Function and Regulation of Anti-Cell Death Genes in Plant Development

Subject: Science
Type: Analytical Essay
Pages: 20
Word count: 5058
Topics: Biology, Experiment, Microbiology


The role played by plants in promoting the wellness of society and enhancing the sustainability of the planet’s ecosystem has rarely been contested since the advent of agriculture. However, with the continuing trends of human development, the transition of plant use for facilitating manufacturing activities continues to weaken the traditional role played by plants. Therefore, several studies have been conducted with the aim of establishing the best ways through which plant development can be assured, taking into consideration the environmental response and evolutionary patterns of the modern society. Through these efforts, scholars established anti-cell death as a method of plant development 

Anti-cell death is a technique adopted by multi-cellular organisms as a defensive and developmental mechanism (Franklin-Tong and Gourlay, pg 390). In animals, morphological distinctions have since been used to distinguish different types of cell deaths, including apoptosis, necrosis and autophagy. On the other hand, similar morphological terms are currently being developed to distinguish different types of cell deaths in plants. Primarily, the aim of anti-cell death in animals is to describe the processes of autophagy and apoptosis, while necrosis is the mechanism for defining the uncontrollable or chaotic mode of death. 

The term anti-cell death is used extensively to describe the observed instances of death in plants. Studies indicate that there are diverse plant developmental systems and a consortium of plant cell culture models being analyzed by different research centers. From the available bulk of literature, it is evident that there are several types of anti-cell deaths in plants. Therefore, there is need for fundamental distinction between the different types and functions of genes that are involved in anti-cell death in plants. 

Evidently, it has been established from the above outline that cell death plays a pivotal role in the innate responses in both animals and plants. The main aim of this paper is to review the pathways that lead to cell death in plants with a purpose of identifying the anti-cell death genes. Additionally, this discussion expands its mandate by analyzing the function and regulation of anti-cell death in plant development. Using relevant sources of literature, the paper delivers a systematic analysis of fascinating analogies between cell death and plant development with respect to the primary functions of cell death as stipulated in the introductory outline of the discussion. At the end of the discussion, significant insights will be developed to paint a picture of the emerging trends in plant development with respect to the topical research on anti-cell death genes.


There have been several attempts to analyze the concept of cell death in plants since the experimental demonstrations in studies conducted in the 1980s and the 1990s with the aim of dissecting the programmed nature of plant cell death (Xinqiang and Hong, pg 354). The dominant discovery in these experiments indicates that there is a heterologous expression of certain genes in plants that can regulate cell death. Since this discovery, the field of plant programmed cell death has continued to grow, with maturity depicted in studies aimed at distinguishing the roles of plant cell deaths in plant development. Majority of the literature and experiments in the field of programmed cell death in plants draw heavily on comparative analysis retrieved from paradigms of animal systems such as apoptosis, necrosis and autophagy. Despite this, there are adaptive characteristics and distinctive features that that distinguish the lifestyle of plants from those of animals, hence the adoption of only distantly related components in revealing the genetic regulations of plant cell death. 

Cell death refers to a series of events that culminate in the organized and controlled destruction of the cell. In plants, cell death is a fundamental process, as it plays the roles of controlling the elimination of cells during plant development and defense in the form of hypersensitive response. The activation of cell death by plants is dependent on the decision by the plant cells based on information that these cells receive from different sources, such as the environment. Other factors have since been linked with the decision by plant cells to activate cell death, including cell survival signals, stress signals, developmental cues, pathogen recognition and metabolic state. However, this decision is largely determined by internal information on factors such as the developmental history of the plant cell and the cellular damage. 

There are different types of cell deaths that occur in plant cells. The most common type of cell death in plant cells is denoted by condensation of the protoplast away from the cell wall. Scholars have managed to visualize this distinctive morphology in plant cells that have died due to stress or hypersensitive responses during their developmental programming phase (Coll, Epple and Dangl, pg 1248). Plant cells can survive mild stress, hence delegating the function of cell death in stress control to particularly higher levels of stress. During high stress levels, plant cells are induced by the stress to initiate a programmed cell death system that results in dead cells with condensed protoplasts. Necrosis is the term often used to define the death of plant cells owing to stress, despite the fact that cells do not always show the distinctive morphology that leads to death from stress. 

Cell death is a physiological process that selectively targets the elimination of unwanted cells. A distinct difference between cell death in plants and animals is the function played by this process. In animals, cell death often results to diseases such as Parkinson’s disease, Alzheimer’s disease, Lou Gehrig’s disease and Huntington’s disease. Cells in animals play a significant role in tissue specialization and homeostasis. Cell death in animals can cause disassembly of the cell, which manifests in shrinkages condensation and fragmentation of the cell nucleus and cytoplasm (Reape and McCabe, pg 18). This destroys the nucleus of the DNA, hence damaging the optimal cell functioning of animals. 

In plants, however, cell death is selective, and purposefully targets the growth and survival of the plant. Primarily, cell death in plants causes the deletion of the suspensor and aleuronic cells that serve temporary functions during plant development. These processes also eliminate the stamen in female flower unisexual plant species. Therefore, cell death in plants causes the formation of leaf lobes and perforation, which play a role in specialization of the cells. 

Clear evidence indicates that cell death in plants involves a process referred to as programmed cell death (PCD) (Kumar, pg 39). Cell death during plant development and interactions with the environment involves the process of PCD. Therefore, cell death in plants occurs during the reproductive phase of plant development. For instance, cell death occurs in the elimination of non-functional spores and their cells in the cell lines of plants. In as much as the relationship between the genes involved in cell death in animals and plants are unknown, significant consideration has been directed towards analyzing the possible evolutionary origins of cell death in plants. 

To understand the complex death mechanisms in plants, it is imperative to examine the particular programmed cell death morphotype. Besides, this process requires the adoption of integrated approaches to cellular observation, including the biochemical and genetic approaches. In light of the divergent approaches to understanding the concept of cell death in plants, this discussion adopts the genetic approach, thus presenting cutting edge knowledge regarding individual specific aspects of cell death. This discussion, therefore, incorporates the classification of plant cell deaths based on the genetic approach. Just like other studies that have classified animal death classification, this study establishes the nomenclature of plant cell death morphology and adopts a unified criterion of their definition based on the genetic approach. 

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Process of cell death in plants

Multi-cellular organisms are developed through the repeated process of programmed cell differentiation and cell division. This is referred to as cell cycle event, which is genetically regulated and programmed. There are several factors that cause deaths in cell tissues. However, in plants, death of cell tissues is more common in older plants, and is attributed to injury, which leads to necrosis, the death of these cells. However, younger and more active cells often die due to injury at the molecular level, which is inflicted on specific cells or on neighboring cells. These are the internal and external factors that explain the need for plants to have the inbuilt sensory mechanism through which the program of cell death is initiated. Cell death often translates to loss in cell tissues. However, through genetic orientations, cell replacement occurs where the quiescent cells are activated to subsequently divide until the lost number of cells is cancelled out (Fannjiang, pg 2788). 

In plant cells, just like animal cells, the death of cells is referred to as necrosis. Necrosis in plant cells mostly occurs when the cells are injured. Besides injury, there are several other factors that cause necrosis in plant cells. During necrosis, plant cells get injured, and punctured by injurious components that cause damage to the neighborhood cells. There are several ways through which necrosis manifests on plant cells. 

Paraptosis refers to the swelling of cells, and development of large bubbles with liquid. This does not employ the caspases, which is often witnessed in animal cells (Kumar, pg 36). Similarly, plant cells can die through developing crates inside, which allow cell organelles to escape from the cell. This leads to destruction of the organelles by proteases within the cell. This type of plant cell death is referred to as autoschizis. In this type of cell death, the normal cells are often left intact and unaffected. This cell death causes exaggerated damage on the cell membrane, which leads to progressive cytoplasm loss. 

Plant cells can also die from oncosis, which refers to the expansion of the cells due to uncontrolled intakes of water. This method of cell death acts largely on the protein, which become denatured hence allowing for the intake of excessive calcium into cells. This death of plant cells can be attributed to the differential distribution of proteins on either side of the mitochondrial membrane. Oncosis is Adenosine Tri-Phosphate independent, thereby explaining why its manifestation can proceed without the mitochondrial function (Daneva et al, pg 453). 

In apoptosis, programmed cell death of plant cells is identified through morphological manifestations. Apoptosis, unlike oncosis, autoschizis and paraptosis, is stimulated by certain factors that will be discussed later in the paper. Apoptosis leads to the fragmentation of DNA and the intracellular organelles. This type of cell death causes the cell to collapse, hence producing blebs and membranous vesicles out of the surface of the cell. Cell death in plants is perfected by the generation of information within the cell structures. Death of plant cells often is preceded by structural modifications of the remaining cells, as the modified dead cells are replaced with other cells that perform specific functions. 

The pathways of cell death in plant cells are activated through responses resulting either from the internal or external environment. The external environment constitutes factors such as those that expose the plant cells to possible injury. On the other hand, the internal factors include the signals from DNAs and cell-survival instruments. The internal pathways for cell death in plants are hinged on the activity balance between the anti- and pro-apoptotic signals. On the other hand, the external pathways begin outside the cell, and manifest through the activation of the pro-apoptotic receptors that are situated on the surface of the cell. 

In the plant cells, apoptosis is often induced by injury and the lack of essential growth inhibitors. Besides, there are certain plant cells that are marked for apoptosis, including the cells that have no function (Franklin-Tong and Gourlay, pg 401). The cells often communicate to establish the cells that are excess, and functionless, thereby subjecting them to death. Besides, plant cells that develops at improper places or during improper period of the developmental cycle is induced to apoptosis. In the course of plant development, different cells play different roles. Upon completing their designated functions, cells are rendered harmful to other cells. Therefore, cells that have completed their function are marked for death due to the harmful threat they present to the other cells.

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Function of Anti-cell death genes in plant development

The plant cell is subjected to constant signals from the external and internal environments. By sensing these signals, plants are forced to act on them. The plant cell should coordinate these signals in order to make a decision to undergo programmed cell death. The mitochondrion plays a significant role in controlling cell death in plant cells (Yang et al., pg 1022). However, minimal information exists on the exact role that the mitochondria plays in executing cell death to realize plant development. From different studies, the contributions of genes, proteins, and individual organelles to cell death can be developed. However, it is unlikely that the any plant organelle or molecule acts alone during cell dead. Similarly, individual molecules and organelles behave in a uniform fashion to facilitate programmed cell death. Therefore, to understand the function of anti-cell death genes in plant development, an analysis of the mitochondrion genes is necessary. 

Cytochrome is a plant protein that contains genes that denote the catalytic activities in plant cells. The cytochromes are located inside the mitochondria, and play a vital role in defining the cell death in plants following stress. Cytochrome is released from the mitochondria during the developmental phase of the plant cell. Plants cells, unlike animal cells, do not have caspases, a factor that disqualifies the occurrence or apoptotic activities caused by events that lead to the death of plant cells. Significant amount of evidence indicates that during plant cell death, the cytochrome generates a string of activities that associate with plant subtilizing (Coll, Epple and Dangl, pg 1254). This breaks down the plant mitochondrion in a cell-free system that results in condensation of chromatin and high molecular with of the DNA. This also leads to laddering of the DNA. 

Genetic functions strongly relates to the release of mitochondrial proteins. During the stress response, cytochrome and other death inducing molecules are subsequently released from the mitochondria. Normally, the outer membrane of the mitochondrion is maintained through a balance of the anti-apoptotic and pro-apoptotic proteins. Therefore, proteins such as cytochrome are prevented from being released from the mitochondria under the normal conditions. However, the endoplasmic reticulum inhibitor induces sell death through initiating a hypertensive response when the plant is exposed to viral vectors. Besides, when this inhibitor is expressed to the plant cell, resistance to death can be conferred by known activities of the cellular genetic composition. 

Anti-cell death genes in plants are activated to sustain the cell survival by reducing the protein accumulation in the endoplasmic reticulum. This is conducted through the process of unfolded protein response, which promotes cell deaths when the endoplasmic reticulum stress is high. In plants, however, the underlying genetic mechanism is less understood, with the key genetic regulators for cell survival in the plant endoplasmic reticulum identified as membrane-associated transcription factors (Yang et al., pg 1036). 

In the plant cells, endoplasmic reticulum is the primary site for the production of organelle proteins and secreted plasma membrane. Plant cells have a unique quality control system that ensures the accuracy of cell death through the optimization of cell death machinery and the endoplasmic reticulum- associated genetic degradation. In order to coordinate the capacity of cell deaths to the demand for cell replacement, signaling pathways are genetically conserved. This conservation encourages the sensing of the accumulated proteins in the endoplasmic reticulum and sustains the homeostatic balance. 

Plant development following cell death envisages the repair of the dilapidated plant cells (Xinqiang and Hong, pg 366). It is difficult to detail and characterize the role that genes play in facilitating the repair of plant cells, though a major component of cell repair is protein. Genes are vital in protein synthesis, a process which is induced immediately after the decision to program cell death is reached. The speed of this recovery, moreover, is dependent on the internal information stored in the genes of the plant cells. In as much as programmed cell death morphology is described in the hypersensitive response in plants, significant literature developed to target morphology during normal growth and development indicates conformity between the plant and animal autophagy. 

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Autophagy in plant cells plays a major role in distinguishing between the apoptotic and necrotic phases. 

In many instances, several developmental cell deaths in plants are not typically autophagic in their description of dying or dead cells. For instance, the tapetum development of angiosperms causes shrinkages in the whole nuclei and cell, as well as condensation of the chromatin at the internal nuclear membrane periphery (Yang et al., pg 1015). Therefore, genes are significant in highlighting the morphological features that occur at different developmental stages of cell death. The genes play a pivotal function in the fragmentation of the nuclear DNA, which condenses the cells and nuclei. The genes, furthermore, explain the existence of suspensor-like cells in embryogenic cell cultures, which display the condensed morphology that is associated with plant cell death. 

The anti-cell death genes play a vital role in understanding the homeostatic role of the main catabolic processes of plan cells. Systematic analyses have been made in an attempt to establish the involvement of these genes in disease resistance and cell death in plants. Findings illustrate that the anti-cell death genes lead to opposing effects on the progression of cell death (Coll, Epple and Dangl, pg 1252). However, several factors determine the validity of these findings, including the age and the patho-system of the infected tissues in the cell. As such, anti-cell death genes help in plant development through explaining the pleitropic impact that defective plant cells have on the physiology of the whole plant. Using similar mechanisms, these genes establish how the death resistance and cell death are affected by the cellular functioning of synthesizing information about cell death.

Plants cells are encased in rigid cell walls that limit the abilities of cells to exhibit dynamic changes in sizes and shape, even after receiving cell death signals. Anti-cell death genes play a significant role in facilitating the changes that characterize intracellular disassembly. These genes conduct such processes through modeling the microfilaments and microtubules. During cell death, structural alterations are common on the cytoskeleton structure of the plant cell. There are diverse models that can be used to identify the causes of cell death in plants. Even so, the anti-cell death genes determine the progression of cell death in plants, hence playing a vital role in signaling the initiation and execution of cellular controls in the plants. The genes, moreover, distinguish the correlating cytoskeleton dynamics that define the death processes of plant cells.

As explained earlier in the discussion, the process of cell death in plants is evolutionary. There are a number of proteolytic pathways that have evolved in plant evolution. These pathway can be categorized either as biochemical or physiological. Consequently, cell death in plants exhibits morphological features that can be compared to the caspase mediated apoptosis in animals. Therefore, plant cell death is executed by proteases (Fannjiang, pg 2790). The recent characterization of cell death associated the anti-cell genes with activities that demonstrate the involvement of plant proteases in plant programmed cell death. The anti-cell death genes, moreover, are responsible for determining the proteolytic activities whose functioning resembles that of animal caspases. 

The process of cell death in plants is regulated by enzymes, which are determined by the anti-cell death genes. There are some proteolytic enzymes that have been found to mediate programmed cell death in plants, including serine proteasts, proteases sub-unit enzymes and enzymes produced for processing vacuoles (Bozhkov and Lam, pg 1240). The role of anti-cell death genes is described in the abiotic and biotic stress-induced cell deaths. One core feature of these genetically determined proteases is that their constitutive activation in the living cells is determined by the genetic composition of the cellular tissues in plant cells. The anti-cell death genes, additionally, facilitate the export of these enzymes to the apoplast, where the cell death stimulus enters the cell. From this illustration, it is evident that the anti-cell death genes play a pivotal role in determining physiological balance between enzymes that activate and export the cell death stimulus. For that reason, anti-cell death genes perform a key function of molecular regulation, which plays a large role in programmed cell death in plants. 

The vacuolar processing enzymes (VPEs) are found inside vacuoles. These enzymes play a pivotal function in the plant development. The lytic vacuoles facilitate programmed cell death in plants at the developmental stages (Vanyushin et al., pg 148). During the execution of programmed cell death in plants, the lytic vacuoles are activated to kill the intercellular pathogens. The anti-cell death genes aid the process of programmed cell death by cleaning up the intracellular contents during development. The plants, therefore, depend on anti-cell death genes to combat the bacterial pathogens that accumulate in the apoplast. These genes activate the lytic vacuoles to develop a defensive mechanism for the plant against pathogens. 

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The plant cell death community and plant biologists have established that structural features developed by genes are important to the cell death processes defined in these plants (Bozhkov and Lam, pg 1239). There are several ways that this discussion has highlighted the role of anti-cell death genes in plant development. They include the specific fragmentation of the cytoplasm, inter-nuclear somatic fragmentation of the DNA nucleus, cessation of nuclear DNA synthesis and synthesis of the mitochondrial DNA. The anti-cell death genes have been linked with inducements on structural changes in the organization of the cellular organelles, as well as the formation of membrane structures in the cytoplasm. 

Regulation of anti-cell death genes in plant development

Just like in animals, programmed cell death can be used in explaining plant developments and adaptations to stressful environments. The control of cell death in plants is however, not the same as that in animals. In animals, with more specificity on mammals, the conserved proteins have been linked with predominantly controlling cell death. On the other hand, no such genes have been identified and subsequently linked with performing similar function in plants. As discussed in the above section, the apoptotic processes in plants involve release of mitochondria proteins. The control of these proteins is done by enzymes. 

Significant amount of research has been directed towards establishing the control and regulation mechanism of cell death in plants (Daneva et al, pg 447). The process of linking this mechanism to the genetic composition of cell tissues can be difficult, considering the fact that it often occurs in small groups of inaccessible cells that are surrounded by healthy tissue. Despite this, the regulation of anti-cell death genes in plants is studied using the cell-culture induced cell death. This concept manifests through certain hallmarks identifiable with animal apoptosis, including DNA degradation, distinct morphology and the release of cytochromes. Cell culture plays a pivotal role in understanding the control and regulation frameworks of anti-cell death genes. 

In plant necrosis, heat shocks in the plant cells are often used to depict the shift from live cells to dead cells. Naturally, it is necessary for plant cells to regulate these shocks. The mitochondrion plays a significant role as a regulator of the activities that lead to all types of cell deaths in plants. This further illustrates that the mitochondria plays the central regulatory role in integrating the stress and cell death signals in plants (Vanyushin et al., pg 168). In the mammalian cells, for instance, the release of apoptotic proteins is responsible for triggering the process of cell death. This release occurs from the inner membrane space of the mitochondrion. There are limited studies that show plant families operating similar to the mammals in regulating the process of apoptosis. In plants, the mitochondrion releases molecules that activate programmed cell death. 

In plant cells, the PT pores play a central role in regulating the process of apoptosis. Besides, the three main components of the PT pore are present in animals, including cyclophilin, adenine nucleotide transporter and voltage dependent anion channel (Franklin-Tong and Gourlay, pg 393). The activation of these elements of the PT pore in plant cells explains the sudden switch that plant cells undergo in necrosis. The opening of the mitochondrial pores indicates that the regulation of activities between the living and necrotic states in plant cells is regulated by the mitochondria. 

The process of necrosis in plant cells is denoted by a chain of events that follow the effectors’ recognition through the plant receptors. There are signaling modules that regulate the receptor proteins, which are the senescence associated genes and the non-race specific disease resistance. These are the two anti-cell death genetic structures linked with the regulation of plant cell death. These two generic systems play a key role in creating the defense responses after the accumulation of the proteins. 

Plants do not have the close caspase homolog, which perform the regulatory functions during the process of cell death in animals. Several studies indicate that despite this, the presence of hypersensitive response protease activities is identifiable with plant necrosis (Fannjiang, pg 2795). The vacuolar processing enzyme (VPE) exhibits a casapase-like activity during the hypersensitive response. During this process, the fusion of vacuoles to the plasma membrane is mediated by caspase like activity. Therefore, the functional relevance of the anti-cell death genes is determined by the regulation of the vacuolar processing enzymes, which is a plant proteasome sub-unit. 

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The plant immune system is integral in the plant development process. This system is associated with the hypersensitive response cell death, and is among the most dramatic manifestations of programmed cell death in biology. The mechanism of regulating hypersensitive response cell death has been discussed above, though limited information exists on the evolutionary trends that can be used to explain this cell death using the anti-cell death genes. The type 1 metacaspase-dependent regulatory module is a genetic feature that translates the immune receptor medicated recognitions of pathogens into the activation of cell death in the downstream. 

The regulation of plant cell death does not end with the vacuolar processing enzymes VPE. The catabolic processes of plant and animal cells are essential in understanding the homeostatic role of autophagy. The systematic analysis aimed at reconciling the contradictions of the regulation of the anti-cell death genes involved in autophagy indicates that there are links between the hypersensitive response cell death and death resistance (Bozhkov and Lam, pg 1240). The analysis further illustrate that ATG genes are leading the opposing effects on the progression of cell death. This is dependent largely on the age and the pathosystem of the infected tissues. 

During plant programmed cell death, control of the method of mitochondria protein release is conducted by an enzyme known as hexokinase. This enzyme catalyzes the initial set-up in the intracellular glucose metabolism. Hexokinase is associated with mitochondria, and plays a vital role in regulating the programmed cell death in plants. The anti-cell death genes, furthermore, are regulated through the binding between hexokinase and the mitochondria. The mitochondrion is maintained by the serine kinase, which performs the function of controlling plant apoptosis in the presence or absence of the signaling genes. 

The life cycle of plants is denoted by continual production of reactive oxygen species (Reape and McCabe, pg 22). These processes occur in the chloroplasts and mitochondria, and are regarded as by-products of metabolic processes such as photosynthesis and respiration. The reactive oxygen species (ROS) regulate the anti-cell death genes through transfer of electrons to oxygen in the form of singlet oxygen, hydroxyl radicals and hydrogen peroxide. The reactive oxygen species are often very toxic, and the ability to oxidize and damage the cell components such as enzymes proteins, membrane lipids and nucleic acids being documented in several studies. The toxic nature of these species is significant in converting the destructive radicals from anti-cell death genes to antioxidants, hence preventing the damage of cells that were not marked for damaging. There is an interface for environmental and metabolic signals that modulate induction of the cell’s acclimation to stress, and subsequent activation of programmed cell death in plants. Therefore, the toxicity of reactive oxygen species is significant in signaling the molecules in plant cells. 

The continuous adaptation to fluctuating environments is a natural feature of plants. However, light is among the major factors that determine the control of growth, development and survival in plants (Daneva et al, pg 461). The plant’s response to biotic and abiotic stress is dependent on light, as well as the progression of the hypersensitive response and the wound response. The chloroplast, just like the mitochondrion, plays a central role in regulating anti-cell death genes. The role of the chloroplasts in regulation of plant development is the regulation of photosynthetic efficiency and inhibition of plant growth. This is conducted through reactive oxygen species that help in catalyzing the excess excitation energy, which is any light that the chloroplasts receive in excess of the required amount for photosynthesis in the photo system. The higher light intensity increases the excess excitation energy, hence regulating the reactions of the anti-cell death genes.


In plants, significant amount of research has been directed towards establishing the main reason behind the occurrence of cell death. Traditionally, the cell death in plants was envisioned as a mechanism through which the plants prevented the growth of pathogens in incompatible plant-pathogen interactions. Today, emerging trends indicate that researchers are using the concept of cell death in plants to explain the causal to disease resistance in plants.

From the discussion above, it is evident that the anti-cell death genes in plants are not responsible for inhibiting the proliferation of cell death in plants. Instead, these genes play a key function in inhibiting the proliferation of pathogens through dictating the interactions between plants and pathogens, hence resulting in resistance without cell death being reported (Vanyushin et al., pg 179). The resistance from cell death in plants inhibits the pathogen-induced dell death devoid of affecting the disease resistance.

This discussion adds onto a new dimension on how the recognition of anti-cell death functions and their subsequent regulations can determine the process of plant development. The implications of this study are essential to plant biologists and cell death researchers, who have dedicated their studies to analyze the restriction of pathogens and cell death.  

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