Feast, Famine & Relatives

 
 

Bacteria rarely live in isolation and often are surround by their close relatives.  As Malthus noted, the rapid growth of organisms can lead to the depletion of resources. 

Under conditions of long term resource depletion/starvation, the major source of raw material are an bacteria's neighbors, which are also its relatives. 

Assume that a population of bacteria is grown under conditions where nutrients are used up or exhausted.   If a cell dies its structural integrity is lost, and it components released and can be absorbed by neighboring organisms. 

Although it may, at first, seem counterintuitive -- the ability of individuals to kill themselves can confer a selective advantage to a population of organisms.
 

If starvation occurs, and no one dies, it is possible that all organisms present will die at about the same time – the population will become extinct. 

In such a situation, there is an obvious advantage to the cell death trait.   It a portion of the population dies, its nutrients can be released and used by its neighbors, who are live longer. 

Of course, another way to gain an advantage would be to acquire a trait, through mutation, that induces neighboring cells to die.   

If such a signal actived the apoptosis mechanism, it could be viewed as a simple form of cell-cell communication.  On the other hand, if it actively killed the neighboring cell, it could be considered a form of predation.  

  
graphic of population
+/- cell death
 
Another way to gain an advantage would be to aquire a trait, through mutation, that induces neighboring cells to commit apoptosis.    Such a trait is a form of cell-cell communication, and could be one of the beginnings of more complex forms of cellular coordination.   
 

Inducing cell death:  One common mechanism of inducing cell death in bacteria involves what is known as addiction modules

These systems were first recognized through their role in the maintenance of parasitic DNA molecules (plasmids), but similar system are present in the the host cell.

They all seem to work according to the same basic scheme: healthy cells synthesize both a stable toxin and an unstable "anti-toxin".

What these molecules do is more or less irrelevant for our purposes, except that in the absence of the anti-toxin, the toxin kills the cell. 

If something happen to block toxin/anti-toxin synthesis, the level of anti-toxin decreases faster than the level of toxin, because anti-toxin is less stable [expand?].

 

This implies that they perform a highly advantageous function, so valuable that they have been reinvented repeatedly.

  • What is the proposed model by which SpoOA expressing cells avoid death even though they synthesize 'killing factor".  
  • Since SpoOA expressing cells secrete the sporulation inhibitor protein SdpC, why isn't sporulation inhibited in all of the cells in a starving culture, even those that fail to make SpoOA?
  • Based on your reading, do you think the activation of the SpoOA gene occurs frequently or infrequently in starving cultures.  
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Use Wikipedia | 19 March 2005 revised 21-Mar-2013