168 The Structure of Protoplasm 



end into an anterior end with a typical hyaline cap. If the pressure 

 against this new anterior end is now increased, the direction of 

 flow again immediately reverses and a hyaline cap again forms at 

 the opposite end. This can be repeated many times on the same 

 individual, provided some little time is allowed for recovery between 

 successive reversals in the direction of pressure." 



Internal pressures may also play a role. As endoplasm is forced 

 forward into the softened anterior end of the slime mold, the internal 

 pressure there increases. It is possible that when the pressure 

 reaches a certain point, gelation may occur and increase until the 

 resulting increase in contractile tension increases the internal 

 pressure to a point where solation results. 



We come now to the regulation a^id polarization of the viscosity 

 changes. It is quite evident that there must be some sort of a 

 regulation of these changes, otherwise progressive locomotion could 

 not occur except accidentally. The continued or periodic softening 

 at the anterior end and the greater contractile tension at the 

 posterior end are necessary for progression. Pseudopodia may be 

 thrust out and withdrawn from various regions of an ameba or a 

 cell without locomotion. Some sort of a polarization is needed. The 

 thickness and the viscosity of the gel layer, which determines its 

 contractile tension, are undoubtedly regulated, as are also the 

 amount and viscosity of the endoplasm. There are probably both 

 internal and external environmental factors involved. 



Various authors have questioned the validity of the theory that 

 the contractile tension of the gel layer plays an essential part in 

 locomotion. The older ideas that surface tension plays a leading 

 role can be dismissed without comment. More recently Marsland 

 and Brown (1936) have questioned the contractile tension theory 

 as will be seen by the following quotation: (p. 177) "Streaming of 

 the plasmasol in a forming pseudopodium is immediately stopped by 

 sudden compression to about 250 atmospheres." (p. 175) "On the 

 hypothesis that the flow is caused by a contraction of the proximal 

 portion of the plasmagel tube, forcing the plasmasol distally into 

 the forming pseudopodium the cessation of movement might be 

 attributed to a loss of tension throughout the entire plasmagel tube 

 due to the liquefying action of the pressure. On this basis the flow- 

 ing of the plasmasol would cease when, as a result of the increased 

 fluidity of the plasmagel, the force exerted by the plasmagel tube 

 becomes too small to overcome the resistance to flow. It is question- 

 able, however, that a constriction in the plasmagel tube is a neces- 



