scholarly journals Genome-Wide Associations Between Hybrid Sterility QTL and Marker Transmission Ratio Distortion

2006 ◽  
Vol 23 (5) ◽  
pp. 973-980 ◽  
Author(s):  
L. C. Moyle
2021 ◽  
Author(s):  
María Gracia Luigi‐Sierra ◽  
Joaquim Casellas ◽  
Amparo Martínez ◽  
Juan Vicente Delgado ◽  
Javier Fernández Álvarez ◽  
...  

2021 ◽  
Author(s):  
Maria Luigi-Sierra ◽  
Joaquim Casellas ◽  
Amparo Martinez ◽  
Juan Vicente Delgado ◽  
Javier Fernandez Alvarez ◽  
...  

Transmission ratio distortion (TRD) is the preferential transmission of one specific allele to offspring at the expense of the other one. The existence of TRD is mostly explained by the segregation of genetic variants with deleterious effects on the developmental processes that go from the formation of gametes to fecundation and birth. A few years ago, a statistical methodology was implemented in order to detect TRD signals on a genome-wide scale as a first step to uncover the biological basis of TRD and reproductive success in domestic species. In the current work, we have analyzed the impact of SNP calling quality on the detection of TRD signals in a population of Murciano-Granadina goats. Seventeen bucks and their offspring (N=288) were typed with the Goat SNP50 BeadChip, while the genotypes of the dams were lacking. Performance of a genome-wide scan revealed the existence of 36 SNPs showing significant evidence of TRD. When we calculated GenTrain scores for each one of the SNPs, we observed that 25 SNPs showed scores below 0.8. The allele frequencies of these SNPs in the offspring were not correlated with the allele frequencies estimated in the dams with statistical methods, thus evidencing that flawed SNP calling quality might lead to the detection of spurious TRD signals. We conclude that, when performing TRD scans, the GenTrain scores of markers should be taken into account to discriminate SNPs that are truly under TRD from those yielding spurious signals due to technical problems.


2017 ◽  
Author(s):  
Rachel E. Kerwin ◽  
Andrea L. Sweigart

ABSTRACTHybrid incompatibilities are a common correlate of genomic divergence and a potentially important contributor to reproductive isolation. However, we do not yet have a detailed understanding of how hybrid incompatibility loci function and evolve within their native species, or why they are dysfunctional in hybrids. Here, we explore these issues for a well-studied, two-locus hybrid incompatibility between hybrid male sterility 1 (hms1) and hybrid male sterility 2 (hms2) in the closely related yellow monkeyflower species Mimulus guttatus and M. nasutus. By performing reciprocal backcrosses with introgression lines, we find evidence for gametic expression of the hms1-hms2 incompatibility. Surprisingly, however, hybrid transmission ratios at hms1 do not reflect this incompatibility, suggesting additional mechanisms counteract the effects of gametic sterility. Indeed, our backcross experiment shows hybrid transmission bias toward M. guttatus through both pollen and ovules, an effect that is particularly strong when hms2 is homozygous for M. nasutus alleles. In contrast, we find little evidence for hms1 transmission bias in crosses within M. guttatus, providing no indication of selfish evolution at this locus. Although we do not yet have sufficient genetic resolution to determine if hybrid sterility and transmission ratio distortion map to the same loci, our preliminary fine-mapping uncovers a genetically independent hybrid lethality system involving at least two loci linked to hms1. This fine-scale dissection of transmission ratio distortion at hms1 and hms2 provides insight into genomic differentiation between closely related Mimulus species and reveals multiple mechanisms of hybrid dysfunction.


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


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