Luria–Delbrück experiment

The Luria–Delbrück experiment (1943) (also called the Fluctuation Test) demonstrated that in bacteria, genetic mutations arise in the absence of selective pressure rather than being a response to it.

Thus, it concluded Darwin's theory of natural selection acting on random mutations applies to bacteria as well as to more complex organisms.

Max Delbrück and Salvador Luria won the 1969 Nobel Prize in Physiology or Medicine in part for this work.

Suppose a single bacterium is introduced to a growth medium with rich nutrients, and allowed to grow for

In particular, if the distribution of survivor number turns out to decay more like a power law than like an exponential, then we can conclude with high statistical likelihood that Darwinian scenario is true.

(Section 4.4 [1]) By the 1940s the ideas of inheritance and mutation were generally accepted, though the role of DNA as the hereditary material had not yet been established.

[2] In their experiment, Luria and Delbrück inoculated a small number of bacteria (Escherichia coli) into separate culture tubes.

After a period of growth, they plated equal volumes of these separate cultures onto agar containing the T1 phage (virus).

This was not what Delbrück and Luria found: Instead the number of resistant colonies on each plate varied drastically: the variance was considerably greater than the mean.

Luria and Delbrück proposed that these results could be explained by the occurrence of a constant rate of random mutations in each generation of bacteria growing in the initial culture tubes.

When both plates were incubated for growth, there were actually as much as 50 times greater number of bacterial colonies on the respread dish.

[6] More recently, the results of Luria and Delbrück were questioned by Cairns and others, who studied mutations in sugar metabolism as a form of environmental stress.

[7] Some scientists suggest that this result may have been caused by selection for gene amplification and/or a higher mutation rate in cells unable to divide.

[8] Others have defended the research and propose mechanisms which account for the observed phenomena consistent with adaptive mutagenesis.

Dilutions are plated onto rich medium to calculate the total number of viable cells ( Nt ).

Numerical comparisons of these two models with realistic values of the parameters has shown that they differ only slightly.

The determination of μ from this equation has proved difficult but a solution was discovered in 2005[citation needed].

The mechanism of resistance to the phage T1 appears to have been due to mutations in the fhuA gene - a membrane protein that acts as the T1 receptor.