ISSN:
1432-0886
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
Notes:
Summary The extensive genetical analysis of the T-locus in mice, carried out by Dunn and his co-workers, has revealed that the breeding pattern of t-alleles is very peculiar. The complexity of the T-locus indicates that some structural rearrangements are involved here. The purpose of the present work was to gain some informations on the structure of chromosomes in which t-alleles are present. 2. The course of spermatogenesis in the lines of mice of the following genotypes was investigated: +/+; T/+; T/t n — namely T/t 0, T/t12, T/tw1, T/tw6, T/tw18; tn/tx — namely t 0/t12, t0/tw18, t12/tw18, tw1/t12, tw1/t0, tw1/tw6, tw1/tw18, and in heterozygotes for translocations T138 and T190, both involving the fragment of linkage group IX in which some t-alleles are present and used as markers. 3. The alleles T and t w1 are not connected with structural rearrangements, as far as detectable by the methods used. The alleles t 0, tw6 and t w18 are interstitial deficiencies involving different chromosomal regions. The most complete data were obtained for t 0: in T/t 0 heterozygotes a loop corresponding to a big interstitial deficiency was present, in all t 0/tn compounds the aberrant structure of one of the bivalents indicated that an interstitial deficiency is here involved. By analysis of translocation T190 the deficiency loop is localized in the chromosome representing linkage group IX. The identification of t w6 as a small interstitial deficiency is based on the analysis of T/t w6 heterozygotes and its localization in linkage group IX on the presence of this deficiency in translocation T138. The description of tw18 as a small interstitial deficiency stems from the analysis of T/tw18 and t 0/tw18, the localization in linkage group IX is shown by its presence in t 0/tw18 in the same bivalent as t 0. The evidence obtained for t 12 indicates that it is either a big terminal deficiency or a small interstitial one inducing constant asynapsis in adjacent terminal segments of the bivalent. 4. The reasons why loops encountered in genotypes involving t 0, tw6 and t w18 are considered as deficiencies and not as duplications are based on available embryological and genetical data. The possible connections between the mode of action of the investigated t-alleles as embryonic lethals and the cytological results on their structure and localization are discussed. 5. Most of the lethal t-alleles suppress crossing-over in the region T-tf. Factors reducing the frequency of recombination in other organisms are discussed in comparison. It is concluded that the pattern of aberation in meiotic behavior of the bivalent carrying t-alleles is for almost each of the studied alleles rather specific and does not permit for suggesting any general mechanism which could account for the action of investigated lethal t-alleles as crossing-over suppressors. 6. A diagram of the presumable localisation of genetical factors in linkage group IX is presented. It is concluded that the so-called T-locus occupies the main part of the long arm of the chromosome corresponding to linkage group IX and that the investigated t-alleles are not unilocal neither with the gene T nor each with other, but scattered along the chromosome. 7. The possible modes of the origin of new t-alleles are discussed, and the hypothesis is advanced that this event might be connected with mistakes of replication of the strand on which a new t-allele arises.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00368143
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