Nov. 8,1915 
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 
pollination 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 fertilization 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 by the 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. 
