Nov. 8. I9I5 Distribution of Virus of Mosaic Disease 255 



ovules, and especially the loose, dry, normally ripened seeds, in producing 

 the mosaic disease in inoculated plants. Although the greatest care may 

 be exercised in removing immature seeds from a succulent placental col- 

 umn, it must be evident that the probability of rupturing and removing 

 some of the placental substance is very great. In the normal ripening 

 process, however, the seeds loosen and fall away from the drying and 

 shrinking placental column so gradually that the minimum amount of 

 placental material is carried away attached to the seeds. 



Malformations caused by the mosaic disease may disturb the normal 

 relations of stamens and pistils to such an extent as to cause sterility in 

 many blossoms, owing to the failure of natural self-pollination. Hand 

 polHnation of these pistils has frequently led to normal seed development. 

 Not infrequently the development of the corolla is almost entirely inhib- 

 ited and the stamens and pistils also fail to develop normally. Even 

 in these blossoms the anthers may contain more or less functioning 

 pollen, which has produced normal fertihzation when transferred to the 

 pistils of healthy blossoms. In some instances the anthers produce 

 little or no functioning pollen. In extreme cases the normal form and 

 structure of the anther sacs is replaced by a mass of irregular prolifera- 

 tions. Generally blossoms affected with the mosaic disease appear to 

 produce viable pollen and ovules quite as freely as those borne by 

 healthy plants (PI. XXIII). 



From the fact that the mosaic disease is not known to occur as the result 

 of embryonic transmission of the disease directly from the mother plant 

 during seed development, it is evident that a very efficient barrier guards 

 against embryonic infection or the subsequent successful continuation 

 of the disease from parent to seedling. In particularly malignant 

 cases of the disease, where few or no viable seed are produced, following 

 pollination with pollen from healthy blossoms, it is possible that the 

 infective agents of the disease have produced embryonic infection 

 which resulted in death. Whether the failure to produce viable seed 

 in these instances is due to actual infection of the ovules or to a general 

 impairment of nutrition and cell division of the capsular structures 

 associated with embryonic development, can not at present be deter- 

 mined. It is possible that embryonic development never proceeds in 

 those ovules actually invaded and infected byvthe virus of the disease. 

 In all experimental tests at least germinable seeds from plants affected 

 with the disease have always produced normal, healthy offspring. 



At this time speculation seems quite fruitless, and one can only wonder 

 what protects the embryo so securely from the mosaic disease, even 

 though intimately associated with and nourished by infective parental 

 tissues. 



