CHROMOSOME ABERRATIONS IN ANIMALS 647 



quence of end-to- end union of sister chromatids at the site of the break, 

 formation of a chromatin bridge between the two separating centromeres 

 at anaphase, and subsequent breakage of the extended strand at an 

 indeterminate position. The irregular cleavage mitoses lead to abnormal 

 embryonic development, and occasionally cellular multiplication may 

 occur without differentiation (Sonnenblick and Henshaw, 1941). 



If the breakage-fusion-bridge cycle occurred in either the fourth 

 chromosome or a sex chromosome, it might not be expected to prove 

 lethal in all cases, since haplo-fourth and XO individuals are viable. 

 Muller (1940) and Pontecorvo (1941) found, however, that the number of 

 individuals surviving loss of a sex chromosome was much lower than 

 expected. It thus appears that the actual mechanism of loss may 

 involve mechanical difficulties that upset the course of mitosis and modify 

 subsequent developmental processes, even though the absence of the 

 chromosome from the complex would not in itself cause death of the 

 embryo (cf. Fano and Demerec, 1944; Catcheside and Lea, 1945b; 

 Catcheside, 1948). Viable losses, which occur with a frequency of about 

 1 per cent at 4000 r according to Pontecorvo (1942), presumably occur 

 when the break is produced close to the centromere, so that a short 

 bridge is formed at anaphase. Formation of daughter nuclei could 

 presumably then proceed without interference from the chromosome in 

 the process of elimination (see also Catcheside, 1948). 



For the reasons indicated, most of the detectable deficiencies induced 

 by irradiation of spermatozoa of Drosophila are intercalary rather than 

 terminal. Some exceptions have been reported, however (Demerec and 

 Hoover, 1936; Sutton, 1940; Catcheside and Lea, 1945a), and it has also 

 been noted that terminal inversions occur in nature (e.g., by Kaufmann, 

 1936 and Kikkawa, 1938, on D. ananassae). These observations present 

 an objection to Muller's suggestion (1941) that the induced losses are 

 always intercalary rather than terminal, the deleted section approaching 

 the tip but not including the terminal band or bands. Muller's assump- 

 tion (1940) that the chromosomes of Drosophila contain specialized 

 terminal chromomeres or telomeres essential to their survival has also 

 been contested, on the basis of an analysis of breaks induced in ring-X 

 chromosomes (Catcheside and Lea, 1945b). 



The extent of an induced intercalary deficiency may be determined 

 roughly by a method designed by Painter and Muller (1929), which 

 measures the suppressing action of genes in the remaining or centric 

 portion of the chromosome. Irradiated males are mated with females 

 having attached-X chromosomes carrying recessive marking genes. 

 When a spermatozoon carrying an X from which a section has been 

 deleted as a result of radiation injury fertilizes an egg with attached-X 

 chromosomes, the individual created has X-chromosome material in 

 excess of that of a normal diploid female. The wild-type genes in the 



