The present study explores the origin of human Robertsonian translocations (RT) 
and the causes of the nonrandom participation of the different acrocentrics in 
them. Satellite associations have been analysed in 966 cells from 8 persons, and 
1266 RT with ascertainment have been collected from the literature. The 
observation that the chromosomes preferentially taking part in satellite 
associations vary between individuals is confirmed. However, since a preferred 
chromosome appears to associate at random with the others, this phenomenon 
should not add to the nonrandomness of the RT. Most RT presumably arise through 
adjacent chromatid exchanges corresponding to mitotic chiasmata, in the 
pericentric regions of the acrocentrics. Our working hypothesis is that there is 
a basic exchange rate between any two acrocentrics. The surplus of t(14q21q) is 
presumed to depend on these two chromosomes having a homologous pericentric 
region. The 10-20 times higher incidence of t(13q14q) as compared with other RT 
is best explained by crossing-over between homologous, but relatively inverted, 
segments in these chromosomes. Of the 246 RT ascertained through repeated 
abortions or infertility, 56 were found through the latter. Of these, chromosome 
14 was involved in 51. The infertility may be caused by a small deletion of 14q, 
as is often the case in 15q in Prader-Willi syndrome. In all RT ascertained 
through 21 or 13 trisomy, respectively, the relevant chromosome is one of the 
participants. Our data thus do not give any support to the idea of 
interchromosomal effects exerted by RT.