenic attacks and stress responses. In animal cells, the process of cell death by either apoptosis or necrosis can be experimentally induced using varying levels of stress. Such inductions have proven to be critical in the laboratories as scientists try to distinguish the different forms of cell deaths and the factors surrounding them. In one of these experiments, researchers subjected tumour cells to several noxious stimuli to determine the threshold required to trigger cell repair and controlled apoptosis. High levels of stress resulted in uncontrolled necrosis. The apoptosis-like programmed cell death morphology is witnessed during the hypersensitive response that is seen in plants. This is a similarity that indicates that both plants and animals used the programmed cell death process a hypersensitive reaction.
In animals, the loss of mitochondrial transmembrane is identified as the committal step in the programmed cell death process. The morphological changes recorded in Type II/ autophagic programmed cell death in animals is similar to those seen in the development and growth of plant programmed cell death. Another similarity between programmed cell death in animals and plants is the central point of regulation. As indicated earlier in the study, the process of cell death required regulation. The mitochondria offer primary regulators that are responsible for all types of cell deaths.
Regulation by the mitochondria is vital in integrating programmed cell death and /or stress signals in both plant and animal cells. The process begins by releasing apoptogenic proteins from the inner membrane space of the mitochondria, which triggers apoptosis. The release of the apoptogenic proteins is regulated by the Bax/Bcl-2 pore or the Permeability Transition (PT) pore. The process is different in animal cells because the Bax/Bcl-2 pore can selectively release IMS proteins which in turn activate the caspases. Formation of permeability transition pores is also not unique to animal cells as there is evidence to support the presence of PT pores that operate in plant cells. These pores also help in the release of programmed cell death activating molecules. This is because the three essential components that make up the PT pores are also present in plants. They include cyclophilin D, adenine nucleotide transporter, and voltage-dependent anion channel. However, plants still lack the classical caspase family that is vital in the true apoptosis process.
The transition process from apoptosis to necrosis is almost identical in both animal and plant cells. Moderate loss of the membrane in the animal cells would result in the release of the mitochondrial IMS proteins in the form of cytochrome c that would activate the caspase-like molecules, which eventually leads to apoptosis. A more severe loss of the membrane would have a catastrophic effect on t...
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