In 1928, Frederick
Griffith encountered a phenomenon now known as genetic transformation.
Colonies of virulent strain
(pathogenic) of pneumonia causing bacterium, Streptococcus pneumonia grown
on nutrient agar, have a smooth (S)
glistering appearance owing to the presence of a type specific, polysaccharide
(a polymer of glucose and glucuronic acid) capsule. The avirulent
(non-pathogenic) strains, on the other hand, lack this capsule and they produce
dull, rough(R) colonies. Smooth (S) and rough (R) characters are directly
related to the presence or absence of the capsule and this trait is known to be
genetically determined. Both S and R forms occur in several types and are
designated as S-I, S-II, S-III, etc., and R-I, R-II, R-III, etc., respectively.
All these subtypes of S and R bacteria differ
with each other in the type of antigens, they produce. The kind of antigen
produced is likewise genetically determined. Smooth (S) forms sometimes mutate to
rough (R) forms, but this change has not been found reversible. In the course
of his work,
Griffith
injected laboratory mice with injected with virulent S-III
pneumococci, the mice suffered from pneumonia and died.He then injected laboratory mice with live R-II
pneumococci; the mice suffered no illness because R-II pneumococci was avirulent. However, when he
injected the heat killed S-III bacteria in mice, they did not suffer from
pneumonia. But, when the mice were injected with the mixture of living
avirulent R-II and heat killed S-III virulent, the unexpected symptoms of
pneumonia appeared and high mortality resulted in them. By postmorteming the
dead mice, it was found that their heart blood had both R-II and S-III
pneumococci. From these results, Griffith concluded that the presence of the heat-killed
S-III bacteria must have caused a transformation
of the living R-II bacteria, so as to
restore to them the capacity for capsule formation they had earlier lost by
gene mutation. This was called “Griffith
effect” or more popularly “bacterial trans-formation”.
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