Examples Of Programmed Cell Death Research Articles

Filling in the gaps: a road map to establish a model system to study developmental programmed cell death

Only a handful of model systems for studying programmed cell death (PCD) exist. The model Arabidopsis thaliana has generated a plethora of knowledge, but it is essential to introduce new models to broaden our understanding of the commonalities of PCD. This review focuses on Aponogeton madagascariensis (the lace plant) as a choice model to study PCD in vivo. PCD plays a key role in plant development and defence. Thus, identifying key regulators across plants is a priority in the field. The formation of perforations in lace plant leaves in areas called areoles is a striking example of PCD. Cells undergoing PCD within areoles can be easily identified from a loss of their anthocyanin pigmentation. In contrast, cells adjacent to veins, non-PCD cells, retain anthocyanins, creating a gradient of cell death. The spatiotemporal pattern of perforation formation, a gradient of cell death within areoles, and the availability of axenic cultures provide an excellent in vivo system to study mechanisms of developmental PCD. The priorities to further develop this model involve sequencing the genome, establishing transformation protocols, and identifying anthocyanin species to determine their medicinal properties. We discuss practical methodologies and challenges associated with developing the lace plant as a model to study PCD.

Programmed cell death in seeds of angiosperms.

During the diversification of angiosperms, seeds have evolved structural, chemical, molecular and physiologically developing changes that specially affect the nucellus and endosperm. All through seed evolution, programmed cell death (PCD) has played a fundamental role. However, examples of PCD during seed development are limited. The present review examines PCD in integuments, nucellus, suspensor and endosperm in those representative examples of seeds studied to date.

Possible Role of Sphingolipids in Developmental Programmed Cell Death of Petunia Petals

A type of programmed cell death (PCD) in animals is due to lysosomal membrane permeabilisation or rupture. One of the suggested reasons is sphingolipid accumulation in the membrane. In plants many examples of PCD, including petal senescence, are due to vacuolar permeabilisation and rupture. Using Petunia flowers, we tested the effect on PCD of sphingolipids and of sphinglolipid synthesis inhibitors. Feeding flowers with five main sphingolipids (sphinganine, phytosphingosine, dihydroceramide, ceramide and sphingosine) hastened PCD. Feeding phytosphingosine together with silver thiosulphate, an inhibitor of ethylene perception, completely prevented the PCD-promoting effect of phytosphingosine, suggesting that its acts through ethylene. Feeding together with the reactive oxygen species scavenger N-acetylcysteine had no effect, while the scavenger ascorbic acid only had a slight alleviating effect. These data suggested that phytosphingosine did not act through reactive oxygen species. Treatments with four inhibitors of sphingolipid synthesis (desipramide, fumonisin B1, myriocin, N,Ndimethylsphingosine) hastened PCD. The data indicate that changes in the endogenous sphingolipid levels resulted in early PCD. The effect of phytosphingosine was abrogated by blocking ethylene perception, suggesting that it acted upstream of ethylene, thus not by directly affecting vacuolar membrane composition.

Hypoxia induced non-apoptotic cellular changes during aerenchyma formation in rice (Oryza sativa L.) roots.

The stress of low oxygen concentrations in a waterlogged environment is minimized in some plants that produce aerenchyma, a tissue characterized by prominent intercellular spaces. It is produced by the predictable collapse of root cortex cells, indicating a programmed cell death (PCD) and facilitates gas diffusion between root and the aerial environment. The objective of this study was to characterize the cellular changes take place during aerenchyma formation in root of rice that accompany PCD. Scanning electron microscopy and transmission electron microscopy were used for cellular analysis of roots. Aerenchyma development was observed in both aerobic and flooded conditions. Structural changes in membranes and organelles were examined during development of root cortex cells to compare with previous examples of PCD. There was an initial collapse which started at a specific position in the mid cortex, indicating loss of turgor, and the cytoplasm became more electron dense. These cells were distinct in shape from those located towards the periphery. Mitochondria and endoplasmic reticulum appeared normal at this early stage though the tonoplast lost its integrity. Subsequently it underwent further degeneration while the plasmalemma retracted from the cell wall followed by death of neighboring cells followed a radial path. However, pycnosis of the nucleus, blebbing of plasma membrane and production of apoptotic bodies were not found which in turn indicated nonapoptotic PCD during aerenchyma formation in rice.

Reduced expression of top1 gene induces programmed cell death and alters ascorbate metabolism in Daucus carota cultured cells

Topoisomerase I (topo I) is a nuclear enzyme which plays a fundamental role in several pathways involving changes in DNA topology. The topo I-mediated reaction is accomplished by the transient covalent binding of the enzyme to DNA (topo I-DNA complex). Stabilization of the topo I-DNA complex, leading to irreversible double-strand breaks, has been reported to occur in animal cells under oxidative stress conditions and during apoptosis. In order to study the existence of a putative link between the topo I-mediated DNA damage and ascorbate (ASC) metabolism, also involved in the responses against oxidative stress and in the apoptotic process in plants, Daucus carota cells showing reduced expression of the top1beta gene encoding the topo Ibeta isoform were produced, using an antisense RNA strategy. Two independent transgenic lines (AT1-beta/22 and beta/36), characterized by a slow growth phenotype, resistance to camptothecin, a specific inhibitor of topo I, but sensitivity to etoposide, an inhibitor of topo II, were investigated in this study. In the absence of external stimuli, AT1-beta/22 and beta/36 cells underwent programmed cell death (PCD) in a precocious phase of the growth curve. ASC metabolism showed remarkable differences in AT1-beta/22 and beta/36 cells, compared with control, and the observed alterations were similar to those occurring in tobacco Yellow Bright-2 cells induced to enter PCD by exogenous stimuli. However, differently from other studied examples of PCD, overproduction of reactive oxygen species was not detected in AT1-beta/22 and beta/36 cells. The relevance of these findings in relation to the signalling pathways leading to PCD is discussed.

Many ways to exit? Cell death categories in plants

Programmed cell death (PCD) is an integral part of plant development and defence. It occurs at all stages of the life cycle, from fertilization of the ovule to death of the whole plant. Without it, tall trees would probably not be possible and plants would more easily succumb to invading microorganisms. Here, we have attempted to categorize plant PCD in relation to three established morphological types of metazoan cell death: apoptosis, autophagy and non-lysosomal PCD. We conclude that (i) no examples of plant PCD conform to the apoptotic type, (ii) many examples of PCD during plant development agree with the autophagic type, and (iii) that other examples are apparently neither apoptotic nor autophagic.

Programmed cell death of tracheary elements as a paradigm in plants.

Plant development involves various programmed cell death (PCD) processes. Among them, cell death occurring during differentiation of procambium into tracheary elements (TEs), which are a major component of vessels or tracheids, has been studied extensively. Recent studies of PCD during TE differentiation mainly using an in vitro differentiation system of Zinnia have revealed that PCD of TEs is a plant-specific one in which the vacuole plays a central role. Furthermore, there are recent findings of several factors that may initiate PCD of TEs and that act at autonomous degradation of cell contents. Herein I summarize the present knowledge about cell death program during TE differentiation as an excellent example of PCD in plants.

Changes in cell structure during the formation of root aerenchyma inSAGITTARIA LANCIFOLIA (Alismataceae)

In many wetland species, root aerenchyma is produced by the predictable collapse of root cortex cells, indicating a programmed cell death (PCD). The objective of this study was to characterize the cellular changes that accompany this PCD in the marsh species Sagittaria lancifolia. Structural changes in membranes and organelles were examined during development of root cortex cells to compare with previous examples of PCD. The organization of cortical microtubule (CMT) arrays in root cells from S. lancifolia was also evaluated as a possible predictor of cell lysis. Nuclear fragmentation and condensation were the earliest changes observed in cells undergoing lysis. Breakdown of the tonoplast and other organelles and disruption of the plasma membrane followed. After loss of cytoplasm, cells collapsed to form gas spaces. These results were compared to collapse of root cortical cells of Zea mays and Oryza sativa during aerenchyma development. Changes in the appearance of the cytoplasm of all three species were similar at later stages of aerenchyma development. The relative timing of disintegration of the tonoplast and middle lamella appeared to differ among the three species. Changes in the organization of CMT arrays did not appear to be a predictor of PCD in S. lancifolia. Aerenchyma production in plants involves a type of PCD that is morphologically distinct from PCD described from many animals.

Role of Ced-3/ICE-family proteases in staurosporine-induced programmed cell death.

In the accompanying paper by Weil et al. (1996) we show that staurosporine (STS), in the presence of cycloheximide (CHX) to inhibit protein synthesis, induces apoptotic cell death in a large variety of nucleated mammalian cell types, suggesting that all nucleated mammalian cells constitutively express all of the proteins required to undergo programmed cell death (PCD). The reliability of that conclusion depends on the evidence that STS-induced, and (STS + CHS)-induced, cell deaths are bona fide examples of PCD. There is rapidly accumulating evidence that some members of the Ced-3/Interleukin-1 beta converting enzyme (ICE) family of cysteine proteases are part of the basic machinery of PCD. Here we show that Z-Val-Ala-Asp-fluoromethylketone (zVAD-fmk), a cell-permeable, irreversible, tripeptide inhibitor of some of these proteases, suppresses STS-induced and (STS + CHX)-induced cell death in a wide variety of mammalian cell types, including anucleate cytoplasts, providing strong evidence that these are all bona fide examples of PCD. We show that the Ced-3/ICE family member CPP32 becomes activated in STS-induced PCD, and that Bcl-2 inhibits this activation. Most important, we show that, in some cells at least, one or more CPP32-family members, but not ICE itself, is required for STS-induced PCD. Finally, we show that zVAD-fmk suppresses PCD in the interdigital webs in developing mouse paws and blocks the removal of web tissue during digit development, suggesting that this inhibition will be a useful tool for investigating the roles of PCD in various developmental processes.