May i, 1825 Necrosis, Hyperplasia, and Adhesions in Tomatoes 
885 
leaves of mosaic tomato, petunia, 
legumes, and raspberry, and a similar 
condition was found by Doolittle (11, 
■p. 17) in cucumber leaves and by Rand 
(26, p. 19) in pecan leaves. Townsend 
(33, pi. 4) showed that the spines on the 
leaf veins of the lower epidermis charac¬ 
teristic of beet curly top were due to 
elongation of cortical cells. Dickson 
(10, p. 35) found hypertrophied cblor- 
enchyma cells associated with the raised 
green areas on mottled mosaic tomato 
fruits, a condition similar to the peri¬ 
carp hypertrophy occasionally met with 
in this study. 
Extensive hyperplasia or prolifera¬ 
tion of cells was found by Allard (1, 
p. 255) in the anthers of mosaic 
tobacco plants. The hyperplastic 
development of a double layer of 
palisade tissue in the dark green leaf 
areas is reported by Hunger (15, p. 
272) and by Dickson (10, p. 26) in 
tobacco mosaic, and Doolittle (ll r 
p. 18) reports hyperplasia in connec¬ 
tion with the projecting knobs on 
mosaic cucumber fruits. 
Of special significance are the obser¬ 
vations of Smith and Boncquet (32, p. 
104 ) on the formation of wound-heal¬ 
ing cells about the phloem necrosis 
in beet curly top, the observations of 
Artschwager (2, p. 569) upon the radial 
stretching or hypertrophy of the cells 
surrounding the necrotic areas in po¬ 
tato leaf-roll and the observations of 
Kunkel (17, pi. 12) upon the elongation 
of the parenchyma cells around the 
necrotic pockets or cavities in the mosaic 
corn stalk, leading, as he says, to incip¬ 
ient gall formation. These areas, 
Kunkel (17, p. 11) states, first “appear 
water soaked and are more turgid than 
the surrounding tissues,” later (17, p. 5) 
“take on a slightly yellow or brown 
color,” and “in a still more advanced 
stage all or a part of the cells in the 
pockets collapse and elongated cavities 
are left within the stalk.” He further 
states (17, p. 9) that “the disease 
usually causes the host cell to enlarge 
.... Many diseased cells die and 
collapse. This may happen even when 
little or no abnormal growth has taken 
place. However, cells that make con¬ 
siderable growth die and break down 
earlier than cells that respond more 
slowly.” These phenomena exhibit 
striking similarities with some of those 
observed in mosaic tomatoes, except 
for the unmistakable hyperplasia in 
the latter. 
It would seem, therefore, that under 
certain conditions the young tomato 
fruit may express a range of rather 
striking symptoms, of which, however, 
some trace has been recorded in the 
mosaic and related diseases of other 
hosts. Malformation and bursting of 
the fruit, external and internal necrotic 
regions, cavities, surface blisters, trans¬ 
lucent tissue with reduced intercellular 
space, elongation of cells around 
necrotic tissues, and hyperplasia have 
been previously noted. In view of the 
profound alterations and derange¬ 
ments in the normal hereditary course 
of development of the embryonic leaf 
tissues brought about by mosaic 
diseases in general, it is not surprising 
to find strikingly aberrant histological 
conditions in the tissues of the young, 
rapidly growing tomato fruit. 
SUMMARY 
The histological abnormalities in the 
young fruits of greenhouse tomato 
plants affected with the severe type of 
mosaic (streak or winter blight) were 
studied by means of unstained free¬ 
hand sections and stained microtome 
sections. 
Normally the tissue of the axile 
placenta grows out between and around 
the ovules, engulfs them, and fills the 
locular cavity with a cellular matrix as 
the ovary enlarges. This placental 
matrix touches, but remains free from 
the carpellary walls and the seed coats. 
Many of the mosaic fruits are charac¬ 
terized by brown necrotic surface dis- 
EXPLANATORY LEGEND FOR PLATE 7 
A .—Cross section of an outer angle of a locule in fruit about 12 mm. in diameter with a double intumescence 
invading and crushing the placental matrix. The normal thickness of the pericarp is shown at lower left 
corner. Two large hyperplastic intumescences, one from the inner surface of the pericarp, one from the 
radial wall, have grown inward and met each other, after which the direction of growth was somewhat 
altered in each case. There is a thin plane of crushed necrotic tissue at the advancing face of the growths 
which have almost reached the ovule shown at the bottom of the figure. These intumescences represent 
an abnormal hyperplaslic growth 2 mm. in length. This constitutes an adhesion between the locule walls 
and the placenta. Photomicrograph X 33. Unstained 
B.—Section of a hyperplastic growth on the inner surface of the pericarp pushing into the placental tissue. 
The palisade columns of rectangular, thin-walled cells indicate the direction of growth and the muriform 
arrangement with the reduced intercellular space explains the translucent appearance of such tissue. The 
advancing face impinges upon a thin plate of crushed necrotic cells and within the hyperplastic tissue a 
secondary necrotic plane is developing, apparently as a result of increased pressure from the tissues between 
this point and the base of the intumescence. The impression is gained from this and similar sections that 
groups of basal cells often begin to divide too rapidly for the more distal cells and crowd into the latter 
from the rear. As in A, this constitutes an abnormal adhesion between locule wall and placenta, since the 
tissues do not usually separate along the necrotic planes. Photomicrdgraph X 33. Unstained 
