May 1, 1925 
881 
Necrosis, Hyperplasia, and Adhesions in Tomatoes 
DISCUSSION 
From a study of these abnormal 
tissues the impression is gained that 
the hypertrophy and hyperplasia are 
responses to the necrosis, possibly an 
effort on the part of the host to repair 
and replace or to isolate and occlude 
the necrotic tissue, possibly a response 
to a stimulus emanating from the 
necrotic tissue. In the surface blisters 
this explanation is tenable, inasmuch 
as the epidermal layer is necrotic. 
The well-developed intumescences on 
the inner walls of the locules occur only 
opposite necrotic regions in the pla¬ 
cental matrix or under necrotic areas 
of the inner epithelium of the pericarp. 
It may be stated as a general rule that 
the hypertrophy and hyperplasia occur 
only in close association with the ne¬ 
crosis. 
Structurally the type of growth re¬ 
sembles that involved in wound tissue 
or cork formation. The fact that the 
smaller cells in the hyperplasias occur 
in proximity to the necrotic tissue 
would indicate that the latter may 
supply the growth stimulus. Riker 
{28, p. 427) found that the smaller cell 
size and the most rapid cell division in 
tomato stems inoculated with the 
crown-gall organism occurred in the 
cells adjacent to the intercellular spaces 
containing the bacteria and hence near¬ 
est to the source of stimulation. How¬ 
ever, in the larger intumescences in the 
mosaic fruits there is evidence of re¬ 
newed waves of growth in the basal 
portions quite distant from the ne¬ 
crotic region. 
The destructive invasion of tissues 
by these proliferations and the ab¬ 
normal tissue fusions may be inter¬ 
preted as incidental consequences of 
the growth response to the necrotic 
condition. However, it may be pos¬ 
sible that hyperplasia, as well as 
necrosis, is a direct effect of the mosaic 
virus. The flattened necrotic plates 
are doubtless the result of the pressure 
of the hyperplastic tissue. 
That the epithelium lining the locules 
in a young tomato is readily reactive 
to a growth stimulus, or to a removal 
of growth inhibition, is shown by the 
ease with which Smith {31, p. 174) was 
able to produce surface proliferations 
by exposing this epithelium to the 
vapor from injections of 20 per cent 
solutions of ammonium carbonate, 
acetate, and tartrate. The greater 
prevalence of necrosis in the tissues of 
the placental matrix may possibly be 
associated with their extremely rapid 
growth. 
A partial review of the literature on 
mosaic and related diseases shows that 
certain of these histological phenomena 
have been previously noted. With 
respect to the malformation and 
rupture of fruits, the bizarre effect of 
the mosaic disease on cucumber fruits 
has been described by Doolittle {11, p. 
13), who also noted that the same 
disease caused a bursting or rupture of 
the pericarp of the wild cucumber fruit. 
Allard ( 1, p. 255) noticed malformation 
of the blossoms in tobacco mosaic 
which interfered with the normal 
development of the pistil and reported 
that mosaic reduced the number and 
the viability of the seeds. The mal¬ 
formation effect of mosaic on tomato 
fruit has been noted by Dickson {10, 
p. 18) and has been reported in con¬ 
nection with winter blight by Howitt 
and Stone {14, p • 164)- Both internal 
and external malformation of the 
tomato fruit were noted by Cobb {9, 
p. 412) in a disease called rosette. The 
necrotic surface-spotting of tomato 
fruits associated with mosaic or related 
diseases has been described by a 
number of observers including Selby 
{30, p. 238), Orton and McKinney {23, 
p. 242), Howitt and Stone {14, p. 163), 
Brittlebank {8, p. 132), Paine and 
Bewley {24, p. 187), McKay {18, p . 
181), Gardner and Kendrick {12, p. 
8), and Poole {25, p. 5). 
Of particular interest in connection 
with the surface blister lesions on 
tomatoes and pericarp-rupture are the 
observations of Atanasoff { 4 , p . 8) upon 
the occurrence of flat translucent 
blisters on very young potato tubers 
of the Schotsche Muis variety affected 
with stipple streak, in which case the 
blisters sink and produce hardened 
EXPLANATORY LEGEND FOR PLATE 5 
A. —Section of an early stage of a fruit blister showing the brown necrosis of the epidermal cells and 
the hyperplasia of the subepidermal cells. Photomicrograph X 126. Stained with gentian violet. 
B. —Cross section of a portion of a surface blister showing radial elongation and transverse division of the 
subepidermal cells to form the hyperplastic tissue of the blister. The necrotic tissue is in the epidermal 
region of the blister. Photomicrograph X 82. Unstained 
C. —Cross section near center of a fruit 1 cm. in diameter showing portions of septa, placenta, and seeds, 
with necrotic areas and a rather marked displacement or abnormal arrangement of the ovules. (1) Thin 
plate of necrotic tissue at the advancing face of a hyperplastic outgrowth from the locule wall. (2) Necrotic 
pocket near an ovule. (3) Necrotic pocket in "the placenta partially surrounded by a zone or whorl 
of hyperplastic tissue. (4) A necrotic ovule. (5) A partially necrotic ovule abnormally oriented. (6) 
A necrotic ovule in contact with a plate of necrotic tissue and an outgrowth from the locule wall. The 
ovule is somewhat changed from its normal location. Photomicrograph X 25. Unstained 
