52 



PHYSIOLOGICAL TRIGGERS 



suggestion that diapause is caused by a quantitative deficiency in energy- 

 yielding enzyme systems, a deficiency which is repaired in some way by PGH. 

 Convincing evidence to the contrary is provided by the curious phenomenon 

 of injury metaboUsm {t,t„ 34). The simple insertion and withdrawal of a fine 

 hypodermic needle in the diapausing pupa evokes a doubling or tripling of the 

 oxygen consumption within 24 hours. After more extensive integumentary 

 injury, metabolism increases 6- to 14-fold and requires more than 2^2 months 

 to return to initial levels. Injury metabolism is unattributable to enhanced 

 muscular activity, or to reactions requiring the participation of either the 

 central nervous system or the insect's endocrine system as presently defined, 

 for surgically isolated anterior and posterior halves of pupae, and pupae from 

 which the entire central nervous system has been extirpated exhibit an injury 

 respiration. Nor can injury metabolism be correlated with localized repair of 

 the wound, for the high metabolism persists for months after repair is apparently 

 completed. It seems to be triggered by substances released at the site of injury, 

 for injury to one member of a parabiotic pair causes an almost equal rise in the 

 metabolism of both animals (30). The injury metabolism is peculiar to the 

 diapausing pupa. It cannot be demonstrated in freshly pupated animals, in 

 animals after the initiation of adult development or in non-diapausing species 

 like the bee moth Galleria mehmella at any stage (34, 40). 



For the present discussion it is of special importance that, though the metab- 

 olism of the diapausing pupa can be increased by injury to levels characteristic 

 of the post-diapausing insect midway in adult development, no development 

 takes place. Thus the diapausing pupa, while capable of respiring at rates that 

 characterize the growing insect, fails to grow in the absence of the proper hor- 

 monal stimulus of the prothoracic glands and the proper quality of metabolism. 

 It appears that the increment of respiration induced by injury cannot be cou- 

 pled to morphogenesis. The injury-stimulated respiration gives assurance that 

 the absence of morphogenesis during diapause is not attributable to a simple 

 quantitative deficiency in the dehydrogenase enzymes which release hydrogen 

 from substrate or the redox enzymes which transmit the hydrogen to oxygen. 

 Nor is it due to an inability to form sufficient high energy bonds, for Telfer and 

 Williams (42) have recently shown that the incorporation of C'^-labeled glycine 

 into pupal proteins is stimulated by injury to about the same degree as respi- 

 ration. Since the incorporation of amino acids into pupal proteins most likely 

 requires the same kinds of high energy phosphate and sulfur bonds as are used 

 in adult development, this finding reemphasizes the qualitative nature of the 

 energetic defect in the diapausing pupa. 



Since it appears to be quality rather than quantity of metabolism that dis- 

 tinguishes the diapausing pupa from the developing adult, let us examine more 

 closely the metabolic differences between the two. It has long been recognized 

 that the over-all gas exchange of diapausing pupae is peculiar in that e.xceed- 



