Metabolism and mode of action 



Lecithin or the corresponding lipoprotein at the outside of the lipoid 

 boundary membrane (top left in diagram) at which accumulation is observed 

 is supposed to form lipoid soluble complexes with salts and so act as the 

 carrier which transfers the salt across the membrane to which as free salt it 

 would be impermeable. 



At the inside (or at the accumulation site; bottom right in diagram) 

 lecithinase-D hydrolyses the complex to choline and phosphatidic acid, 

 liberating the salt. The choline is then converted to acetylcholine by the 

 acetylase system, the energy for this step being derived from ATP ultimately. 

 Choline-esterase is known to act as a transferase in at least one reaction, i.e. 

 acetylcholine+butyric acid ^ butyrylcholine+acetic acid. It is suggested 

 here that the choline-esterase of accumulating membranes similarly transfers 

 choline from the acetyl to the phosphatidyl radical, thus resynthesising lecithin 

 at the outside of the membrane. 



A phosphatide cycle is thus postulated as the carrier mechanism. The 

 cycle is obviously stopped by inhibitors of lecithinase, like rhodamine, by 

 choline-esterase inhibition, and by interference with ATP phosphorylation 

 such as is produced by dinitrophenal. All of these inhibitors apparently 

 cause an inhibition in ion-uptake. 



One should not over-emphasize any teleological argument, but it is 

 noteworthy that choline-esterase is singularly active in the electric organ of 

 Electrophorus. which must be a site of remarkable ion-secreting activity. 

 Phosphatides are noteworthy structural constituents of plant and animal 

 membranes. The enzyme systems referred to certainly exist and presumably 

 have some function. 



It is suggested that the phosphatide-cycle might also form a water-secreting 

 system, as lecithin-water complexes are well known. Furthermore, carbo- 

 hydrate complexes, particularly with inositol-phosphatides, have been 

 isolated, and a corresponding carbohydrate accumulation system is conceiv- 

 able which might be blocked by certain esterase inhibitors. 



THE ACTION OF lAA ON COLEOPTILES 



At high concentrations, 5XlO-*M and over, lAA causes a brief rapid 

 extension which is replaced in short time, 2 to 4 hours, depending on the 

 concentration, by either cessation of further extension or even by shrinkage. 

 This 'toxic' effect, it is suggested, is due to paralysis of the water and salt 

 accumulation system operated by the postulated phosphatide cycle. There 

 is experimentally demonstrated paralysis of accumulation whatever the 

 mechanism may happen to be. 



The striking extensions produced at concentrations between 10~* and 

 10-^ M are, it is suggested, due to interference with the pectin of the walls 

 and removal of Ca++ and/or Mg++ and replacement of calcium pectate 

 in part by free — COOH and in part by — COOCH3. 



One final point may be noted in this connection, we have found in this 

 laboratory that 10-^ to IQ-^ M dimethylthetin chloride, [(CH3)2 ' S • 

 +CH2CObH]Cr, is an active promoter of extension growth during a 

 limited period, behaving rather like a concentrated (10"^ M) lAA solution. 

 This it seems may be related to its known behaviour as a methyl-donor. 



The fact should again be emphasized that the chitin-containing and 



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