scholarly journals Severe inbreeding depression is predicted by the “rare allele load” in Mimulus guttatus *

Evolution ◽  
2019 ◽  
Vol 74 (3) ◽  
pp. 587-596 ◽  
Author(s):  
Keely E. Brown ◽  
John K. Kelly
Keyword(s):  
Inbreeding Depression ◽  
Rare Allele ◽  
Mimulus Guttatus

scholarly journals Evidence for the partial dominance of viability genes contributing to inbreeding depression in Mimulus guttatus.

Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 323-331
Author(s):  
Y B Fu ◽  
K Ritland
Keyword(s):  
Inbreeding Depression ◽  
Wild Plant ◽  
Mimulus Guttatus ◽  
Selfed Progeny ◽  
Partial Dominance ◽  
Complete Dominance ◽  
Model Free ◽  
Segregation Ratios ◽  
Marker Loci ◽  
In The Wild

Abstract The relative importance of different modes of gene expression of viability genes contributing to inbreeding depression was investigated in the wild plant, Mimulus guttatus. Viability genes were identified by self-fertilizing 31 outbred plants, each heterozygous for three to nine unlinked allozyme markers, and analyzing segregation ratios of selfed progeny at maturity for deviations from 1:2:1 ratios. In this study, 24 linkages of viability genes to marker loci were detected. To infer the nature of gene action for these viability genes, a "model-free" graphical method was developed that examines the "space" of segregation ratios allowed by each of seven selection models (i.e., overdominance, complete recessivity, partial recessivity, additivity, partial dominance, complete dominance and underdominance). Using this method, we found that, of 24 linkages detected, 18 were consistent with either partial dominance, complete dominance or underdominance. Six were consistent with either partial recessivity, complete recessivity or overdominance. This finding indicates that, in these chromosomal segments identified by allozyme markers, partial dominance plays the predominant role in inbreeding depression. This is inconsistent with either the dominance or overdominance hypotheses proposed to account for inbreeding depression.

Marker-based inferences about fecundity genes contributing to inbreeding depression in Mimulus guttatus

Genome ◽  
1994 ◽  
Vol 37 (6) ◽  
pp. 1005-1010 ◽  
Author(s):  
Yong-Bi Fu ◽  
Kermit Ritland
Keyword(s):  
Genetic Markers ◽  
Inbreeding Depression ◽  
Phenotypic Variation ◽  
Mimulus Guttatus ◽  
Selfed Progeny ◽  
Partial Dominance ◽  
Number Of Genes ◽  
Isozyme Loci ◽  
Deleterious Genes

Eight unlinked isozyme loci were used as genetic markers to characterize fecundity genes contributing to inbreeding depression in two selfed progeny arrays of Mimulus guttatus. Five fecundity traits were measured. Six of eight marked chromosomal segments were significantly associated with the expression of these traits. The number of genes detected for five traits in two progeny arrays varied, with an average of 2.8 genes per trait. Individual segments explained 1.44–9.29%, and together accounted for 3.85–11.32%, of phenotypic variation. Of 20 significant associations, 10 could be interpreted as exhibiting partial dominance, 7 overdominance, 3 partial recessivity, and 0 underdominance. Significant pairwise epistasis was rare. The results of this study suggest that inbreeding depression is caused by many deleterious genes of relatively small, partially dominant effects.Key words: linkage, isozymes, QTLs, inbreeding depression, Mimulus guttatus.

scholarly journals Inbreeding Load, Average Dominance and the Mutation Rate for Mildly Deleterious Alleles in Mimulus guttatus

Genetics ◽  
1999 ◽  
Vol 153 (4) ◽  
pp. 1885-1898 ◽  
Author(s):  
John H Willis
Keyword(s):  
Inbreeding Depression ◽  
Deleterious Mutations ◽  
Mimulus Guttatus ◽  
Fitness Component ◽  
Fitness Effects ◽  
Fitness Traits ◽  
Deleterious Alleles ◽  
Degree Of Dominance ◽  
Almost All ◽  
Load Average

Abstract The goal of this study is to provide information on the genetics of inbreeding depression in a primarily outcrossing population of Mimulus guttatus. Previous studies of this population indicate that there is tremendous inbreeding depression for nearly every fitness component and that almost all of this inbreeding depression is due to mildly deleterious alleles rather than recessive lethals or steriles. In this article I assayed the homozygous and heterozygous fitnesses of 184 highly inbred lines extracted from a natural population. Natural selection during the five generations of selfing involved in line formation essentially eliminated major deleterious alleles but was ineffective in purging alleles with minor fitness effects and did not appreciably diminish overall levels of inbreeding depression. Estimates of the average degree of dominance of these mildly deleterious alleles, obtained from the regression of heterozygous fitness on the sum of parental homozygous fitness, indicate that the detrimental alleles are partially recessive for most fitness traits, with h~∼0.15 for cumulative measures of fitness. The inbreeding load, B, for total fitness is ~1.0 in this experiment. These results are consistent with the hypothesis that spontaneous mildly deleterious mutations occur at a rate >0.1 mutation per genome per generation.

On the evolution of genetic incompatibility systems. VI. A three-locus modifier model for the origin of gametophytic self-incompatibility.

Genetics ◽  
1991 ◽  
Vol 128 (2) ◽  
pp. 453-469
Author(s):  
M K Uyenoyama
Keyword(s):  
Inbreeding Depression ◽  
Genetic System ◽  
Rare Allele ◽  
Self Incompatibility ◽  
S Locus ◽  
Genetic Incompatibility ◽  
Genetic Determination ◽  
Modifier Locus ◽  
Coordinated Expression ◽  
Conventional Models

Abstract Recent genetic analyses have demonstrated that self-incompatibility in flowering plants derives from the coordinated expression of a system of loci. To address the selective mechanisms through which a genetic system of this kind evolves, I present a three-locus model for the origin of gametophytic self-incompatibility. Conventional models assume that a single locus encodes all physiological effects associated with self-incompatibility and that the viability of offspring depends only on whether they were derived by selfing or outcrossing. My model explicitly represents the genetic determination of offspring viability by a locus subject to symmetrically overdominant selection. Initially, the level of expression of the proto-S locus is insufficient to induce self-incompatibility. Weak gametophytic self-incompatibility arises upon the introduction of a rare allele at an unlinked modifier locus which enhances the expression of the proto-S locus. While conventional models predict that the origin of self-incompatibility requires at least two- to threefold levels of inbreeding depression, I find that the comparatively low levels of inbreeding depression generated by a single overdominant locus can ensure the invasion of an enhancer of self-incompatibility under sufficiently high rates of receipt of self-pollen. Associations among components of the incompatibility system promote the origin of self-incompatibility. Enhancement of heterozygosity at the initially neutral proto-S locus improves offspring viability through associative overdominance. Further, the modifier that enhances the expression of self-incompatibility develops a direct association with heterozygosity at the overdominant viability locus. These results suggest that the evolutionary processes by which incompatibility systems originate may differ significantly from those associated with their breakdown. The genetic mechanism explored here may apply to the evolution of other systems that restrict reproduction, including maternal-fetal incompatibility in mammals.

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