Date Endosperm for Self- Digestion, 63 
(extracts) seemed to have had any effect, at least the quantity of ground 
cellulose had not apparently diminished.’ However, another portion of the 
cotyledon extract was found by Fehling’s test to have formed reducing 
sugar by its action on manufactured cotton fibre, while a similar portion 
boiled to destroy the enzyme was found to have no action on cotton fibre. 
From these results, and an examination of the cotyledon-structure, Green 
concludes that the ferment exists only in the epidermal cells of the coty- 
ledon, and since the endosperm extract seemed to yield no sugar after 
contact with the ground resting endosperms, he finally says regarding the 
endosperm, ‘ there was no evidence that the extract of the endosperm had 
any action on cellulose at all. Evidently in it there is no ferment and the 
change is due to agencies quite external to its cells.’ 
Brown and Morris, after an extended study of the barley endosperm, 
agreed with Van Tieghem that the amylaceous endosperm of the grasses 
is a ‘dead store house’ of reserve material. In the same paper (’ 90 , 
p. 480) the possibility is left open that the aleurone layer may contain 
some residual vitality, but the starch-bearing cells do not, and the con- 
clusion including the ‘ dead store house ’ applies only to these starch-grain- 
cells. They further found (’ 90 , p. 525) that the diastatic capacity of 
scutellum-cells is destroyed by treatment with vapour of chloroform. But 
when * portions of the integuments of germinating barley, with their 
adherent aleurone layer, are treated in a similar way with chloroform 
vapour, we have found that their diastatic power is not in the least impaired , 
the starch under such sections being as quickly and completely attacked 
as under sections which have not been treated. Moreover, we have 
observed the same thing even after the fragments have been immersed for 
some time in absolute alcohol.’ These authors assume that such treatment 
must have destroyed vitality, yet they acknowledge that the diastatic 
capacity remains undiminished. If then diastatic activity can proceed in 
dead tissue, how did these authors conclude that the amylaceous tissue of 
the endosperm constitutes a ‘ dead store house ’ because it does not possess 
diastatic activity ? The inference of course is, that if such cells had been 
found able to do enzyme work they would have been regarded as living. 
As a matter of fact, their conclusion is that the aleurone cells are living 
because they show diastatic activity, and yet this activity was manifested 
under conditions which must have prohibited vitality. This affords an 
excellent example of the trouble which arises when vitality and enzyme 
activity are confused. It must be said here that these authors probably 
do not hold such views at the present time, but in a review of this kind 
it is necessary to deal with the literature as it stands. They further find 
(’ 90 , p. 509) that translocation diastase is probably produced in the 
endosperm-cells by the embryo during its ante-resting development and 
that residual translocation diastase constitutes the diastase of the resting 
