How does the regular spacing of heterocysts arise?
Cells can't count. How then does the regular pattern of heterocysts -- one in ten cells -- arise? Wolk & Quine (1975) put forth a simple idea to explain patterned heterocyst differentiation. This model rests on two assumptions:

     1. Random initiation: There is no prior pattern. The first cells to differentiate are chosen at random.
     2. Lateral inhibition: Differentiating cells release a diffusible inhibitor that acts on adjacent cells.

These two assumptions are sufficient to explain the appearance of pattern, as shown in the accompanying figure.

The Wolk & Quine model is sufficient, but is it true? If it is, then the following predictions should be fulfilled:

Predictions/Assumptions of Wolk & Quine

     1. Sparse initial pattern: First committed cells should be rare, distant from one another

In fact, the mature pattern of heterocysts is preceded by an intermediate pattern of strings of differentiating cells. This can be perceived only by making visible the patterned expression of genes.

     2. Pattern requires diffusible inhibitor: A mutant lacking the inhibitor should have a random pattern

In fact, such a mutant appears to exist. The result is not a random pattern of heterocysts but rather fixation of the intermediate pattern of strings of heterocysts.

     3. Rapid pattern formation: Time from first cell commited to last should be less than 2 hours

In fact, left to themselves, some cells seem to commit immediately while others require many hours.

Wolk & Quine's model is too simple to explain patterned heterocyst differentiation.

Regular spacing explained by a Turing-like model

Back to Table of Contents