not fuse with broken ends; but, in the second paper, 
published after Reeves (36) had made use of Longley’s 
interpretation as a possible illustration of how terminal 
knobs might become intercalary, he states: ‘‘. .. it isa 
well-known fact that chromosome fusion occurs only be- 
tween recently broken ends...*’ And referring to the 
additional chromatin in abnormal chromosome 10, he 
states: “‘It is a segment that has replaced the terminal 
one-sixth of the long arm of chromosome 10, as Rhoades 
(40) has clearly shown.”’ 
The facts are that Rhoades (88, 40) discussed the ques- 
tion of the origin of abnormal chromosome 10 and later 
(41) referred to it again, without stating a conclusion. 
He did point out that a short terminal region of abnormal 
chromosome 10 has achromomere pattern differing from 
that of the corresponding region of normal 10, and that 
crossing over is reduced in this region. This might indi- 
cate that abnormal 10 originated by the replacement of 
a short terminal segment with a much longer non- 
homologous segment. But he pointed out that this ex- 
planation would require plants homozygous for abnormal 
chromosome 10 to be homozygous deficient for certain 
loci found in the terminal region of normal chromosome 
10. This is unlikely, because plants homozygous for ab- 
normal chromosome 10 are not noticeably different in 
phenotype from their sibs carrying only the normal 
chromosome 10. 
Recently, Ting (48) reported cytological evidence in- 
dicating that an abnormal chromosome 10 did originate 
by simple translocation. A fragment, containing a cen- 
tromere, of a B-chromosome became attached to the 
natural end of the long arm of chromosome 10. 
In the absence of a completely satisfactory explana- 
tion, however, it may be said that the tripartite theory 
accounts for the fact that the number of knobs in teosinte 
[ 875 ] 
