MECHANISMS OF LIFE-SPAN SHORTENING 239 



out of both daughter-nuclei, becomes so stretched out by the opposing pulls 

 that each of its opposite centromeric portions succeeds in entering the 

 daughter-nucleus nearer it, and the thread between them forms a chromatin 

 bridge that hampers the effectiveness and upsets the orderliness of chromo- 

 some distribution in subsequent mitoses. This causes the death of the 

 descendant cells even if the affected chromosome material were not really 

 needed, as when a normal homologous chromosome was present that would 

 have sufficed. The bridge, then, may prove lethal even to a diploid or polyploid 

 cell. Thus with a given dose, cells having higher ploidy, being possessed of 

 more chromosomes to form bridges, are killed by this method at a correspon- 

 dingly higher rate than cells with lower ploidy. Work by Pontecorvo and me 

 on Drosophila (1941; Muller and Pontecorvo, 1942; Pontecorvo, 1942), and 

 by Whiting (1945 et seq.) as well as by Heidenthal (1945) on Hahrohracon, 

 showed that deaths by bridge formation in early zygote stages are the usual 

 cause of the dominant lethals found amoung early zygotes after irradiation 

 of spermatozoa, perhaps because the daughter-nuclei in early zygotes do not 

 usually move so far apart as to render a bridge ineffective. 



In experiments reported by Rowena Lamy and myself (1941) on the com- 

 paratively high mortality (some 50%) caused by irradiation of early embryos of 

 Droso2)hila with rather low doses (500 r), we could find no connection between 

 ploidy, or sex, and survival — a result recently supported in our laboratory by 

 results obtained by Helen Meyer and me (unpublished), using a different 

 genetic set-up for testing the matter. Lamy and I had concluded that this 

 damage was probably cytoplasmic or at least not by chromosome breakage. 

 It has recently been found by the Valencias (1962a, b) that there is about this 

 same death-rate if eggs are irradiated shortly before they are to be fertilized 

 (by unirradiated sperm), or shortly after their fertilization (in which case the 

 sperm nucleus also is irradiated), or in the stage of embryos containing some 

 4 to 8 nuclei. This result, as well as the comparatively small number of 

 recessive lethal mutations which they found by genetic testmg to have been 

 induced by the same irradiation, helps to confirm the cytoplasmic interpreta- 

 tion as the main cause of death here. But this effect cannot be termed a kind 

 of senescence since the survivors are not permanently weakened (see also 

 Clark and Mitchell, 1952, for results with Hahrohracon embryos). From species 

 to species this cytoplasmic effect in eggs is very variable, since somewhat more 

 than 15,000 r are needed to cause the egg cytoplasm of Hahrohracon to give 

 rise to much embryonic mortality if the effective nucleus (the paternal one) 

 of the merogonically developing embryo were not irradiated, while in the 

 sOlrworm Astaurov and Ostriakova-Varshaver (1957) find that the egg 

 cytoplasm can well tolerate 540,000 r. 



That such cytoplasmic effects play a negligible role, if any, in the seeming 

 senescence induced by the irradiation of stages beyond those of the early 



