606 PLANT GROWTH AND PLANT COMMUNITIES 



been shown to be effective in this respect. Radiant energy, irritation, 

 many structurally very different chemical substances, as well as micro- 

 organisms and viruses, have been found to be tumorigenic. The effec- 

 tiveness of these agencies in eliciting tumors appears, moreover, to be 

 a function of the hereditary constitution of the host to which they are 

 applied. 



A major point at issue in the tumor problem today is whether 

 tumors in general result from an intrinsic cellular change involving a 

 somatic mutation (at the chromosomal, genie, or cytoplasmic level) or 

 from an extrinsic factor such as a virus. In either case, the end result 

 can be looked upon as involving a change in cellular heredity, since in 

 the case of the virus-induced tumors the infected host cell has acquired 

 new genetic information as a result of the presence of the virus. If, 

 nevertheless, it could be established experimentally that the generality 

 of tumors is caused by viruses, or that most are the result of somatic 

 mutations, it would still not explain enough. The question would re- 

 main as to how either a virus or a somatic change induces the tumorous 

 state in a cell. I should like now to examine this question by analyzing 

 three non-self-limiting tumorous diseases of plants, each of which has 

 a different and quite distinct proximate cause, to learn whether some 

 common underlying mechanism can be characterized that will permit 

 us to gain insight into the nature of autonomous growth in representa- 

 tive plant-tumor cell types. 



The first of these non-self-limiting neoplastic diseases is known as 

 Black's wound-tumor disease (Black, 1949). This disease is caused by 

 a typical virus, which has been isolated and pictured with the aid of 

 the electron microscope. The virus particle has been found to be a 

 polyhedron having a diameter of approximately 80 millimicrons 

 (Brakke et al., 1954). Although this disease is caused by a virus, its 

 expression in a host is limited to areas of irritation such as those caused 

 by wounds. In addition to the virus and an area of irritation, the genetic 

 constitution of the host plays an important role in the expression of this 

 disease (Black, 1951). The genetic constitution may determine sus- 

 ceptibility of the host to the virus or it may determine the response of 

 the cells to the presence of the virus. Thus the virus (1) may fail to 

 multiply in a particular host species, ( 2 ) may multiply but fail to elicit 

 tumors, or (3) may multiply and produce tumors. In the third category, 

 and within the same plant species, various clones may show striking 

 differences with respect to the frequency, distribution, size, and shape 

 ©f the resulting tumor. It is significant that the inbred B21 clone of 

 sweet clover, which responds readily to virus infection with tumor for- 

 mation, also occasionally gives rise to tumors spontaneously in the 

 non-infective state (Littau and Black, 1952). This situation is com- 

 parable to that observed in strain CsHb mice which have lost the 



