PLASMAGENES 399 



from individual to individual (although this can be achieved if the graft 

 is small enough not to provoke an intense anti-body formation by the 

 host), hi this it is very different from most viruses. Secondly, the plasma- 

 gene does not possess complete genetic continuity, but must arise anew 

 during the development of the melanocytes from the neural crest; pre- 

 sumably the initiation is gene-controlled, although the difficulty of inter- 

 individual transplantation makes it difficult to prove this formally. Again, 

 one must remember that the pigment-forming cells are peculiarly adapted 

 to make contact w^ith their neighbours, and are known to pass pigment 

 granules into cells, e.g. in the hair follicles, which are themselves incapable 

 of manufacturing pigment. Thus the situation which enables us to recog- 

 nise the existence of these plasmagenes by their transmission from cell 

 to cell is a very unusual one. One might deduce from this that many such 

 particles might exist in other cells, without our being able to detect them; 

 equally one might argue that it is only because the melanocytes provide 

 this peculiar mechanism of passing granules into contiguous cells that 

 particles which can multiply and preserve their genetic character have been 

 evolved to take advantage of it. Finally, the relations between the particles 

 and the genetic factors in the nucleus remain obscure because we do not 

 understand what genetic difference, if any, exists between a white and a 

 dark area in a piebald guinea-pig ; both areas are, of course, derived from 

 a single fertilised egg, and probably both contain exactly the same genes, 

 although some authors have suggested that the piebald pattern is due to 

 mutation of a colour-controlling gene in some of the somatic cells. It 

 remains obscure, therefore, whether, when the pigment-forming plasma- 

 gene is passed into a white cell and proceeds to multiply there, it is aided 

 in doing so by the gene which initiated it, or whether that gene has 

 mutated to an inactive form and the plasmagene is wholly responsible 

 for the maintenance of its genetic character. 



Some suggestive but indirect evidence for the existence of cytoplasmic 

 plasmagene-hke particles in normal cells can be found in some of the 

 studies which have been made on tumour-inducing 'agents' of the kind 

 which are often classed as viruses. These agents seem to be particulate in 

 nature, and when suspensions of the particles are injected into appropriate 

 healthy cells, they can multiply and cause the cells to develop into tumours. 

 One important point in the present connection is that particles extremely 

 similar to those of the tumour-virus can also be found in normal healthy 

 cells; they are in fact the microsomes (Claude 1940). Further, when normal 

 cells are acted on by certain carcinogenic chemical substances, the tumours 

 which are induced are foimd to contain cytoplasmic particles capable of 

 acting as tumour-viruses ; and it is certainly simplest to suppose that these 



