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4.6: Defense against social cheaters

Now an interesting question arises: within a social organization, such as a group of cooperating microbes or hunters127, we can expect that, through mutation (or through other behavioral mechanisms), cheaters will arise. What do we mean by a cheater? Imagine a bacterium within a swarm, a cell in an organism, or an animal in a social group that fails to obey the rules. In the case of slime mold aggregates, imagine that a cell can avoid becoming a non-reproductive stalk, but rather always differentiates to form a reproductively competent spore. What happens over time? One plausible scenario would be that this spore cell begins its own clone of migratory amoeba, but when conditions change so that aggregation and fruiting body formation occur, most of the cells avoid forming the stalk. We would predict that the resulting stalk, required to lift the spore forming region above the soil and necessary for spore dispersal, would be short or non-existent and so would reduce the efficiency of dispersion between different aggregates as a function of the number of individuals with a cheater phenotype present. If dispersion is important for reproductive success, there would be selection for those who maintain it and against cheaters.

Now the question is, once a social behavior has evolved, under what conditions can evolutionary mechanisms maintain it. One approach is to link the ability to join a social group with various internal and external mechanisms. This makes cooperators recognizable and works to maintain a cooperative or altruistic trait even in the face of individual costs. There are a number of plausible mechanisms associated with specific social traits. This is, however, a topic that can be easily expanded into an entire course. We will focus on common strategies with occasional references to specific situations. To illustrate these mechanisms, we will use human tissues as an example. We can consider the multicellular organism as a social system. The cells that compose it have given up their ability to reproduce a new organism for the ability to enhance the reproductive success of the whole organism. In this context cancer, particularly early on-set and childhood cancers, are diseases that arises from mutations that lead to a loss of social control. Cells whose survival and reproduction is normally strictly controlled lose that control; they become anti-social and begin to divide in an uncontrolled manner, disrupting the normal organization of the tissue in which they find themselves, and can even breakaway, migrate, and colonize other areas of the body, a process known as metastasis. The controlled growth of the primary tumor and these metastatic colonies leads eventually to the death of the organism as a whole.

When we think about maintaining a social behavior, we can think of two general mechanisms: intrinsic and extrinsic policing. For example, assume that a trait associated with the social behavior is also linked to or required for cellular survival. In this case, a mutation that leads to the loss of the social trait may lead to cell death. Consider this in the context of cancer. Normal cells can be considered to be addicted to normality. When their normality is disrupted they undergo apoptosis, a type of active cell death (see above). A cell carrying a mutation that enables it to grow in an uncontrolled and inappropriate manner will likely kill itself before it can produce significant damage128. For a tumor to grow and progress, other mutations must somehow disrupt and inactivate the apoptotic process. The apoptotic process reflects an intrinsic-mode of social control. It is a little like the guilt experienced by (some) people when they break social rules or transgress social norms. The loss of social guilt or embarrassment is analogous to the inhibition of apoptosis in response to various cues associated with abnormal behavior.

In humans, and in a number of other organisms, there is also an extrinsic social control system. This is analogous to the presence of external policeman (guilt and apoptosis are internal policemen). Mutations associated with the loss of social integration – that is, the transformation of a cell to a cancerous state – can lead to changes in the character of the cell. Specialized cells of the immune system can recognize these changes and kill the mutant cell129. Of course, given that tumors occur and kill people, we can assume that there are mutations that enable tumor cells to avoid such immune system surveillance. As we will see, one part of the cancerous phenotype is often a loss of normal mutation and genome repair systems. In effect, the mutant cell has increased the number of mutations, and consequently, the genetic variation in the cancer cell population. While many of these variants are lethal, the overall effect is to increase the rate of cancer cell evolution. This leads to an evolutionary race. If the cancer is killed by intrinsic and extrinsic social control systems, no disease occurs. If, however, the cancer evolves fast enough to avoid death by these systems, the cancer will progress and spread. As we look at a range of social systems, from cooperating bacteria to complex societies, we see examples of intrinsic and extrinsic control.

Questions to answer & to ponder

  • Why does a quorum signal need to be secreted (released) from the organism?
  • What components are necessary for quorum signaling?
  • Why is r (the relationship between organisms) never 0 (although it can be quite small).
  • What types of mechanisms can be used to address the effects of cheaters in a population?
  • How would these mechanisms apply to social interactions?
  • Make a model of the mechanisms that can lead to the evolution of social interactions within an organism and within a population.


127 An interesting read: The stag hunt and the evolution of social structure.

128 Apoptosis in cancer:

129 Immune recognition of self in immunity against cancer: New generations of anti-cancer drugs work by reactivating immune survalience: see


  • Michael W. Klymkowsky (University of Colorado Boulder) and Melanie M. Cooper (Michigan State University) with significant contributions by Emina Begovic & some editorial assistance of Rebecca Klymkowsky.