scholarly journals No evidence for biased co-transmission of speciation islands in Anopheles gambiae

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.

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.


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 ◽  
...  

1991 ◽  
Vol 57 (2) ◽  
pp. 153-157 ◽  
Author(s):  
William Garside ◽  
Christine Ruangvoravat ◽  
Patricia Dolan ◽  
Nina Hillman

SummaryThe effects of different types of insemination (normal and delayed matings and in vitro fertilization) on the transmission ratio distortion (TRD) of three t haplotypes were determined. The tw73 haplotype which contains all of the loci known to affect TRD is transmitted at equivalent frequencies in normal matings and in in vitro fertilizations (0·84 and 0·85, respectively) but at a significantly lower frequency (0·62) in delayed matings. The distal partial th18 haplotype is transmitted at equivalent frequencies in all types of insemination (0·66 to 0·70) while the proximal partial tw18 haplotype is transmitted in Mendelian frequencies in normal matings and in in vitro inseminations but at a significantly lower frequency in delayed matings. The results are discussed with reference to the current genetic model for transmission ratio distortion.


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