scholarly journals DEVELOPMENTAL STAGES OF GENOME ELIMINATION RESULTING IN TRANSMISSION RATIO DISTORTION OF THE T-007 MALE RECOMBINATION (MR) CHROMOSOME OF DROSOPHILA MELANOGASTER

Genetics ◽  
1981 ◽  
Vol 97 (1) ◽  
pp. 95-111
Author(s):  
Kathleen A Matthews

ABSTRACT T-007 is a Male Recombination (MR) second chromosome that induces transmission ratio distortion (at its own expense) when heterozygous with many laboratory marker chromosomes. The developmental timing of elimination of T-007 chromosomes has been investigated. About 21% of the T-007 chromosomes expected to be recovered among the progeny of heterozygous T-007 males are lost at some point between fertilization and eclosion (representing 29% of the total distortion observed in young males). Another 52% of the expected number of T-007 chromosomes are lost as a result of spermatid abortion during spermiogenesis (representing 71% of the total distortion). Abnormalities in both the number of spermatids per bundle and the structure of spermatid tails are seen at the earliest stages of spermiogenesis in T-007 males.

2012 ◽  
Vol 367 (1587) ◽  
pp. 374-384 ◽  
Author(s):  
Matthew W. Hahn ◽  
Bradley J. White ◽  
Christopher D. Muir ◽  
Nora J. Besansky

Genome-scale scans have revealed highly heterogeneous levels of divergence between closely related taxa in many systems. Generally, a small number of regions show high differentiation, with the rest of the genome showing no or only low levels of divergence. These patterns have been interpreted as evidence for ongoing speciation-with-gene-flow, with introgression homogenizing the whole genome except loci involved in reproductive isolation. However, as the number of selected loci increases, the probability of introgression at unselected loci decreases unless there is a transmission ratio distortion causing an over-representation of specific combinations of alleles. Here we examine the transmission of three ‘speciation islands’ that contain fixed differences between the M and S forms of the mosquito, Anopheles gambiae . We made reciprocal crosses between M and S parents and genotyped over 2000 F 2 individuals, developing a hierarchical likelihood model to identify specific genotypes that are under- or over-represented among the recombinant offspring. Though our overall results did not match the expected number of F 2 genotypes, we found no biased co-transmission among M or S alleles in the three islands. Our likelihood model did identify transmission ratio distortion at two of the three islands, but this distortion was small (approx. 3%) and in opposite directions for the two islands. We discuss how our results impinge on hypotheses of current gene flow between M and S and ongoing speciation-with-gene-flow in this system.


1979 ◽  
Vol 33 (2) ◽  
pp. 137-146 ◽  
Author(s):  
William R. Engels

SUMMARYMale sterility, male recombination, and transmission ratio distortion – all examples of a syndrome known as hybrid dysgenesis in Drosophila melanogaster – were found to involve chromosome–cytoplasm interactions. The latter two have temperature optima near 25° and involve pre-meiotic events. In addition, sex ratio distortion, and induction of certain translocations of the X and Y chromosomes (but not the autosomes) were found to be part of hybrid dysgenesis. Both are caused by chromosome–cytoplasm interactions with pre-meiotic events playing a crucial role. The results agree with previous data on female sterility in hybrid dysgenesis, which also has cytoplasmic components and premeiotic origins.


Genetics ◽  
1977 ◽  
Vol 86 (4) ◽  
pp. 813-833 ◽  
Author(s):  
Margaret G Kidwell ◽  
James F Kidwell ◽  
John A Sved

ABSTRACT A syndrome of associated aberrant traits is described in Drosophila melanogaster. Six of these traits, mutation, sterility, male recombination, transmission ratio distortion, chromosomal aberrations and local increases in female recombination, have previously been reported. A seventh trait, nondisjunction, is described for the first time. All of the traits we have examined are found nonreciprocally in F1 hybrids. We present evidence that at least four of the traits are not found in nonhybrids. Therefore we have proposed the name hybrid dysgenesis to describe this syndrome.—A partition of tested strains into two types, designated P and M, was made according to the paternal or maternal contribution required to produce hybrid dysgenesis. This classification seems to hold for crosses of strains from within the United States and Australia, as well as for crosses between strains from the two countries. Strains collected recently from natural populations are typically of the P type and those having a long laboratory history are generally of the M type. However, a group of six strains collected from the wild in the 1960's are unambiguously divided equally between the P and M types. The dichotomy of this latter group raises interesting questions concerning possible implications for speciation.—Temperature often has a critical effect on the manifestation of hybrid dysgenesis. High F1 developmental temperatures tend to increase the expression of sterility, sometimes to extreme levels. Conversely, low developmental temperatures tend to inhibit the expression of some dysgenic traits.—There are potentially important practical implications of hybrid dysgenesis for laboratory experimentation. The results suggest that care should be exercised in planning experiments involving strain crosses.


2006 ◽  
Vol 14 (3) ◽  
pp. 299-306 ◽  
Author(s):  
Nicola L Dean ◽  
J Concepción Loredo-Osti ◽  
T Mary Fujiwara ◽  
Kenneth Morgan ◽  
Seang Lin Tan ◽  
...  

Genetics ◽  
1996 ◽  
Vol 142 (4) ◽  
pp. 1299-1304
Author(s):  
F Pardo-Manuel de Villena ◽  
C Slamka ◽  
M Fonseca ◽  
A K Naumova ◽  
J Paquette ◽  
...  

Abstract We determined the genotypes of >200 offspring that are survivors of matings between female reciprocal F1 hybrids (between the DDK and C57BL/6J inbred mouse strains) and C57BL/6J males at markers linked to the Ovum mutant (Om) locus on chromosome 11. In contrast to the expectations of our previous genetic model to explain the “DDK syndrome,” the genotypes of these offspring do not reflect preferential survival of individuals that receive C57BL/6J alleles from the F1 females in the region of chromosome 11 to which the Om locus has been mapped. In fact, we observe significant transmission-ratio distortion in favor of DDK alleles in this region. These results are also in contrast to the expectations of Wakasugi's genetic model for the inheritance of Om, in which he proposed equal transmission of DDK and non-DDK alleles from F1 females. We propose that the results of these experiments may be explained by reduced expression of the maternal DDK Om allele or expression of the maternal DDK Om allele in only a portion of the ova of F1 females


2006 ◽  
Vol 17 (3) ◽  
pp. 239-247 ◽  
Author(s):  
Reiner Schulz ◽  
Lara A. Underkoffler ◽  
Joelle N. Collins ◽  
Rebecca J. Oakey

Genomics ◽  
1992 ◽  
Vol 12 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Stephen H. Pilder ◽  
Cindy L. Decker ◽  
Salim Islam ◽  
Christine Buck ◽  
Judith A. Cebra-Thomas ◽  
...  

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