44 PHYSIOLOGICAL GENETICS 



Similarly, merogonic tissue in Amphibia dies, except when grafted 

 or grown upon a normal host (Baltzer, 1933). The same applies 

 to haploid Drosophila tissue (Bridges, 1930). Otherwise 

 doomed tissues of a lethal brachyuric mouse may be grown in 

 vitro (Ephrussi, 1935), and lethal deficiencies may exist as mosaic 

 spots (Ephrussi, 1934). All these cases show a physiological 

 damage produced by mutant genes or lack of chromosome mate- 

 rial, which spreads within the tissues and may therefore be 

 counteracted by the presence of normal tissue. These facts do 

 not, then, belong to the problems discussed in this chapter. 

 The same applies to genie interactions which might produce 

 lethal effects by lack of some coordination. Kosswig (19296) 

 and also Goodrich (1935) showed that in hybrids of the fishes 

 Platypoecilus and Xiphophorus the pigment cells produce such 

 an excess of pigment that actually fatal melanotic tumors occur. 

 A similar effect in early development would, of course, also be 

 lethal. 



D. Preliminary Conclusions 



The study of the phenocopies, the sensitive periods, and the 

 development of mutants already permits some conclusions which 

 have been partly anticipated at different points of the description. 

 Two different sets of facts are pertinent. First, we consider the 

 cases where the phenotypic expression of a mutant trait is a 

 function of temperature within the physiological limits of adapta- 

 tion to temperatures (in Drosophila ca. 16 to 30°). In these 

 cases, e.g., Bar eye in Drosophila, the effect follows the well- 

 known rules for temperature action upon life processes. In this 

 connection, it is of no importance whether this effect is described 

 in terms of the Van't Hoff or the Arrhenius or any other formula. 

 The fact is decisive that the effect is of the same type as observed 

 in certain chemical reactions, without any additional features, 

 roughly described in the terms of the Van't Hoff formula as an 

 increase of two to three times for 10° rise of temperature within 

 the physiological temperature zone. In these cases, some of the 

 multiple alleles of the mutant produce an effect at normal tem- 

 perature that is situated within the range of the experimentally 

 varied effect at different temperatures. If, then, the effect of 

 raising the temperature is to increase the velocity of some reac- 

 tions or processes, it seems that the mutant (multiple) allelomorph 



