Section 7 — Cytogenetics 



trasted to those observed independently for 

 nullo-X: diplo-X (6:1) and nullo-4: diplo-4 

 (20:1), yet these same ratios of X and 4 egg types 

 concomitant to chromosome-2 nondisjunction 

 were essentially unchanged. 



This investigation was supported by U.S. 

 Public Health Service Predoctoral Fellowship 

 No. GPM-13,926-C1 from the National 

 Institutes of Health. 



7.32. Nondisjunction in Drosophila hydei. 

 T. G. Gregg (Oxford, U.S.A.). 



A previous report on nondisjunction in 

 Drosophila hydei^ indicated that the rate of 

 primary nondisjunction in hydei females was 

 somewhat higher than the rate in Drosophila 

 melanogaster females. On the basis of recent 

 work ( 2 ) it has become apparent that primary 

 nondisjunction in melanogaster females results 

 from the failure of two x-chromosomes from a no 

 exchange tetrad to engage in distributive 

 pairing during meiosis. It also seems that dis- 

 tributive pairing depends largely, although not 

 exclusively, on the centric heterochromatin. 

 On the basis of these latter observations one 

 might expect the rate of primary nondisjunction 

 in hydei females to be much lower than the rate 

 in melanogaster females, provided the mecha- 

 nisms involved in meiosis are similar in the two 

 species. This expectation is based on the unusual- 

 ly large amount of heterochromatin in the 

 hydei X which should facilitate distributive 

 pairing, and on the fact that the genetic length 

 of the hydei X is twice as great as the melano- 

 gaster X which should result in fewer no exchange 

 tetrads. Data have been collected that indicate 

 that the rate of primary nondisjunction in hydei 

 females actually is markedly and significantly 

 lower than the rate in melanogaster females. The 

 difference in rate between this report and Spen- 

 cer's report probably lies in Spencer's use of the 

 markers bobbed and Notch, which he himself 

 suggested might increase the rate of nondis- 

 junction. Data in this report also indicate that 

 in hydei females the rate of nondisjunction does 

 not increase with age. 



1. spencer, J. Ohio Acad. Sci. 1930. 



2. See especially grell, Proc. Natl. Acad. Sci. 

 U.S. 1962. 



7.33. Evidence from Some Unusual Mutants Con- 

 cerning the Nature of t-alleles in the Mouse. 



M. F. Lyon (Harwell, Great Britain). 



"Mutation" of ^-alleles in the mouse results 

 usually from crossing-over in an abnormal 

 chromosome region. Study of the "mutants" 

 should therefore reveal whether the different 

 properties of r-alleles can be ascribed to 

 linearly arranged factors or depend on the 

 whole length of abnormal chromosome. The 

 properties of the allele t 6 include: modification of 

 expression of dominant alleles at the T-locus, 

 homozygous lethality, male sterility, abnormal 

 male segregation ratio, and crossover sup- 

 pression. Mutants derived from t 6 show that the 

 lethal factor is not at the T-locus but is close to 

 the nearby locus of tf, while the T-modifying 

 factor is very close to the T-locus. The allele 

 t h7 , derived from / 6 , decreases the expression of 

 T rather than enhancing it as / 6 does, and can 

 mutate back, by crossing-over, to the /"-en- 

 hancing form. This suggests that it carries a 

 duplication of the T-modifying factor, and 

 hence that this factor has a gene activity which 

 is reduced, but greater than half normal. 

 Another mutant, t hl5 , also derived from t h7 by 

 crossing-over, has a new lethal factor, comple- 

 mentary to the t 6 lethal factor. 



These facts suggest the hypothesis that the 

 fundamental chromosome abnormality in t- 

 alleles is reduced gene activity combined with 

 loss of specific pairing. This would lead to 

 crossover suppression, unequal crossing-over, 

 and hence to duplications and deficiencies. A 

 functional change in nucleic acid (e.g. to hetero- 

 chromatin) would provide a better explanation 

 than a structural one (e.g. inversion). 



7.34, Cytological Investigation on the T-locus in Mus 

 musculus L. Irene Geyer-Duszynska (New 

 York, U.S.A.). 



The T-locus in mice is known as a most complex 

 and odd one. Cytological analysis has revealed, 

 that this complexity is due to the fact that 

 lethal t-alleles are not point mutations but 

 deficiencies located in various regions of the 

 chromosome. The size and the position of the 

 deficiency is for a given t-allele constant. The 

 analysis of compounds and translocations T190 

 and T138 gave additional evidence that the defic- 

 iencies found are located in the chromosome of 

 linkage IX group, and connected with t-alleles. 

 Cytogenetically this chromosome can be de- 

 scribed as follows: centromere — T — tf — Ki — 

 Fu—H2— small deficiencies (t wl8 and t w6 )— 



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