Nature Publishing Group, publisher of Nature, and other science journals and reference works
Nature
my account e-alerts subscribe register
   
Monday 16 November 2009
Journal Home
Current Issue
AOP
Archive
Download PDF
References
Export citation
Export references
Send to a friend
More articles like this

Letters to Nature
Nature 274, 163 - 164 (13 July 1978); doi:10.1038/274163a0

Deletion mapping of the t complex of chromosome 17 of the mouse

ROBERT P. ERICKSON, SUSAN E. LEWIS & KAREN S. SLUSSER

Department of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan 48109

THE dominant T mutation in the t complex on chromosome 17 of the mouse causes a shortening of the tail in heterozygotes and embryonic lethality in homozygotes1. Recessive t alleles are defined by their interaction with T to cause tail-lessness in double heterozygotes (T/t) and are often associated with three other properties: (1) homozygous lethality at several different embryonic stages, (2) effects on male reproduction including sterility and transmission ratio distortion, and (3) crossover suppression2,3. Although the multiplicity of these effects suggests that several genes are involved, crossover suppression has made classical genetic analysis of the region difficult. As T/t animals are viable, the lethal factors associated with recessive t homozygosity cannot be allelic to those associated with T homozygosity. Lyon et al. studied exceptional crossovers and found evidence that the homozygous lethality of t alleles and their property of interacting with T to cause tail-lessness were specified at different genetic loci4,5. We have studied a presumed deletion, T orl in crosses with recessive t alleles as well as with alleles at closely linked loci to map further the multiple effects associated with the t complex. We report here that factors associated with t lethality are distal to the T orl deletion and separable from those responsible for at least one kind ot t allele-associated male sterility apparently included in the deletion.

------------------

References
1. Chesley, P. J. exp. Zool. 70, 429–459 (1935).
2. Gluecksohn-Waelsch, S. & Erickson, R. P. Curr. Topics devl Biol. 5, 281–316 (1970).
3. Bennett, D. Cell 6, 441–454 (1975).
4. Lyon, M. F. & Meredith, R. Heredity 19, 301–312 (1964).
5. Lyon, M. F. & Meredith, R. Heredity 19, 313–325 (1964).
6. Moutier, R. Mouse News Lett. 48, 38 (1973); 49, 42 (1973).
7. Bennett, D. et al. Genet. Res. 26, 95–108 (1975).
8. Gluecksohn-Schoenheimer, S. J. exp. Zool. 110, 47–76 (1949).
9. Wroblewska, J. Cryogenetics 10, 199–207 (1971).
10. Lyon, M. F. & Mason, I. Genet. Res. 29, 255–266 (1977).
11. Lyon, M. F. & Bechtol, K. B. Genet. Res. 30, 63–76 (1977).
12. Bennett, W. I., Gall, A. M., Southard, J. L. & Sidman, R. L. Biol. Reprod. 5, 30–58 (1971).
13. Dooher, G. B. & Bennett, D. J. Embryol. exp. Morph. 32, 749–761 (1974).
14. Hammerberg, G. & Klein, J. Genet. Res. 26, 203–211 (1975).
15. Dickie, M. M. Mouse News Lett. 40, 29 (1969).
16. Bennett, D. & Dunn, L. C. Proc. Symp. Immunogenet. H–2 System, 90–103 (Liblice, Prague, 1970).



© 1978 Nature Publishing Group
Privacy Policy