Since the discovery of the recessive lethal mutation to as reported by Dobrovolskaia-Zawadskaia and Kobozieff ( '32) and Chesley and Dunn ('36) a considerable amount of research has been devoted to the remarkable series of recessive mutant alleles that have since been shown to occur at this locus (T
Embryological tests of genetic male sterility in the house mouse
β Scribed by Gluecksohn-Schoenheimer, S. ;Segal, Ruth ;Fitch, Naomi
- Publisher
- John Wiley and Sons
- Year
- 1950
- Tongue
- English
- Weight
- 568 KB
- Volume
- 113
- Category
- Article
- ISSN
- 0022-104X
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β¦ Synopsis
I n previous papers the existence of male sterility in the house mouse caused hy the combination of diff erent recessive mutations of the t type was reported (Eryson, '44; Dunn and Gluecksohn-Schoenheimer, '43). These mutations all occur in one linkage group (no. TX) and do not show any crossing o r e r with each other. Three of them have been shown to suppress crossing over in a region of 1-5 crossover units in chromosome IX and they all are probably coniiected with chromosonial rearrangernents of one kind or another.
The first mutation of this kind to be discovered was t o (Chesley and Dunn, '36). I n combiiiatioii with T (dominant short tail mutation) it produces taillessness, while in homozygous condition ( t " / V ) it is lethal and t O / P embryos die soon after implantation in the uterus. another recessive mutation related closely to t" is tl ; it also produces taillessness in combination with T and is lethal when homozygous, the tl/fl zygotes d j k g even before implantation ; the combination t"/t', however, resnlts in normal tailed progeny (Dunn, '37). While such normal tailed females t o / t l breed normally, the males are sterile (Dunn arid Gluecksoliii-Schoenheimer, '43). 9 third mutation in this series (t') turned out to be identical with t' (Dunn, '39). Recently, still another mutation in this series ( P I was analyzed. It also produces taillessness in conibinanation with T a i d does not show any crossing over with the other mutatioiis in the l' series, lout the homozygotes ( i 3 / t 3 )
This work was aidcd by n grant froin the American Cancer Society o n the recommendation of the Coriirriittce on Growth of the National Research Council.
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