Apoptosis and development
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Role of caspases and the apoptosome. The cytoskeleton. Adhesion molecules. Cell polarity and chemotaxis. Membrane ruffling. Apoptosis occurs during the normal development of multicellular organisms and continues throughout adult life.
The combination of apoptosis and cell proliferation is responsible for shaping tissues and organs in developing embryos. For example the apoptosis of cells located in-between the toes allows for their separation. Apoptosis is also an important part of the regulation of the immune system.
T lymphocytes are cells of the immune system that are responsible for destroying infected or damaged cells in the body. They mature in the thymus, but before they can enter the bloodstream they are tested to ensure that they are effective against foreign antigens and are also not reactive against normal, healthy cells. Any ineffective or self-reactive T-cells are removed through the induction of apoptosis. Problems with the regulation of apoptosis have been implicated in a number of diseases. Cancer is a disease that is often characterized by too little apoptosis. Cancer cells typically possess a number of mutations that have allowed them to ignore normal cellular signals regulating their growth and become more proliferative than normal.
Under normal circumstances damaged cells will undergo apoptosis, but in the case of cancer cells mutations may have occurred that prevent cells from undergoing apoptosis. In these cases there is no check on the cellular proliferation and consequently the disease can progress to the formation of tumors. In many cases these tumors can be difficult to kill as many cancer treatments rely on damaging the cells with radiation or chemicals and mutations in the apoptotic pathway often produce cells that are resistant to this type of attack.
Means were obtained by examining between 14 and 18 embryos for each category. A minimum of 4 and a maximum of 14 sections were examined for each embryo. Pooled data from multiple experiments. If pro-apoptotic factors facilitate apoptosis during metamorphosis of tadpoles into frogs, we would expect over-expression of the anti-apoptotic XR11 to impede metamorphosis.
However, XR11 transgenic tadpoles developed as apparently normal larvae that underwent metamorphosis, losing their transient larval structures, such as gills and tails Fig.
Regulation of apoptosis
The loss of gills is evident by the slimming of the body profile in the pharyngeal region arrow in A. The remnant of the tail is indicated by the arrow in B. Loss of these structures occurs via apoptosis during metamorphosis in response to thyroid hormone [ 42 ]. Metamorphosis of XR11 transgenic tadpoles and responses to exogenous thyroid hormone T 3. An XR11 transgenic froglet undergoing metamorphosis. Responses of one-week old approximately stage 45 transgenic tadpoles to thyroid hormone T 3.
The apoptotic response of one-week old transgenic tadpoles approximately stage 45 to T 3 was assessed in cross-sections through the velum. Demonstration of XR11 over-expression in tadpoles by immunoprecipitation. This experiment was repeated once.
Intestinal development and homeostasis require activation and apoptosis of diet-reactive T cells
To address more specifically whether apoptosis can be triggered by thyroid hormone in XR11 transgenics, we used the metamorphosis induction assay described by Tata [ 43 ] and Huang et al. One-week tadpoles were exposed to triiodothyronine T 3 for five days. As shown in Figure 3C—J , tadpoles transgenic for XR11 displayed the same gross responses to thyroid hormone, including gill resorption, as shown by the GFP transgenics with no discernable delay. The gill apparatus, which is visible in the absence of T 3 arrow in H , regresses after T 3 treatment in both cases.
Discovery of programmed cell death
Meckel's cartilage the lower jaw shows a dramatic beak-like reshaping arrows in F and J. To determine whether apoptosis was occurring equally in the GFP and XR11 transgenic tadpoles, we focused on the ventral velum, a portion of the larval filter feeding apparatus that has a chevron shape in cross section before it dissociates through apoptosis during metamorphosis [ 45 ]. These results indicate that apoptosis that occurred in response to thyroid hormone was unaffected by over-expression of XR One possible explanation for the extensive apoptosis in the XR11 transgenic tadpoles is that the XR11 protein was no longer over-expressed.
However, as shown in Figure 3S , immunoblotting with an antibody to XR11 confirmed that the 22 kDa XR11 protein was over-expressed in the transgenic tadpoles. Proteins were extracted from individual tadpoles at approximately stage 45, separated by electrophoresis, blotted and probed as described in Methods. These tadpoles had been treated with triiodothyronine T 3. Similar results were obtained with samples from untreated tadpoles data not shown. The variation in the GFP signal reflected the intensity of GFP fluorescence in the live tadpoles, presumably reflecting differences in the number of integrated copies of GFP.
The failure of XR11 over-expression to prevent metamorphosis enabled us to rear the resultant frogs to sexual maturity. We induced ovulation in adult females and used the sperm from adult males to obtain second-generation embryos overexpressing XR The results of representative crosses are shown in Table 1. Individual parents were designated by number i.
Crossing the XR male with a wild-type female gave a ratio of transgene positive to transgene negative progeny, suggesting that his genome had integrated the transgene at a single site. Crossing him with the XR female gave a ratio, a result consistent with a single transgene integration site. However, crossing him with the XR female yielded a ratio, suggesting that this female had two transgene integration sites. Consistent with the literature [ 15 ], wild-type embryos subjected to -radiation before the MBT did not undergo apoptosis before the MBT data not shown.
After exposure to 10 Gy Fig. More extensive damage was seen after exposure to 20 Gy Fig. TUNEL-positive nuclei were pervasive. Dissociation of the embryos was so extensive that the embryos often fragmented during the TUNEL procedure. Maternal and paternal expression of the XR11 transgene. A-C , Wild-type embryos. A , Representative control embryos. Arrow indicates the blastopore lip. No evidence of apoptosis is apparent. Embryos that had been exposed to 10 Gy are shown in B.
More extensive damage is seen after exposure to 20 Gy C.
This experiment was conducted three times using eggs from four XR11 females. This experiment was conducted twice using sperm from two XR11 males. Reduced damage from radiation was always observed after exposure to 10 Gy, but protection from 20 Gy was variable from experiment to experiment, suggesting that overexpression of XR11 was not always sufficient to overcome the effects of 20 Gy.
To investigate whether protection from radiation-induced damage was due to maternal or zygotic expression of the transgene, we irradiated embryos derived from fertilizing eggs of wild-type females with sperm from XR11 males and compared them to wild-type embryos. Instead, all embryos resembled irradiated wild-type embryos compare Fig. These results are consistent with a requirement for a maternal source of radiation protection at these early stages. According to the literature, embryos irradiated after the MBT do not undergo apoptosis [ 17 , 19 , 20 ].
Indeed, embryos that were irradiated after the MBT stage However, TUNEL assays showed that irradiation enhanced apoptosis in wild-type embryos, predominantly in the brain, eyes, pharynx and tail bud. Hence, we sought to determine whether the maternal effect of the XR11 transgene was sustained after the MBT and whether zygotic expression of the transgene could also confer radiation tolerance. To do this, we segregated the XR11 transgenic embryos of over-expressing XR11 females from their non-transgenic siblings based upon their expression of the GFP reporter gene under control of the cardiac actin promoter.
Results show that maternal expression of the XR11 transgene protected embryos irradiated at stage When embryos were irradiated during the mid stages late tail bud and examined 12 hours later, the protection afforded by maternal expression of XR11 had diminished significantly in the head and pharynx, although the tail tips were still protected Fig. However, zygotic expression of XR11 was very effective in conferring global protection from apoptosis Fig. Embryos were irradiated at stage GFP-negative embryos lacking the XR11 transgene.
A , Control. GFP-positive embryos containing the XR11 transgene. D , Control.
This experiment was conducted four times using eggs from six XR11 females. This experiment was conducted once using eggs from two XR11 females. To examine the effects of zygotic XR11 transgene expression in the absence of maternal expression, we irradiated stage Progeny were scored 12 hours later for GFP expression directed by the cardiac actin promoter to confirm the presence of the transgene.
Apoptosis in Embryonic Development | The Embryo Project Encyclopedia
As shown in Figure 6A—F , there was extensive apoptosis in both the heads, pharynges and tail tips of irradiated neurula-stage embryos and no discernable difference in the levels of apoptosis observed between the GFP-positive and GFP-negative embryos. Embryos that received 20 Gy radiation Figs.
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These results suggest that zygotic expression of the transgene had little effect in preventing apoptosis at this stage. However, when sibling embryos were irradiated in the mid stages and examined 12 hours later, the transgene conferred global protection from apoptosis Fig. Note particularly the extensive apoptosis that is evident in the otic capsules arrows in Fig. GFP-negative embryos. This experiment was conducted three times using sperm from five XR11 males.
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This experiment was conducted once using sperm from two XR11 males. The experiment could not be repeated due to the unavailability of additional XR11 males. To correlate transgene expression with repression of radiation-induced apoptosis, we monitored XR11 RNA expression and protein levels Fig. On the contrary, there was no evidence for expression of the XR11 transgene in embryos derived from wild-type eggs fertilized by XR11 sperm. Immunoblots Fig. This experiment was conducted once.
Because the XR11 protein is membrane-bound, it is difficult to separate it from yolk, which is abundant in embryos. The presence of yolk during electrophoresis results in wavy bands in the gel.