An analysis of the “pleiotropic” effects of a new lethal mutation in the rat ( Mus norvegicus )

Abstract

The number of observable “characters” in an organism is infinite. The number of genes which control development is limited. It follows that many, perhaps most, genes must not affect only one organ or character, but several at a time. Their effect is manifold, and the term “pleiotropism” has been coined to cover this diversity of actions of a single gene. The question arises: How does a gene produce its “pleiotropic” effects ? An agent X which produces the effects a and b can do so in three different ways. X may produce a and b directly, but in two independent and different ways ( X → a → b ). Or X may produce a and b directly, but in essentially the same way ( X —→ a → b ). Or X may produce one of its effects ( a ) directly, and this primary product in turn conditions the other effect ( b ). This is a causal chain, ( X → a → b or X → b → a ),one effect being subordinated to the other and following it in time. The primary effect may still be notice­ able when the secondary effect has developed; then we observe “pleiotropism” in space, whereas otherwise we observe it only in time. If more than two effects are conditioned by X , combinations of these three funda­mental ways of causation may occur.