"Cell Executioner" Gene 203
slantyyz writes: "A fascinating and possibly scary scientific discovery -- Toronto scientists have discovered a "chisel of life" gene that kills cells. Apparently this ancient gene, dubbed AIF [apoptosis (death) inducing factor] is found across all forms of life and acts as a cell executioner. While this could have uses in killing cancer cells, it could potentially open the discovery of a true fountain of youth." Nature has more, if you're a subscriber.
THIS IS OLD ! (Score:1)
Re:Could be useful. (Score:1)
What about immediate age (Score:1)
/. idiots post shit I can't read (Score:1)
article that most of us can't read because
you NEED A PAID SUBSCRIPTION. That's really
/.gay. What the hell, michael? At least
write a detailed summary or something,
the abstract...and the full test (Score:1)
Programmed cell death is a fundamental requirement for embryogenesis, organ metamorphosis and tissue homeostasis. In mammals, release of mitochondrial cytochrome c leads to the cytosolic assembly of the apoptosome-a caspase activation complex involving Apaf1 and caspase-9 that induces hallmarks of apoptosis. There are, however, mitochondrially regulated cell death pathways that are independent of Apaf1/caspase-9. We have previously cloned a molecule associated with programmed cell death called apoptosis-inducing factor (AIF). Like cytochrome c, AIF is localized to mitochondria and released in response to death stimuli. Here we show that genetic inactivation of AIF renders embryonic stem cells resistant to cell death after serum deprivation. Moreover, AIF is essential for programmed cell death during cavitation of embryoid bodies-the very first wave of cell death indispensable for mouse morphogenesis. AIF-dependent cell death displays structural features of apoptosis, and can be genetically uncoupled from Apaf1 and caspase-9 expression. Our data provide genetic evidence for a caspase-independent pathway of programmed cell death that controls early morphogenesis.
Programmed cell death (PCD) is a fundamental property of all multicellular organisms. It is crucial for plant and animal development, insect and amphibian metamorphosis, organ morphogenesis, tissue homeostasis, ageing, and the removal of infected or damaged cells1. The biochemical and ultrastructural features of apoptosis are highly conserved throughout the evolution of multicellular animals1-4. PCD has been linked to the CED9/Bcl-2, CED4/Apaf1 and CED3/caspase-9 genes that are essential for PCD in Caenorhabditis elegans and vertebrates5-8. In response to death stimuli, mitochondrial membranes are permeabilized9, 10, and cytochrome c is released from mitochondria3, 11, 12 and associates with Apaf1 and pro-caspase-9 to trigger a caspase activation cascade that culminates in cell death characterized by apoptotic morphology7, 13-15. Failure to invoke appropriate cell death can result in cancer or autoimmunity, whereas increased PCD can lead to degenerative processes such as immunodeficiency and neurodegenerative disease16.
Although the cytochrome c/Apaf1/caspase-9 apoptosome is essential for several PCD pathways, cells deficient in these molecules can still die3. Indeed, cytochrome c, apaf1 and caspase-9 knockout mouse embryos undergo normal, albeit delayed, morphogenesis17-21. Moreover, cell lines derived from these mutant mice are not uniformly resistant to death stimuli, but instead undergo PCD in a manner specific to both cell type and death signal19. It has also been shown that Bcl-2 preserves the integrity of mitochondrial membranes and protects cells from death independently of Apaf1 and caspases, implying that Bcl-2 interferes with two different mitochondrion-dependent death effector cascades22, 23. Thus, a death effector system other than cytochrome c/Apaf1/caspase-9 must be able to induce PCD.
We previously cloned apoptosis-inducing factor (AIF), which, like cytochrome c, is normally present in the mitochondrial intermembrane space and is released in response to death stimuli24, 25. Extramitochondrial targeting of AIF, micro-injection of recombinant AIF protein into cells, or addition of AIF to isolated nuclei leads to the generation of apoptotic phenotypes, such as chromatin condensation and phosphatidylserine exposure on the cell surface24. AIF has also been implicated in the control of apoptosis in syncytia induced by the HIV type-1 envelope glycoprotein26, indicating that AIF may be involved in the pathogenesis of HIV infections. But although AIF can induce certain aspects of cell death in cultured cells, whether it is essential for PCD in vivo remains unresolved. Moreover, AIF has never been linked to PCD at the genetic level.
To explore the role of AIF in the control of PCD during animal development, we disrupted the mouse aif gene by homologous recombination. We report here that AIF is essential for the first wave of PCD required for embryonic morphogenesis and cavitation. Moreover, inactivation of AIF renders embryonic stem cells resistant to cell death after serum starvation. These results provide the first genetic evidence of a second, mitochondrially regulated cell death pathway in mammalian cells that is critical for morphogenesis and PCD after withdrawal of survival factors.
Gene targeting of aif in embryonic stem cells The murine aif gene was ablated in embryonic stem (ES) cells using a targeting vector that deleted exon 3, corresponding to the amino terminus of the mature protein (nucleotides 247-346, amino acids 83-115). Three independent aif-targeted ES cell clones were obtained. Because the aif gene maps to the X chromosome24, mutation of one aif allele resulted in a complete knockout in XY male ES cells and absence of aif expression by northern and western blotting (see Supplementary Information Fig. 1). As a control for changes to ES cells during G418 selection, ES cell clones were isolated in which the neomycin resistance cassette had integrated randomly into the genome (aif neo/Y).
Three independent aif -/Y ES cell clones were injected into C57BL/6 blastocysts to generate chimaeric mice, and into rag1-/- blastocysts for lymphocyte reconstitution27. Whereas all parental wild-type ES cell clones (aif +/Y) and all aif neo/Y ES cell clones could contribute to adult tissues in chimaeric mice and reconstitute T- and B-cell lineages in rag1-/- mice, we failed to observe any chimaerism using all three aif -/Y ES cells clones. Using in vitro ES cell differentiation and formation of teratocarcinoma-like tumours in vivo28, however, aif -/Y ES cell clones differentiated into cells from all three germ layers, including cartilage, muscle, neuronal tissue, epithelium, B cells, myeloid and erythroid cells (see Supplementary Information Fig. 1)29. Thus, aif -/Y ES cells retain their capacity to differentiate into cells from all three germ layers.
aif -/Y ES cells are resistant to growth factor deprivation The aif -/Y ES cell lines exhibited normal proliferation in vitro. Unlike cytochrome c-/-, apaf1-/- and caspase-9-/- ES cells17, 19, 21, aif -/Y ES cell lines displayed normal susceptibility to death, which was preceded by the dissipation of the mitochondrial transmembrane potential (m), in response to staurosporine, etoposide, azide, tert-butylhydroperoxide (Fig. 1a), anisomycin or ultraviolet irradiation (data not shown). This normal susceptibility to cell-death induction was observed both in the absence and in the presence of the pan-caspase inhibitor Z-VAD.fmk (Fig. 1a). Whereas serum withdrawal results in cell death of aif +/Y, aif neo/Y and apaf1-/- ES cells23, all three aif -/Y ES cell lines largely conserved their viability and normal mitochondrial membrane integrity (m) when cultured in the absence of serum (Fig. 1b). Moreover, in the presence (but not the absence) of Z-VAD.fmk, aif -/Y ES cell lines failed to die in response to the pro-apoptotic agent vitamin K3 (menadione) (Fig. 1b). Thus, AIF is rate-limiting for some pathways of death induction. In particular, aif -/Y ES cells are resistant to death after growth factor withdrawal.
AIF is essential for cavitation of embryoid bodies The absence of overt chimaerism in whole organisms, yet the apparently normal differentiation potential of aif -/Y ES cells in vitro and in vivo, suggested that AIF might be required for normal PCD during early embryonic development. PCD occurs throughout mammalian development, beginning with apoptosis of the initially solid embryonic ectoderm to generate the proamniotic cavity30. This early developmental process can be mimicked in vitro by culturing aggregates of ES cells in the absence of leukaemia inhibitory factor and feeder cells31. Under these culture conditions, ES cells form undifferentiated cell aggregates that develop into simple embryoid bodies (EBs), defined as multicellular aggregates containing an outer layer of endodermal cells and a solid core of undifferentiated ectodermal cells (Fig. 2a, left). The inner cells of simple EBs subsequently undergo PCD to form cystic EBs (Fig. 2a, top centre), a process called cavitation. As cystic embryoid bodies are cultured in vitro, the cavity expands (Fig. 2a, top right). The removal of cells of the inner core to form a cavitated or cystic EB is the first known wave of PCD during mouse morphogenesis30.
When aif -/Y ES cells were tested in the EB formation assay, they were able to form simple EBs at frequencies and with kinetics comparable to those of aif +/Y and aif neo/Y controls (Fig. 2). But whereas a significant proportion of aif +/Y and aif neo/Y EBs underwent cavitation to form cystic EBs, EBs from all three differentiated aif -/YES cell lines exhibited a complete block in cavitation (Fig. 2a, b; and Supplementary Information Fig. 2). As cavitation is essential for the initiation of gastrulation and thus subsequent steps in embryogenesis32, defective cavitation by aif -/Y EBs probably explains the inability of aif -/Y ES cells to lead readily to adult tissue in chimaeric mice.
AIF controls PCD during early morphogenesis Impaired cavitation might be due to either increased proliferation and/or impaired PCD of the cells that form the inner core. To investigate whether EB cell proliferation was increased in the absence of AIF, we examined BrdU (5-bromodeoxyuridine) incorporation by wild-type and aif -/Y EBs. Although aif -/Y EBs displayed abnormal morphology (Fig. 3a, left) and histology (Fig. 3b, left), no evidence was obtained for increased proliferation of the inner cells of aif -/Y EBs at day 3, day 5, or at any later time point as compared with wild-type EBs (data not shown). To assay for PCD, the inner cells from wild-type and aif -/Y EBs were analysed by DAPI (4',6-diamidino-2-phenylindole dihydrochloride) staining to detect chromatin condensation (Fig. 3c, left) and by assays for in situ caspase-3 activation (Fig. 3d, left). Massive apoptosis was observed in the wild-type EBs, but no signs of cell death were found among the inner cells of aif -/Y EBs. These results indicate that impaired cavitation in aif -/Y EBs is not caused by enhanced proliferation but is due to a failure of inner cells to undergo PCD.
The outer endoderm cells have been suggested to provide death signals to inner cells required for cavitation30; however, histological and electron microscopy analyses showed that simple aif -/Y EBs do not lack endodermal tissue. Furthermore, aif -/Y EBs expressed the endoderm-specific32, 33 markers BMP2, BMP4, GATA-4, -fetoprotein and HNF-4 (data not shown). To establish that the defects of aif -/Y cells are autonomous to inner cells, we generated chimaeric EBs by mixing aif -/Y and wild-type ES cells expressing a lacZ reporter (aif +/Y; lacZ) (Fig. 4a). Although cavitation was partially rescued in these chimaeric EBs (Fig. 4b), cell death was restricted to wild-type (blue) inner cells (Fig. 4b-e). Our mixing experiments also showed that aif -/Y cells can differentiate into columnar epithelium (Fig. 4f). These results indicate that impaired cavitation in aif -/Y EBs is not caused by defective endoderm formation. Instead, impaired cavitation is due to an intrinsic failure of AIF-deficient inner cells to undergo PCD.
Apaf1 and caspase-9 are not required for cavitation The death of inner cells in wild-type EBs was found to be accompanied by the activation of caspase-3 (Fig. 3d, left), an effector caspase downstream of the cytochrome c/Apaf1/caspase-9 apoptosome. We therefore explored the contribution of Apaf1 and caspase-9 to cavitation by analysing the development of EBs from apaf1-/- and caspase-9-/- ES cells17, 19. Genetic inactivation of the apaf1 and caspase-9 genes abolished caspase-3 activation (Fig. 3d, right). However, loss of Apaf1 or caspase-9 expression had no apparent effect on cavitation (Fig. 3a, b; and Supplementary Information Fig. 3) or the death of inner cells (Fig. 3c). The kinetics and extent of cells that undergo chromatin condensation were comparable among wild-type, apaf1-/- and caspase-9-/- EBs (n = 5 per group). Adding the broad-spectrum caspase inhibitor z-VAD.fmk to developing wild-type EBs also failed to block cell death and subsequent cavitation. These results show that the PCD required for EB cavitation can occur in the absence of caspase-3 activation and can be genetically uncoupled from Apaf1 and caspase-9.
We next examined the intracellular localization of AIF in EBs and the effect of mutations of apaf1, caspase-9 or aif on AIF and cytochrome c mobilization. In response to death stimuli AIF translocates from the mitochondria to the nucleus, whereas cytochrome c localizes to the cytosol24. AIF (Fig. 5a, red colour) was found to translocate from the mitochondria to the nucleus (green DNA stain) in inner cells, but not in the outer endodermal cells of wild-type, apaf1-/- and caspase-9-/- EBs. Cytochrome c was also released from mitochondria of wild-type, apaf1-/- and caspase-9-/- inner cells (Fig. 5b). There was no detectable cytochrome c translocation from mitochondria to the cytosol in inner cells of aif -/Y EBs, indicating that mitochondrial membranes fail to permeabilize. This result is consistent with the failure of aif -/Y inner cells to activate caspase-3 (Fig. 3d), a defect that presumably results from deficient assembly of the apoptosome. These findings indicate that AIF acts upstream of cytochrome c and independently of the cytochrome c/Apaf1-triggered caspase activation cascade during cavitation.
AIF-regulated PCD has characteristic features of apoptosis It has been reported that cell death of apaf1-/- and caspase-9-/- ES cells in response to ultraviolet radiation exhibits the morphological features of necrosis rather than apoptosis19, 23. To establish whether AIF-controlled cell death in EBs has the ultrastructural characteristics of apoptosis, inner cells from wild-type and aif -/Y EBs were compared using electron microscopy. Dying inner cells in wild-type EBs displayed typical apoptotic morphology (Fig. 6a), including the presence of chromatin condensation, plasma membrane blebbing, formation of apoptotic bodies, and a preserved ultrastructure of cytoplasmic organelles. Inner cells from aif -/Y EBs retained a healthy phenotype (Fig. 6b). Intriguingly, the inner cells from both caspase-9-/- and apaf1-/- EBs exhibited typical features of apoptosis, such as intact nuclear and plasma membranes, chromatin condensation (Fig. 6c-f, asterisks), plasma membrane blebbing (Fig. 6c, d, arrows), formation of apoptotic bodies (Fig. 6e), and preserved ultrastructure of mitochondria (Fig. 6c, f, solid arrowheads) and rough endoplasmic reticula (Fig. 6c, f, '>'). These features were similar to those in wild-type inner cells.
Consistent with the absence of caspase-3 activation, caspase-9-/- and apaf1-/- EBs do not manifest an advanced pattern of chromatin compaction (Fig. 6a). Instead, a peripheral type of chromatin compaction predominated (Fig. 6c-f). Thus, with the exception of caspase-dependent advanced chromatin compaction, the AIF-regulated pathway of PCD required for embryonic cavitation exhibits classical ultrastructural features of apoptosis and is independent of the Apaf1/caspase-9-mediated PCD pathway.
Discussion In C. elegans, genetic evidence suggested that apoptosis is strictly dependent on caspase activation5. We provide genetic evidence here that not all apoptosis of mammalian cells is dependent on caspases, and that an AIF-dependent, caspase-independent PCD pathway exists that is crucial for cell death following growth factor deprivation and early mammalian development.
AIF and mitochondrial control of apoptosis. Numerous reports have shown that caspase inhibition prevents mammalian cell death or blocks the acquisition of morphological and biochemical characteristics of apoptosis34. Moreover, mutational analyses of cytochrome c (ref. 21), caspases19, 20 and Apaf1 (ref. 17) showed that these molecules contribute to apoptosis in a manner specific to both cell type and death signal. Similarly, aif -/Y ES cells, unlike apaf1-/- and caspase-9-/- ES cells, are sensitive to various apoptotic stimuli, such as staurosporine, anisomycin, ultraviolet irradiation and etoposide. However, aif -/Y ES cells are resistant to serum withdrawal and AIF is essential for the first wave of cell death during mouse morphogenesis. These data indicate the coexistence of two separate pathways linking the mitochondria to apoptosis, one that requires AIF and the other that relies on caspase activation.
The results of our study provide definitive genetic evidence that AIF inactivation abolishes all signs of cell death in early morphogenesis, including the mitochondrial release of cytochrome c. Moreover, AIF is a rate-limiting factor of ES cell death induced by menadione (only if caspases are simultaneously blocked) or by serum withdrawal (independently of caspase inhibition), indicating a stimulus-dependent contribution of AIF to the apoptotic cascade. The exact hierarchies and communication between AIF and the cytochrome c/Apaf1/caspase-9 apoptosome in cell-type- and death-signal-specific PCD remain to be determined.
Morphogenesis of multicellular organisms. PCD is essential during early animal development for the sculpting of digits, the palate and the eyes, the formation of hollow organs and the neural tube, and the generation of sexual organs1. In early mouse embryos, the proamniotic cavity is formed by the death of the ectodermal cells in the core of the developing embryo30. Thus, PCD is an integral part of morphogenesis and metamorphosis at all stages of animal development. Because developmental PCD exhibits the structural hallmarks of apoptosis, the finding that C. elegans bearing mutations of their caspase (CED-3) or Apaf1 (CED-4) orthologues have normal lifespans2 was originally surprising. Moreover, morphogenesis and organ sculpting are also normal in cytochrome c, apaf1 and caspase-9 knockout mouse embryos, albeit delayed17-21. These observations pointed to the existence of another PCD pathway that can compensate for the absence of caspase-dependent apoptosis and that is highly conserved through evolution. As AIF messenger RNA and protein expression can be detected throughout murine embryogenesis and in all developing organs (see Supplementary Information Fig. 4), it is likely that AIF contributes to morphogenesis at later stages of embryogenesis.
We have shown that the genetic inactivation of AIF abolishes the first wave of developmental cell death occurring during early mouse embryogenesis. Assuming that ontogenesis recapitulates phylogeny, it is tempting to speculate that AIF represents a pathway of apoptosis that predates the caspase pathway. Whereas AIF homologues have been found in all metazoan phyla35, no evidence for caspases has been reported in plants, fungi or unicellular organisms such as the Trypanosoma cruzi epimastigote, all of which can nevertheless undergo PCD1. We propose that AIF and the AIF-regulated cell death pathway constitute an ancient and conserved process required for the morphogenesis of multicellular organisms. The identification of the molecules involved in this PCD pathway and their genetic and functional characterization should yield new insights into the basic physiology of cell death, and might allow us to develop strategies for the modulation of the cell death machinery.
Methods aif-deficient ES cells and chimaeric mice The aif gene was cloned from a 129/SVJ mouse genomic library using a mouse aif probe (nucleotides 247-346). A targeting vector (600 base pairs short arm, and 6 kilobases long arm) flanking a PGK-Neo cassette was electroporated into male E14K ES cells. ES cell colonies resistant to G418 (300 g ml-1) were screened for homologous recombination by polymerase chain reaction (sense primer, 5'-GGGATTAGATAAATGCCTGCTCTT-3'; antisense primer, 5'-CCCCCAAACTTATATCAGCCTACCTTC-3'). Recombinant colonies were confirmed by Southern blotting of HindIII-digested genomic DNA hybridized to a flanking probe. Total RNA was extracted from aif -/Y ES cells and subjected to northern blotting using full-length AIF complementary DNA. Absence of AIF protein in aif -/Y ES cells was determined by western blotting using an antibody reactive to residues 151-200 of murine AIF24. Antibodies to Apaf1 (Upstate Biotechnology) and actin (Sigma) were used as controls. To test contribution to adult tissues, aif -/Y ES cells were injected into blastocysts from rag1-/- mice27 and C57BL/6 mice to generate chimaeric animals. Mice were maintained at the animal facilities of the Ontario Cancer Institute in accordance with institutional guidelines. Equivalent results and phenotypes were obtained for three independent aif -/Y ES cell clones. apaf1-/- and caspase-9-/- ES cells have been described17, 19.
ES cell differentiation Parental wild-type aif +/Y, three aif -/Y ES cell clones and ES cell clones in which Neo was randomly integrated (aif neo/Y) were cultured under conditions promoting differentiation into EBs29, 36. Chimaeric EBs were generated using aif -/Y ES cell clones (lacZ-negative) and aif +/Y ES cells constitutively expressing lacZ (aif +/Y; lacZ). The aif +/Y; lacZ ES cell clone contains a randomly integrated copy of the lacZ gene fused to the chicken -actin promoter37. For colony assays, single EB cell suspensions were replated in methylcellulose. Blood islands were detected using benzidine. ES cells were further differentiated into primitive mesodermal cells by co-culture with OP9 bone marrow stromal cells for 5 d. Single-cell suspensions from these cultures were either used for FACS analysis of Flk1+ hemangioblasts or replated onto OP9 cells and grown for an additional 5-12 d. Colonies were counted 10-14 d later and stained with Wright-Giemsa to analyse morphology, and with anti-CD45, CD11b, CD19 and TER-119 monoclonal antibodies38. In vivo tumour formation of ES cells in athymic nu/nu mice and detection of differentiated tissues have been described 28.
Quantification of cell death We cultured ES cells in the presence of 10% fetal calf serum and leukaemia inhibitory factor. Cell death was induced by addition of staurosporine (2 M, 24 h), etoposide (100 M, 24 h), sodium azide (15 M, 48 h), tert-butylhydroperoxide (200 M, 48 h) or menadione (150 M, 24 h), or by serum withdrawal (0%, 72 h), in the presence or absence of Z-VAD.fmk (50 M). Death was quantified by staining with propidium iodide (PI; 5 g ml-1) and DiOC6(3) (40 nM).
Immunostaining and in situ procedures For in situ localization of AIF and cytochrome c (ref. 25), paraformaldehyde-fixed EBs were stained with rabbit antiserum raised against residues 151-200 of AIF, or anti-cytochrome c monoclonal antibody (clone 6H2.B4, Pharmingen) followed by PE-conjugated goat anti-rabbit IgG (anti-AIF) or PE-conjugated goat anti-mouse IgG (anti-cytochrome c). Cells were counterstained with 10 nM Sytox Green (Molecular Probes). Staining was detected by confocal scanning fluorescence microscopy. Electron microscopy and in situ DAPI staining to detect chromatin condensation were as described19. Activated caspase-3 was detected using an antibody specific for the cleaved (active) form of caspase-3 (New England BioLabs). In situ hybridization of murine embryos at distinct stages of development was done using sense and antisense probes from murine aif cDNA (nucleotides 456-1607).
Re:THIS IS OLD ! (Score:1)
apoptosis is not one cell killing another cell. it is programmed cell death, and although it might be induced by external factors, the killing process occurs from within the cell itself.
it is amazing how people react to this subject. i would not consider to put my opinion forward on a subject i do not know a lot about, unless i was very very sure that i was not talking b(*&(hit
think before you post, please.
Re:Maybe cells die because there is no O2? (Score:1)
So your heart cells may really be apoptosing in a stroke or heart attack. The question then is: will it really help to prevent this? Maybe, if medical attention can save the cells if they can be stopped from committing suicide, but if not, blocking apoptosis will just lead to necrosis and lots of enzymes, damaged DNA, and other cellular crud floating around.
Re:Who wants to live forever (Score:2)
Every time a new technology is discovered/invented to do with people there's the silly bastard reaction that we're messing with nature (the awful unsaid meme being that humans are outside nature). Everything we do impacts on what would have happened without our efforts - we impose our will on others and animals and the universe. When we save a beached whale it probably would have died - but I think we did a good thing (although blowing it up is quite entertaining too - and i'm a vegetarian). So, really, it's not about messing with nature (the very idea of that reeks of a religious 'greater plan') but instead about what benefits the world. Medicine has proven to be a good thing - as has surgery, yet because these are ingrained we don't consider them "unnatural" anymore. Yet they extend life from an average of 40yrs to perhaps 80. Screw this 'good and short life' crap - Billy Corgan was right, it's not live fast die young, it's live fast live long.
Does living a few years longer benefit the world? Yes, it does.
Poll: Name for the "cell executioner" gene (Score:4)
Re:Who wants to live forever (Score:2)
Isn't that a Chinese curse?
easy.. (Score:2)
We give them all tiny little swords and declare, "There can be only one!"
Re:The quality of Old Age (Score:2)
Death defines life ; and it's the very fact that we have a finite time in this body that gives us the drive to squeeze the most out of it while we still have it.
Of course, the same factors create some of the stupidity we see today. Nobody in charge seems to be worried about global warming. This is in part because they and everyone they know will be safely dead before things progress to 'Damnation Alley' like proportions. If they thought they might have to live in the future they're creating (and suffer like everyone else), they might be more careful to create a good one.
There is no question that extending the human lifespan would change things. Some problems would go away, others would take their place.
Just increasing the quality of late life will have an impact. We will then have people in their seventh and eighth decade who have the energy and vigor to participate more fully in society. Some will be deeply set in their ways, others will have decided that most social 'problems' which plague their younger collegues really don't matter very much. For example, would a person who had actually seen civilization survive the 'terribly destructive' influence of the novel, radio, television, Elvis, The Beatles, etc. be as concerned about violent video games as the numbskulls in Washington today? (Yes, all of those things were at one time considered terribly destructive and decried as the downfall of civilization by some group or another).
The question is, who would 'win', those dedicated to the status quo, or those who had already seen too many changes to care about the status quo anymore?
Re:Who wants to live forever? (Score:2)
Re:Who wants to live forever? (Score:1)
Re:Accidents, Poisson distribution (Score:1)
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Re:Useful for cancer, not for immortality (Score:1)
That wouldn't work: gene transfer is always extremely inefficient, maybe 1 in a hundred or in a thousand cells will take up and incorporate the gene correctly. Those few cells will then apoptose soon after, leaving the rest of the cancer cells multiplying happily.
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another vaporware... (Score:1)
But wait a minute, I am already immortal, as far as I remember, I have always been alive.
Re:Who wants to live forever? (Score:2)
Of all the people that have ever lived, only half have died. So you may be overstating your case.
Source: some smithsonian natural history exhibit or other.
Re:Who wants to live forever? (Score:2)
Damn, my chances have just gone down a lot. Thanks for the correction though.
Re:Immortality is impossible (Score:3)
Indeed, but a lot of effort tends to be focused on the leading killers. So if all natural/disease based death were gone, accidents would be next on the chopping block.
New cars would make today's volvos look like deathtraps. Buckets would have little sensors that would detect drowning, and open drain holes. Ladders would automatically drill themselves into the floor or ground.
Accidents would still kill, but that 600 number would slowly drift ever higher.
Re:Could be useful. (Score:4)
Biologically there is something quite right with it. There is a theory that old age death is very good for a species. It can't really be tested at this time, of corse. The closest you can do is take a genetic programming package, find a problem it can solve, and then change it to remove old age death. Then see if it can still solve it, and if it can if that takes more generations or not. My meager experiments with the "simplified ants looking for food" problem shows a huge increase in the number of generations needed to find the solution. But don't take my word for it, it's a pretty easy experiment, go try it. (note you still kill off the bad performers, you only let the "old" ones live if they are in the top few percent)
Socially it looks like old age death is a good idea. Most mathmations (for example) make their good discoveries early, and then don't do a whole lot. Or so I have been told. Plus think of the divorce rate if we don't have the death escape hatch 50% of marriages use :-)
All kidding aside, for social effects the only place I have seen them investigated is science fiction, and the results vary quite a bit. Many of those societies I wouldn't enjoy as much as this one, except of corse, I would have far more time to enjoy them....
Economically losing old age death would be a disaster if we didn't also lose old age (forget our current social security problems, if the avg. age shot up to 150 we would be sunk!). If we lost old age as well things wouldn't be as bad, but the increasing population would make jobs a bit scarce (unless birth rates dropped dramatically).
Personally, I would love to live forever (assuming I get to do it in fairly good health, and in a more or less normal mental state). It only causes a problem when we all get to do it :-)
A suitable quote. (Score:1)
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It could be coffe.... or it could just be some warm brown liquid containing lots of caffeen.
Re:A suitable quote. (Score:1)
:-)
// yendor
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It could be coffe.... or it could just be some warm brown liquid containing lots of caffeen.
Re:Could be useful. (Score:2)
Well, nobody's suggesting that this gene should be eliminated -- just controlled a bit better. The purpose of apoptosis is to kill cells that appear to be abnormal (i.e. mutated cells and tumor cells). But the system is hardly perfect and many perfectly good cells are killed while many tumor cells are allowed to live.
The fact is that natural selection doesn't work that well to improve such a system because generally cancer occurs to old people past child-bearing age and so there is no selective pressure.
Re:Could be useful. (Score:2)
Cell death for development is important but it isn't the primary function of apoptosis or AIF in general.
Re:Who wants to live forever? (Score:1)
There's no time for us
There's no place for us
What is this thing that fills our dreams
Yet slips away from us?
There's no chance for us
It's all decided for us
This world has only one sweet moment
Set aside for us.
Who wants to live forever?
Who wants to live forever
Oh_______ when love must die?
Touch my tears
With your lips
Touch my world
With your fingertips
And we can have forever
And we can love forever
Forever....
Forever....
Forever... is our today.
Who wants to live forever?
Who wants to love forever?
Who dares to love forever?
Oh________
Who waits forever anyway?
(I would attribute this properly, but any self-respecting person should know it..)
Re:Who wants to live forever? (Score:2)
It doesnt prevent car crashes, cancer...
Actually, the same technology might be used to prevent cancer by selectively killing off only cancer cells... but I get your point.
Cellular death (Score:1)
I suspect this product was a hoad, but back in the days of analog cellphones it was actually very easy to build a device that does this: the frequency spacing between the transmit and receive frequency was exactly 40MHz. You could build a cheap device that receives the strongest signal around, mixes it with a 40MHz oscillator and transmits the result back. Multipying two sines results in the sum and difference of their frequencies - one of them will jam the receiver side of the phone very efficiently.
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(oops, hoad-hoax) (Score:1)
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The quality of Old Age (Score:1)
What is of interest and importance to me is the quality of life and in particular, health, as we get older. I remember seeing a documentary on TV about a treatment given to OAP's derived from embryo research (I don't remember the species or nature of the drug) but the net effect was increased energy, hardening of the bones (curing osteoporosis) and thickening of the skin to levels more common in youth. If science can deliver a way to keep me more alert and 'bouncy' until it's my time to pass on, then I'll be a very happy man in deed.
Who wants to live forever
Macka
Re:Who wants to live forever? (Score:1)
Credit Mr Adams why doncha?
Re:Who wants to live forever? (Score:2)
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Accidents, Poisson distribution (Score:2)
Immortality is impossible (Score:3)
One might argue that medical science's ability to clean up after our accidents will improve with time, but I doubt it is every going to figure out a way to put our brains back together if they are splattered all over the road in the course of being struck by a car.
So there is an upper bound to our life span even if we are technically 'immortal'.
-josh
Re:Missing? (Score:1)
AIF would not be usefull in fighting standard viruses. It COULD be usefull in fighting cancer by telling the cancer cells to self destruct (which would be much less invasive than physically removing the cancerous tissue). Then again, one slight mistake and you could easily kill the patient, either by making all of their cells die immediately, or making them all live forever, which (I think) would make the patient's entire body cancerous. In short, AIF seems like a very sharp double edge sword.
Re:Could be useful. (Score:1)
Re:Could be useful. (Score:1)
I'm obsessed with a much more pragmatic question: why doesn't anyone on the Internet use apostrophes in their contractions any more? I've gotten used to seeing people totally confuse "your" and "you're" (not to mention "there" and "their"), but come on - "dont" and "Im" aren't even words! (Although I suppose you could partially blame "dont" on the automatic crosswalk signs that flash "WALK" and "DONT WALK" at you - would it really cost the city that much more to buy an appropriately-located apostrophe?)
Maybe I'm just grumpy today, but this article seems to have attracted more than its (note: not "it's") share of failed communicators. The parent post is a particularly egregious example. I remember when even trolls could communicate better than this!
I know, I know: flamebait. Still true, though.
Re:Not fountain of youth (Score:1)
OK, how exactly was that flamebait? Overrated, perhaps, but there was certainly no incitement to a flamewar. What color is the sky in your world, O Moderator? C'mon, meta-moderation!
Re:OT --- Re:Could be useful. (Score:1)
You're right; consider me suitably chastened. I guess I am grumpy today...
Re:Not fountain of youth (Score:2)
nitpick:
Not exactly - your cells must die for you to remain healthy. Dead cells aren't very healthy themselves :)
Re:Who wants to live forever? (Score:1)
Nice way to put that story in though. Almost word for word the story of the brunungee (killed the spelling there sorry) on the show.
What's wrong with dying (Score:2)
The problem with dying of old age is that it is "only" natural. Just because something is compatable with your genes' interests, doesn't mean it's compatable with your interests.
You can worship nature or the gods, and marry and reproduce and care for your offspring and then die to make room for your genes' newer hosts. Let the pre-ordained program have its way.
Or you can have a ambition and a real ego, and declare that your mind is what matters and your personal agenda is more important than the biological program. When you take that approach, attempting to defy nature and conquer mortality may make a lot of sense.
Such attempts may be futile, and trying to apply engineering principles to a complex system that is the product of long-term evolution, is difficult and can run into a lot of pitfalls (ask anyone who has maintained ancient legacy code ;-) but it's heroic to try anyway.
---
Re:Who wants to live forever? (Score:2)
I feel that you should have the right to attempt to accept the offer. But success is not guaranteed. (OTOH, you may instead choose the first option, where success will be guaranteed.)
Caution: Now approaching the (technological) singularity.
Compare to lifespans in the book of Genesis (Score:2)
---
How can we be sure... (Score:2)
I bet next week it'll be on CNN, and then it'll start to run amok and kill people randomly, and then there'll be talk of bioterrorism of a kind never before heard, controlled by something that can't be human...
Hey, in this day and age, even Nature magazine can be called into question. (Don't you think they would accept it if Columbia or Universal or whoever offered them a ridiculously large amount of money to run with this?)
Just my two paranoid cents.
Re:Who wants to live forever? (Score:2)
Gee, thanks for telling the rest of the species what it shouldn't do and think. Just don't find it weird when all the biologists utterly ignore your orders and go on developing this technology as far as possible like they have always done, regardless of whether anyone (especially Slashdot posters) thinks they shouldn't.
-- Kaufmann
This keeps happening to me (Score:2)
Stupid. No wonder I don't spend much time at Slashdot anymore.
Re:yeah... but also... (Score:1)
Re:Who wants to live forever? (Score:1)
And yes: I believe people really DO want to live forever. Just look at the worlds religions. They all result in eternity. If it's not for the body, than it is for the soul.
Also our western science is hopelessly trying to find the key to eternal life. That's what the research for this gene is all about: trying to let humans life forever.
You are probably right when an avarage guy at this moment discovers that he's immortal: he would get bored eventually, or get very paranoid.
However, I do think that when the human mind is provided with enough chalanges he can live forever without getting bored. And look at the universe: there is enough to be discoverd.
So, in my opinion people should NOT stop believing in God or science (or whatever it is that provides them with the hope of eternity), because this hope is what drives the human mind to discover new things (which is something unique among the creatures that live on this planet).
Re:Who wants to live forever? (Score:1)
You see? He said I think. He didn't think for you
Re:Profession (Score:1)
Re:Ack! (Score:1)
Re:Who wants to live forever? (Score:2)
The gene modification would stop dying from old age, but it doesnt make one imortal.
It doesnt prevent car crashes, cancer, toxic poisoning, etc
So while life might be greatly extended, it wont be imortality, and the question of life or death will be as real as before. If nothing more, it will become more of an uncertainty, will you die at the age of five, or at the age of five hundred
?
Next to all that, i also think the human brain has a limited capacity of adjusting, and remebering.. What happens after 4000 years of adjusting and remebering? I think people will choose their own end. I know i prolly would
-- Chris Chabot
"I dont suffer from insanity, i enjoy every minute of it!"
Not fountain of youth (Score:4)
Do not hype this too much! (Score:1)
Most the proteins involved in the regulation of cell cycle fall into this category. Any dysfunction of these proteins can result in anything from cell death (cell cycle arest, apoptosis) to uncontrolled cellular division (cancer).
Apparently this is Just One More Piece to fit in the puzzle.
The complexity of signalling pathways is such that simply perturbing one component can have completely unexpected results, in the short- medium- and long-term.
One step closer to cure for cancer (Score:3)
There is a protein called p53 that's responsible for (among other things) detecting damage in a cell, and then either trying to fix the cell, or kill it (apoptosis). The levels of this protein are elevated when cells are in distress -- for example from ultraviolet radiation, starvation, etc. Levels are also affected by mitosis phase, etc etc. In any case, if it is possible to design something that detects high levels of p53 in a cell, and then nondeterministically triggers massive expression of the apoptosis gene (this thing they discovered) then this method could be used to treat some cancers, because in some cancers, levels of p53 are elevated. While this method will likely kill a lot of cells in the middle of mitosis, in a healthy tissue only a small fraction are dividing at any one time.
In some cancers, the p53 gene is damaged and does not get expressed, so in that case some other metric would have to be used to trigger apoptosis.
Anyway, between approaches like this, chemo, surgical removal, and whatever else there is, cancer is slowly becoming a survivable disease.
Useful for cancer, not for immortality (Score:3)
AIF is important because it's likely that many cancers will have a defective copy of it. With advances in gene therapy, it should soon be possible to insert new copies of the gene into the cancerous cells thereby triggering apoptosis in them and destroyin the tumour. However, it's not much use for making you live forever. You don't die because cells decide that you've lived for too long - you die due to disease or failure of organs induced by wear and tear and picking up of mutations. It's possible that inhibiting AIF might lead to some individuals living slightly longer, but only because cells that are defective would hang around until they broke down completely rather than killing themselves cleanly. It wouldn't be terribly pleasant.
(Note: IAAB)
Re:Who wants to live forever? (Score:1)
risk is part of life. the struggle of life would not disapeer. only change. if you lived forever would you exept the artificial and arbitrary standards we now life under?
IMHO people would change to be something better. why? because scare tacties based on dealth and restriction become useless, with unlimited supply.
we are already seeing this with the unlimited supply of the information on the internet.
do you really think that the massess would work as they do now? eternal hard boring work is the classic defintion of HELL. no, the masses would DEMAD changes. they would see how us hackers play / with our work and DEMAD the same. not that they would become hackers, but do that which they enjoy at the monent and like doing.
IMHO those that can't accept unlimited life. will do themselfs in, or change. with limitless time, this is really no reason to have petty greed, (what would you be greedly for?) or fear. if do didnt do it right today there is a limitless supply of tomarrows...
nmarshall
The law is that which it boldly asserted and plausibly maintained..
Is this really a good idea? (Score:2)
I would also venture to say that the CPU isn't like the CPU in our computers which are imutable, but change as the cells specialize. The "Stem Cells" are virgin cells which haven't specialized yet, thus the same DNA strands would produce different results in different cells after they specialize.
We know that DNA is very vulerable to coruption from all kinds of bad things like radiation, carcinigans, lab research on rats. I think the best comparison might be memory leaks, inadquate bounds checking, or pointer errors in our world.
The cell self-destruction might be safe guard against bigger problems. Kind of like a like rebooting your system every so often.
Cheers
yeah... but also... (Score:3)
Re:Required reading (Score:1)
Profession (Score:1)
"Living forever".. unlikely.. longer, maybe. (Score:5)
Ok, for starters: I really recommend that anyone interested in this stuff pick up a (modern) book on biology and genetics, there's a lot of stuff been discovered in the past 10 years, and we're only just scratching the surface. (Someone will make a lot of money selling computers to process all that info :).
This gene has been predicted (if not known about) for some time. It's needed, because your cells die all the time, they're supposed to. Over time, you get problems - errors - in DNA, and this is one of the problems with making cells that duplicate forever, eventually, they won't do the same things anymore (IIRC, brewing companies need to change the yeast they use periodically, because mutations that occur over time change the taste of the beer). The cells in yeast aren't all that different from the cells in your own body! (Actually, anyone who has problems with evoloution would be shocked at how much your cellular processes are (identical) to any other furry mammal).
The biggest application of this kind of technology is the real limit on human lifespan - brain cells. We can eventually replace almost everything else, somehow, but your brain is what and who you are. Once it deteriorates, you're not the same person anymore. Figuring out how to prevent brain cells from dying - brain cells are unique, in that they do not reproduce, ever - just the supporting (gidal?) cells do.
Nobody will be living forever until nanotech becomes rampant - no other mechanism to repair nerve and cellular damage is possible (and even then, it might not be enough). I wouldn't mind retaining my mental facilities until I reach the end of my lifespan, though. If you figure you'll probably live to 80, but will be signifigantly handicapped after 60 or 65, that's a 15 year productive increase.
Who wants to live forever (Score:1)
I think more emphasis should be placed on the quality of life, not on the quantity.
Most of these measure we take to preserve life just mean a few more years in the retirement home.... again am I missing the plot???
When you think about it, you are dead for so long, that in the grander scheme of things, a couple of years will not make a difference.
Also, most of us cannot find stuff to keep us entertained when we are on holiday, yet we want to live forever.
Here's to la dolce vita.... the sweet life, or as the Chinese would say, may you live in interesting times.
Missing? (Score:1)
If it is applied to cells that a virus would attack, then the cells will not die, so the virus will be unable to reproduce, and therefore will die out.
Re:Required reading (Score:1)
Re:What about immediate age (Score:1)
Re:Who wants to live forever? (Score:1)
Re:Who wants to live forever? (Score:2)
No, I seriously doubt it. In fact, I take the opposite view. People would became incredible risk-takers. If you've lived 300 years, you'd probably become pretty bored and start jumping out of airplanes (or space shuttles or whatever), because you just didn't care any more.
It's really basic psych.
Re:Who wants to live forever? (Score:2)
Re:I pity all you misguided people (Score:1)
Re:Very good news. (Score:1)
That is why you age, and when the damage accumulated is too much, you die.
If a the cells can be made to perform perfect dna duplication always, then you would not age.
And if the dna sequence are more redudent and self-repairing, (or some other way so that damgage will not accumulate) you will have a indefinite life span.
Go into biological research if you wish to live long.
Re:Who wants to live forever? (Score:2)
Re:Immortality this ISN'T (Score:1)
Ack! (Score:2)
Er... Boss? How do we kill them?
Re:yeah... but also... (Score:1)
Not immortality, but it has its uses (Score:3)
The stimuli that invoke apoptosis are usually factors that will kill the cell anyway--starvation, poisoning, radiation damage. Apoptosis is the cellular equivalent of euthanasia. Without it, the cell will still die anyway, except more slowly, and it will rupture and spew its contents to surrounding cells, possibly causing those cells to die as well. The process of aging and death of a multicellular organism is ultimately mediated by entropy, not genetics, so until we can figure out a way to repair the ultrastructure of a cell with nanotechnology, immortality is still a long way away.
What this discovery does allow us to do, however, is stop apoptosis in very specific situations (assuming that we have figured out all the cascade mechanisms, which is probably not likely at this stage). For example, in the aftermath of a heart attack, a stroke, or hypotensive shock, even if blood supply is restored, cells will still commit suicide because the apoptotic pathways have been activated. Experimentally, it has been shown that if you can block the stimuli that initiate apoptosis (such as the excess glutamate released in a stroke), then in these specific situations, the cells will probably do fine once the blood supply is restored.
So there are ways to shut off genes transiently--antisense RNA, competitive inhibitors of transcription factors, etc.--preventing much of the sequelae of these vascular events.
Still, shutting off apoptosis, even transiently, has the risk of inducing cancer. In stroke, for example, the excess glutamate triggers a cascade that generates factors that damage DNA. (These DNA-damaging factors are what directly activate the apoptotic pathways.)
So it's a choice: would you rather be paralyzed, or would you rather have a tumor? The odds are probably not even, so there would be a better choice, but ultimately, entropy can't be stopped, so achieving immortality would probably entail a lot of micromanagement.
Re:Could be useful. (Score:2)
You're only half wrong. You can't kill the cells directly. But if you can quickly kill the cells which are harbouring the virus quickly, then you can stop it reproducing.
Cells have this clever way of grabbing parts of the viral capsids you've described and displaying them on the cell membrane, their surface. So what you do is program a virus with your AIF, then culture that virus within your patient's cells. if it's the right kind of virus (bear with me here, I'm skipping two years of college biology to explain this quickly) you get a virus which is encapsulated in your own cell membrane, and will be accepted by other cells.
Now, in a method as-yet not determined, you get the virus to target cells with the viral fragments on the surface. The custom made virus then infects these cells, and quickly exterminates them, thus your virus won't keep spreading.
Please bear in mind that this is really science fiction - but there are biological entities which perform all of the above. Give protein function and viral vectors fifty years and I would expect this to be a valid reality.
Re:yeah... but also... (Score:2)
Well, Ebola is certainly not one of the smarter ones. HIV is infinitely smarter, because not only does it target certain cells, it's a slow developer, thus being able to spread much further.
What makes it smart is more its method of transport than anything else: being a retrovirus, it has a nasty 'cloaking' mechanism of encapsulating itself within its host's cell membrane, thus making itself appear 'local'.
What makes a virus smart isn't how good it is at killing cells, but how good it is at reproducing. Turning on a viral promoter for programmed cell death will just kill, kill, kill. It's not going to spread very far now, is it?
Re:Who wants to live forever? (Score:2)
----
Re:Who wants to live forever? (Score:2)
"Hope I die before I get old" - The Who, song
"I hope I'm not still rocking on when I'm middle aged, that would be sad" (paraphrased)- Elton John, Parkinson interview
The moral: The you 20, 40, 400 years down the line is a different person to you now. Don't go making decisions for them now.
Rich
Prgrammed Cell Death (Score:2)
So is this new? Perhaps it is the discovery of the gene that is new, but nto the knowledge that cells can commit suicide.
What gave the cell away? (Score:2)
DanH
Cav Pilot's Reference Page [cavalrypilot.com]
Old news? (Score:2)
If I recall, the gene is activated whenever the cell's DNA structure tends to get too old, measured with respect to the tail of the chromosomes.
Anyone got any idea whether this is the same thing?
<()>
Who wants to live forever? (Score:3)
Interesting article, and I can only hope that this research pays dividends when it comes to medical research into curing such modern diseases as cancer and Alzheimer's which cause so much misery and grief.
But the idea of living forever... who would really want to live forever?
It's the sort of idea that sounds like a utopian fantasy when you first hear it. After all, nobody but Hamas suicide bombers wants to die - the fear of death is an inherent part of what makes us human. In olden days berserkers were feared for this reason - they would attack and attack without regard for their own safety, and would invariably take many down with them.
But living forever would pervert this part of what makes us human. At first it would seem like a wonderful freedom - all that time to do new things, to experiance more without worrying about not having enough time. But soon the wonder would fade and the fear would set in. Fear of death, fear of any risk which could injure yourself and fear of not being able to afford to live in a reasonable manner.
This fear would overcome any benefit eternal life could bring. People would stay in their houses, attempting to stay safe. They'd stick with their confortable jobs, never taking any risks, never letting their ambition thrive. And when you live forever, enemies are easy to make and friends easy to lose. When there's a lot more to risk, people won't want to risk it.
So I think that living forever is something that we shouldn't want, and shouldn't work towards. Humans just aren't ready to accept eternal life in this world, and we won't be unless we overcome our petty greed and our fears. And Star Trek aside, I just don't see that happening any time soon. There are too many people with too much to lose from disturbing the status quo.
Re:Could be useful. (Score:2)
Yeah, why invent antibiotes and life-prolonging medical techniques because, after all, we all die.
This just in form the Darwin awards... (Score:3)
In other news, the average IQ of the world has gone up dramatically in the past few weeks, leaving researchers puzzled.
Kurdt
Wow! (Score:3)
Triggering agent (Score:2)
The REAL jabber has the /. user id: 13196
Re:Could be useful. (Score:3)
Being able to kill off cancer cells and other types of viruses(maybe) this could have huge value to people.
IANAB, but I as far as I know, viruses are not cells. From this article [uct.ac.za] on viruses structure, here are the components of a virus:
The bottom line is: this cell killer gene will not help fighting the flu.
--Immortality this ISN'T (Score:5)
The rest is also quite interesting. Read it!
Ron Obvious
Very good news. (Score:3)
Fight censors!
Clarification for those who say it's old news (Score:5)
What the article is describing is the discovery of a factor that leads to apoptosis apart from the previously elucidated mechanism, which involves a protein (cytochrome c) leaking out from the mitochodria into the cytosol of the cell, where it shouldn't be. Essentially, if the cell detects that, it knows that the there is something terribly wrong, and it should suicide - which is essentially what apoptosis is.
Now, it had been arleady known that there was another mechanism, because if they knocked out the genes responsible for the known mechanism, they could still get apoptosis, though not as readily. This lead to the search of what was causing it. This article describes that discovery, which is AIF.
Interesting work. The reason that this is a more likely candidate that the previous method for fighting cancer is that cytochrome c is a very large, complex protein. Injecting it into cancer cells to initiate apoptosis would be difficult, to say the least. I didn't see enough of the article to see how large AIF is, but I bet it is smaller, and may be easier to get into cells that cystochrome c.
The thing that has me curious is if they could knock out the gene temporarily. They showed that cells were less likely to induce apoptosis under conditions of serum deprivation (starvation). Starving cells is one of the steps toward prepping the nucleus for use in cloning. If they keep more of the cells alive during that process, they might have a better success rate in cloning.
Chew on that one for a while.
Could be useful. (Score:2)
I think this discovery could be very very useful to science and medicine. Being able to kill off cancer cells and other types of viruses(maybe) this could have huge value to people. The thing I dont understand is this. Common sense leads me to believe that keeping cells alive longer than nature intended might be a bad idea. Cells replenish when they die. The reason they die is they get too old. If cells DID NOT NEED to die, this gene would not exist. Therefore keeping cells alive longer might have BAD consequences.
Why are people obsessed with the fountain of youth. Is there something so wrong with getting old and eventually dying? Make the most of the time you are alive and dont worry about dying. Eventually we all die, accept it, and go do something productive and enjoyable.
Arathres
Not really that great (Score:2)
However, and to quote
Josa, Susin et. al. Nature 410, 549It says quite clearly that this isn't the only way for cells to die. They just do it in a different way that isn't as good. This isn't a wonder chemical/pathway/whatever, it's just an advance in understanding the intricacies of biological systems. This development alone is not going to improve your life at all. Yes, it's interesting, if you're a biologist, but that's all.
Chisler Gene (Score:3)
Accidents as an upper bound (Score:3)
If the average human lives 600 years, how long does the exceptional human live?
More to the point, how do accidents represent an "upper bound"? When I get to 600 without walking in front of a car or falling on a pair of scissors, are the Probability Police going to come hunt me down so I don't "throw off the statistics"?
--
Living Forever? (Score:2)
So we age becouse we have imperfect copies of cell, that make imperfect copies of themselves. This causes the tissue degenetation.
I believe that making cell live longer, will just make us to have more cells (since it wouldn't stop them from reproducing).
However, the discovery of making them die, can be a huge step on finding the cure of cancer, if them can 'program' the targget cells, leaving the healthy cells alive.
Re:Living Forever? (Score:2)
Re:Could be useful. (Score:2)
It is all about freedom of choice. A lot of people would like to have it for as much as possible. That is what this whole 'science' thing keeps going.