Bitter Pit in A'jyples. 25 



Mc Alpines theory of Bittpr Pit. 



This is in brief (p. 73) that when the supply of water is abundant 

 the vascular network may not enlarge as rapidly as the pulp cells. 

 " a mesh here and there will be left unfinished, the cells adjoining 

 will not receive their regular supplies of nourishment through the 

 regular channels, and collapse and death will ensue." 



If the supply of water is deficient, " even if the mesh was cum- 

 pletely formed, wherever the mesh of the network of vessels failed 

 in conducting water, there the adjoining cells would collapse, and 

 the entire patch shrivel and become brown." 



McAlpine is apparently unaware of the fact that water can pass 

 readily from one pulp cell to another, and that the starch grains 

 usually present in abundance in bitter pit tissue, are carried to the 

 cells through the vascular bundles in the form of sugar, showing 

 that the bundles are functioning normally. It would be easy to 

 obtain evidence of such interruption if it took place. No such 

 evidence is brought forward, and none is to be obtained by the 

 examination of bitter pit tissue. Furthermore, where the bitter 

 pit tissue may form a continuous layer near the surface, as in some 

 confluent forms of "crinkle," living tissue may occur outside the 

 affected portion of the vascular network, from which on McAlpine's 

 theory it should be cut off. His theory is based upon a series of 

 assumptions, some of which are quite incorrect, and no experi- 

 mental or anatomical evidence is brought forward to support it. 

 The exciting cause demanded is either an excess or a deficiency of 

 water, i.e., diametric opposites producing the same result. 



Finally, I have shown that single pulp cells, or small groups of 

 them, in immature bitter pits may retain their starch grains and 

 remain living and turgid until the apple is fully adult, i.e., after 

 the apple has been plucked and the flow of water and food materials 

 through the vascular bundles has ceased. In such cases we are 

 dealing with an inhibition of ferment action by an agency not 

 strong enough to immediately kill the protoplasm, and the death 

 of the starch-containing cells is simply hastened somewhat as com- 

 pared with sugar-containing cells, possibly partly as the result of 

 starvation. Under normal circumstances the sap of each cell is 

 able to hold all the sugar produced from its starch, and since the 

 protoplasm produces its own diastase, it is impossible to see how 

 an interruption of the vascular system could prevent the conversii>n 

 of the starch into sugar. 



