232 Cytoplasm as Seat of Genetic Properties 



ferent hypothesis, by which the problem entered the field of cyto- 

 plasmic inheritance while doing away with plastid mutation and 

 sorting out. He "assumed that in the cases of status albomaculatus the 

 cytoplasm is in a labile condition between normal and "sick," the latter 

 not permitting the plastids to become green. Unknown conditions 

 (i.e., chance) decide which condition prevails and remains constant 

 (we might speak of an alternative norm of reaction decided by un- 

 known causes). From the point of view of cytoplasmic inheritance, 

 this explanation puts the case in the same category as all the other 

 previously discussed ones of the type of cytoplasm as substrate, with 

 additional alternative norm of reaction. 



Rhoades ( 1947 ) , who generally agrees with Correns' position, likes 

 to go a step farther. He bases his views on the work of Anderson 

 (1923) and Demerec (1927), who found that in maize the maternally 

 inherited variegation results in green, yellow, and striped seedlings not 

 distributed at random on the ear. To Rhoades this indicates that 

 segregation of some discrete cytoplasmic component controlling plastid 

 development occurs, which might be called a plasmagene. He thinks 

 that there are two possibilities: either a plasmagene affecting plastid 

 development exists in a normal or abnormal form; or only one type of 

 plasmagene exists which is not present in sufficient numbers to be 

 handed equally to both daughter cells, one of which does not receive 

 enough. "On the basis of the first alternative, the ratio of abnormal to 

 normal plasmagenes would determine the type of plastid development. 

 Those cells with a critical percentage of abnormal plasmagenes would 

 contain poorly developed plastids, while those cells with higher pro- 

 portions of normal plasmagenes would have more normally developed 

 plastids. The occurrence in Anderson's strain of a transition zone — with 

 graded intermediate plastid colors — between green and yellow stripes 

 that have different cell lineages, suggests that these plasmagenes are 

 able to pass through cell membranes. It also argues in favor of the 

 first alternative . . ." 



I do not think that this argument is very convincing, apart from 

 the objection which Correns already made on the basis of showing 

 that such a sorting out does not work when considered in detail, and 

 apart from the rather offensive idea of genes passing through the cell 

 membrane. The hypothesis tries to explain the facts in terms of dif- 

 ferent particulate determiners and their shuffling. As long as it is 

 possible to understand the facts on a physiological basis ( i.e., actions ) , 

 such an explanation seems to be simpler. If, in green-white variegation, 

 an all-or-none effect of a specific ("sick") cytoplasm is involved, there 



