Genic Control of Development 401 



the development of Drosophila with more or less large and different 

 lethal deficiencies in homozygous condition, in order to find out the 

 time of action of the loci the absence of which causes death. It turned 

 out that eggs without an X-chromosome — the extreme — stopped de- 

 velopment during the first hour. The blastoderm nuclei do not succeed 

 in reaching the surface in most parts. If only the right half of the X 

 is missing, death occurs in the second hour and only an incomplete 

 blastoderm is formed. With the other half of the X missing, a blasto- 

 derm is formed but no germinal layers, and death occurs in the third 

 hour. With different Notch deficiencies, the stoppage of development 

 occurs after six hours when the first organs are formed. The nervous 

 system hypertrophies; mesodermal organs and entoderm are lacking. 

 It can be shown that these effects are not simply a result of the missing 

 quantity of chromatin. As all Notch deficiencies of very different length 

 give the same result, it is clearly the absence of definite sections which 

 is responsible. From this it is concluded that individual "genes" con- 

 trol the major developmental processes from the very beginning and 

 that each has its definite time of action. Specifically it is concluded 

 that one such locus (facet-Notch) is indispensable for the formation 

 of some of the organ primordia. Another such locus with a lethal ac- 

 tion, if absent, is the white locus; all deficiencies containing it produce 

 lethality after twelve to sixteen hours. 



Hadorn, who made comparable studies involving transplanta- 

 tions of organs between normal and lethal larvae, proposes the fol- 

 lowing interpretation. He distinguishes between vital loci, the absence 

 of which is always lethal, and less vital loci which might fall out with- 

 out major harm. The deficiency effects found by Poulson are always due 

 to one such vital locus: the one which has an irreplaceable function at 

 the earliest time of embryonic development. To each of these a time 

 is allocated at which the deficiency effects become visible; this, of 

 course, is not the same as saying that the locus begins action at this 

 time, but only that the lack of action becomes critical at this time. 

 (This means to me a threshold type effect, conditioned by the other 

 simultaneous genic actions.) Hadorn concludes (now extrapolating 

 upon the normal function) that definite genes are already in specific 

 control of the first processes of embryogenesis, and that the loci in the 

 chromosomes of embryonic nuclei act in a set order, one after the 

 other, upon early differentiation. This is the old problem of "activation 

 of the genes," which we studied previously. As we have seen, it re- 

 quires much more than an intrinsic order of genic functionality (see 

 III 5 B c). Lethality, as analyzed by Poulson, is of course an effect of 



