134 Hazen: NEW SPECIES OF LOBOMONAS 
much upon external environmental influences to account for 
the requisite local variability, though this element is not neces- 
sarily involved in either theory. 
The beginning of the more recent undermining of the surface 
tension explanation of form change is found in the work of 
Jennings (14), who from painstaking direct observation reported 
that the currents in a moving Amoeba as a whole ‘are not similar 
to those of a drop of inorganic fluid that is moving or elongating 
as a result of a local increase or decrease in surface tension’, and 
in particular that ‘the movements of material in a forming 
pseudopodium are not like those in a projection which is pro- 
duced in a drop of inorganic fluid as a result of a local decrease in 
surface tension’. From these observations Jennings was forced 
to the conclusion ‘that changes in the surface tension of the 
body are not the primary factors in the movements and reac- 
tions of Amoeba’. Similar conclusions from direct observation 
were announced two years Jater by Dellinger (10), whose clever 
photographs of Amoeba viewed from the side reveal the locomo- 
tion of the organism as a sort of ‘walking,’ rather than a flowing of 
a fluid substance upon the substratum. These negatory con- 
clusions have been reinforced and extended by a series of recent 
researches in the field of microdissection (15, 21, 13). From 
these there is general agreement that the structure of Amoeba 
(and probably of many other rhizopods and cells of primitive 
organization) is not of the nature of a simple fluid mass governed 
chiefly by surface tension forces, but rather that it is a highly 
non-homogeneous system, consisting of comparatively fluid 
endoplasm surrounded by an ectoplasm which has often the 
character of a semi-rigid gel, possessing a considerable elasticity, 
though the two regions may very probably grade into one an- 
sage imperceptibly. 
Finally, the experiments of Hyman (13) reveal in each 
pseudopodium of Amoeba a gradient in susceptibility to potas- 
sium cyanide, the susceptibility being greatest at the distal end 
and decreasing proximally. This susceptibility gradient is re- 
garded as being a metabolic gradient which arises before the 
pseudopodium appears, ‘and hence the metabolic change which 
produces increased susceptibility is the primary cause of pseud- 
opodium formation.’ Liquefaction or solation is regarded as 
the cause of the extension of a pseudopodium, and coagulation 
or gelation as the cause of its retraction: the liquefaction is be- 
lieved to be brought about by the metabolic change just re- 
