Cell death
According to evolutionary theory, biological variation that supports or enhances reproduction will increase in future generations—a process known as natural selection. The corollary to this is that biological variation that degrades reproduction will not be selected for. Clearly, natural selection could not result in destructive behavior. Here are two representative statements from Origins:
we may feel sure that any [biological] variation in the least degree injurious would be rigidly destroyed. (Darwin, 63)
Natural selection will never produce in a being any structure more injurious than beneficial to that being, for natural selection acts solely by and for the good of each. (Darwin, 162-3)
But are not examples of such “injurious” behavior obvious? When the rattlesnake rattles its tail, is this not injurious to its hunt for food, and ultimately to its reproductive chances? Darwin argued that this and other such examples are signals to frighten away enemies, not warn the intended prey.
But today we have many examples of injurious behavior that falsify Darwin’s prediction that natural selection “will never produce in a being any structure more injurious than beneficial to that being.” In bacteria, for example, phenomenally complicated mechanisms carefully and precisely destroy the individual. Clearly, this suicide mechanism is more injurious than beneficial to the bacteria’s future prospects.
One such mechanism consists of a toxic gene coupled with an antitoxic gene. The toxic gene codes for a protein that sets the act of suicide into motion and so ultimately kills the bacteria. The antitoxic gene inhibits the toxic gene from executing its mission. Except, that is, when certain problems arise. Lack of proper nutrients, radiation damage and problems due to antibiotics can all cause the antitoxin to be diluted, thus allowing the toxin to perform its mission. (Chaloupka, Vinter; Engelberg-Kulka, Hazan, Amitai; Engelberg-Kulka, Amitai, Kolodkin-Gal, Hazan; University Of Nebraska)
This bacterial suicide is probably good for the bacteria population on the whole. If nutrients are running low, then better for some bacteria to die off so the neighbors can live on. Not only will the reduced population require less nutrients, but the dismantled bacteria help to replenish the food supply. Therefore evolutionists can explain the suicide mechanism as having evolved not for the individual bacteria, but for the population. But the explanation introduces major problems for the theory.
Suicide is probably good for the bacteria population, on the whole, in challenging conditions. Since gene sharing within a bacteria population is at its maximum, evolutionists have no problem explaining such altruism as a result of kin selection (see Altruism). Such a facile response, however, misses the profound problem of how such a design could arise in the first place, for the mechanism is immensely complex.
In this example of bacteria suicide, the antitoxic gene normally inhibits the toxic gene from executing its mission. When the antitoxic gene is diluted then the toxic gene can perform its mission. The toxin does not, however, single-handedly destroy the cell. The toxin is an enzyme that cuts up the copies of DNA (i.e., messenger RNA, or mRNA) that are used to make other proteins. By slicing up the mRNAs, the cell no longer produces the proteins essential for normal operation. But the toxin does not cut up all mRNAs. Some mRNAs escape unscathed, and consequently a small number of proteins are produced by the cell. These include death proteins that efficiently carry out the task of disassembling the cell.
Death proteins are not the only proteins that the toxin allows to be produced. As researchers reported, the toxin “activates a complex network of proteins.” (Amitai) While some of the proteins bring death to the bacteria, others can help the cell to survive. The result is that most cells in the population are destroyed, but a fraction is spared. This of course makes sense. The suicide mechanism would not help the bacteria population if every individual was destroyed. Instead, some survive, and they can be the founders of a new population when conditions improve.
This suicide mechanism and “behavior” is altruistic. Some bacteria die off to save others. And the explanation that this bacteria suicide is due to kin selection adds tremendous complexity to the theory of evolution. Kin selection can select from only that which is available. This elaborate suicide mechanism must have just happened to arise from some combination of random mutations, and then remained in place until the time when it would succeed in surviving a stressful environment. The toxin and antitoxin genes with their clever functionality, the death and survival proteins, the inter cellular communications—all these were needed to be in place and to be coordinated before the kin selection could even begin to act. This is highly unlikely and adds considerable complexity to the theory.
References
Amitai, Shahar, Ilana Kolodkin-Gal, Mirit Hananya-Meltabashi, Ayelet Sacher, Hanna Engelberg-Kulka. 2009. “Escherichia coli MazF leads to the simultaneous selective synthesis of both ‘death proteins’ and ‘survival proteins’.” PLoS Genetics 5:e1000390.
Chaloupka, J., V. Vinter. 1996. “Programmed cell death in bacteria.” Folia Microbiologica, 41:6.
Engelberg-Kulka, Hanna, Ronen Hazan, Shahar Amitai. 2005. “mazEF: a chromosomal toxin-antitoxin module that triggers programmed cell death in bacteria.” J Cell Science 118:4327-4332.
Engelberg-Kulka, Hanna, Shahar Amitai, Ilana Kolodkin-Gal, Ronen Hazan. 2006. “Bacterial programmed cell death and multicellular behavior in bacteria,” PLoS Genetics 2:e135.
University Of Nebraska. 2007. “New Hope For Fighting Antibiotic Resistance,” ScienceDaily April 27.
According to evolutionary theory, biological variation that supports or enhances reproduction will increase in future generations—a process known as natural selection. The corollary to this is that biological variation that degrades reproduction will not be selected for. Clearly, natural selection could not result in destructive behavior. Here are two representative statements from Origins:
we may feel sure that any [biological] variation in the least degree injurious would be rigidly destroyed. (Darwin, 63)
Natural selection will never produce in a being any structure more injurious than beneficial to that being, for natural selection acts solely by and for the good of each. (Darwin, 162-3)
But are not examples of such “injurious” behavior obvious? When the rattlesnake rattles its tail, is this not injurious to its hunt for food, and ultimately to its reproductive chances? Darwin argued that this and other such examples are signals to frighten away enemies, not warn the intended prey.
But today we have many examples of injurious behavior that falsify Darwin’s prediction that natural selection “will never produce in a being any structure more injurious than beneficial to that being.” In bacteria, for example, phenomenally complicated mechanisms carefully and precisely destroy the individual. Clearly, this suicide mechanism is more injurious than beneficial to the bacteria’s future prospects.
One such mechanism consists of a toxic gene coupled with an antitoxic gene. The toxic gene codes for a protein that sets the act of suicide into motion and so ultimately kills the bacteria. The antitoxic gene inhibits the toxic gene from executing its mission. Except, that is, when certain problems arise. Lack of proper nutrients, radiation damage and problems due to antibiotics can all cause the antitoxin to be diluted, thus allowing the toxin to perform its mission. (Chaloupka, Vinter; Engelberg-Kulka, Hazan, Amitai; Engelberg-Kulka, Amitai, Kolodkin-Gal, Hazan; University Of Nebraska)
This bacterial suicide is probably good for the bacteria population on the whole. If nutrients are running low, then better for some bacteria to die off so the neighbors can live on. Not only will the reduced population require less nutrients, but the dismantled bacteria help to replenish the food supply. Therefore evolutionists can explain the suicide mechanism as having evolved not for the individual bacteria, but for the population. But the explanation introduces major problems for the theory.
Suicide is probably good for the bacteria population, on the whole, in challenging conditions. Since gene sharing within a bacteria population is at its maximum, evolutionists have no problem explaining such altruism as a result of kin selection (see Altruism). Such a facile response, however, misses the profound problem of how such a design could arise in the first place, for the mechanism is immensely complex.
In this example of bacteria suicide, the antitoxic gene normally inhibits the toxic gene from executing its mission. When the antitoxic gene is diluted then the toxic gene can perform its mission. The toxin does not, however, single-handedly destroy the cell. The toxin is an enzyme that cuts up the copies of DNA (i.e., messenger RNA, or mRNA) that are used to make other proteins. By slicing up the mRNAs, the cell no longer produces the proteins essential for normal operation. But the toxin does not cut up all mRNAs. Some mRNAs escape unscathed, and consequently a small number of proteins are produced by the cell. These include death proteins that efficiently carry out the task of disassembling the cell.
Death proteins are not the only proteins that the toxin allows to be produced. As researchers reported, the toxin “activates a complex network of proteins.” (Amitai) While some of the proteins bring death to the bacteria, others can help the cell to survive. The result is that most cells in the population are destroyed, but a fraction is spared. This of course makes sense. The suicide mechanism would not help the bacteria population if every individual was destroyed. Instead, some survive, and they can be the founders of a new population when conditions improve.
This suicide mechanism and “behavior” is altruistic. Some bacteria die off to save others. And the explanation that this bacteria suicide is due to kin selection adds tremendous complexity to the theory of evolution. Kin selection can select from only that which is available. This elaborate suicide mechanism must have just happened to arise from some combination of random mutations, and then remained in place until the time when it would succeed in surviving a stressful environment. The toxin and antitoxin genes with their clever functionality, the death and survival proteins, the inter cellular communications—all these were needed to be in place and to be coordinated before the kin selection could even begin to act. This is highly unlikely and adds considerable complexity to the theory.
References
Amitai, Shahar, Ilana Kolodkin-Gal, Mirit Hananya-Meltabashi, Ayelet Sacher, Hanna Engelberg-Kulka. 2009. “Escherichia coli MazF leads to the simultaneous selective synthesis of both ‘death proteins’ and ‘survival proteins’.” PLoS Genetics 5:e1000390.
Chaloupka, J., V. Vinter. 1996. “Programmed cell death in bacteria.” Folia Microbiologica, 41:6.
Engelberg-Kulka, Hanna, Ronen Hazan, Shahar Amitai. 2005. “mazEF: a chromosomal toxin-antitoxin module that triggers programmed cell death in bacteria.” J Cell Science 118:4327-4332.
Engelberg-Kulka, Hanna, Shahar Amitai, Ilana Kolodkin-Gal, Ronen Hazan. 2006. “Bacterial programmed cell death and multicellular behavior in bacteria,” PLoS Genetics 2:e135.
University Of Nebraska. 2007. “New Hope For Fighting Antibiotic Resistance,” ScienceDaily April 27.
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