scholarly journals Genetic basis of sperm and testis length differences and epistatic effect on hybrid inviability and sperm motility between Drosophila simulans and D. sechellia

Heredity ◽  
1997 ◽  
Vol 78 (4) ◽  
pp. 354-362 ◽  
Author(s):  
Dominique Joly ◽  
Claude Bazin ◽  
Ling-Wen Zeng ◽  
Rama S Singh
Keyword(s):  
Sperm Motility ◽  
Genetic Basis ◽  
Epistatic Effect ◽  
Drosophila Simulans ◽  
Hybrid Inviability

Maternal effect and speciation: maternal effect contributes to the evolution of hybrid inviability between Drosophila simulans and Drosophila mauritiana

Genome ◽  
2015 ◽  
Vol 58 (9) ◽  
pp. 405-413
Author(s):  
Sogol Eizadshenass ◽  
Rama S. Singh
Keyword(s):  
Maternal Effects ◽  
Maternal Effect ◽  
Genetic Basis ◽  
Drosophila Simulans ◽  
Hybrid Male ◽  
Egg Hatching ◽  
Hybrid Inviability ◽  
F1 Hybrid ◽  
Drosophila Mauritiana ◽  
Negative Effect

Haldane’s rule has been the basis of speciation research during the last 30 years. Most studies have focused on the nature of incompatibilities in the hybrid male, but not much attention has been given to the genetic basis of fertility and inviability in hybrid females. Hybridizations between Drosophila simulans and Drosophila mauritiana produce fertile females and sterile males. Here, we re-examined the level of fertility in reciprocal F1 females of these two species and looked for the presence of maternal effects. Our results show that the reciprocal F1 females of D. simulans and D. mauritiana hybridizations are fully fertile and in fact show a significant level of heterosis in the rate of oviposition but display reduced egg hatching in one direction. Reduced egg hatching was observed in the progenies of F1 hybrid females with D. mauritiana as mother, the same cross that showed a stronger negative effect on F1 male fertility. A review of the literature on the hybridizations in Lepidoptera also showed a maternal effect on inviability when reciprocal crosses produced asymmetric results. Our findings point to the importance of maternal effects in the evolution of embryo inviability and thus enhancing the process of speciation through the evolution of hybrid inviability.

scholarly journals Genetic basis to hybrid inviability is more complex than hybrid male sterility in Caenorhabditis nematodes

Heredity ◽  
2018 ◽  
Vol 121 (2) ◽  
pp. 169-182 ◽  
Author(s):  
Joanna D. Bundus ◽  
Donglin Wang ◽  
Asher D. Cutter
Keyword(s):  
Male Sterility ◽  
Genetic Basis ◽  
Hybrid Male ◽  
Hybrid Male Sterility ◽  
Hybrid Inviability

scholarly journals The genetic basis of hybrid inviability in the grasshopper Podisma pedestris

Heredity ◽  
1981 ◽  
Vol 47 (3) ◽  
pp. 367-383 ◽  
Author(s):  
N H Barton ◽  
G M Hewitt
Keyword(s):  
Genetic Basis ◽  
Hybrid Inviability

scholarly journals Cytoplasmic-nuclear incompatibility between wild-isolates of Caenorhabditis nouraguensis

2016 ◽  
Author(s):  
Piero Lamelza ◽  
Michael Ailion
Keyword(s):  
Genetic Basis ◽  
Hybrid Sterility ◽  
Reproductive Barrier ◽  
Reproductive Barriers ◽  
Cytoplasmic Factor ◽  
Hybrid Inviability ◽  
Hybrid Incompatibility ◽  
Endosymbiotic Bacteria ◽  
Nuclear Locus ◽  
Shed Light

ABSTRACTHow species arise is a fundamental question in biology. Species can be defined as populations of interbreeding individuals that are reproductively isolated from other such populations. Therefore, understanding how reproductive barriers evolve between populations is essential for understanding the process of speciation. Hybrid incompatibility (e.g. hybrid sterility and lethality) is a common and strong reproductive barrier in nature, but few studies have molecularly identified its genetic basis. Here we report a lethal incompatibility between two wild-isolates of the nematode Caenorhabditis nouraguensis. Hybrid inviability results from the incompatibility between a maternally inherited cytoplasmic factor from each strain and a recessive nuclear locus from the other. We have excluded the possibility that maternally inherited endosymbiotic bacteria cause the incompatibility by treating both strains with tetracycline and show that hybrid death is unaffected. Furthermore, cytoplasmic-nuclear incompatibility commonly occurs between other wild-isolates, indicating that this is a significant reproductive barrier within C. nouraguensis. We hypothesize that the maternally inherited cytoplasmic factor is the mitochondrial genome and that mitochondrial dysfunction underlies hybrid death. This system has the potential to shed light on the dynamics of divergent mitochondrial-nuclear coevolution and its role in promoting speciation.

scholarly journals The genetic basis of Haldane's rule and the nature of asymmetric hybrid male sterility among Drosophila simulans, Drosophila mauritiana and Drosophila sechellia.

Genetics ◽  
1993 ◽  
Vol 134 (1) ◽  
pp. 251-260 ◽  
Author(s):  
L W Zeng ◽  
R S Singh
Keyword(s):  
Male Sterility ◽  
Y Chromosome ◽  
Genetic Basis ◽  
Drosophila Simulans ◽  
Hybrid Male ◽  
Hybrid Male Sterility ◽  
Haldane’S Rule ◽  
Drosophila Sechellia ◽  
Haldane's Rule ◽  
Drosophila Mauritiana

Abstract Haldane's rule (i.e., the preferential hybrid sterility and inviability of heterogametic sex) has been known for 70 years, but its genetic basis, which is crucial to the understanding of the process of species formation, remains unclear. In the present study, we have investigated the genetic basis of hybrid male sterility using Drosophila simulans, Drosophila mauritiana and Drosophila sechellia. An introgression of D. sechellia Y chromosome into a fairly homogenous background of D. simulans did not show any effect of the introgressed Y on male sterility. The substitution of D. simulans Y chromosome into D. sechellia, and both reciprocal Y chromosome substitutions between D. simulans and D. mauritiana were unsuccessful. Introgressions of cytoplasm between D. simulans and D. mauritiana (or D. sechellia) also did not have any effect on hybrid male sterility. These results rule out the X-Y interaction hypothesis as a general explanation of Haldane's rule in this species group and indicate an involvement of an X-autosome interaction. Models of symmetrical and asymmetrical X-autosome interaction have been developed which explain the Y chromosome substitution results and suggest that evolution of interactions between different genetic elements in the early stages of speciation is more likely to be of an asymmetrical nature. The model of asymmetrical X-autosome interaction also predicts that different sets of interacting genes may be involved in different pairs of related species and can account for the observation that hybrid male sterility in many partially isolated species is often nonreciprocal or unidirectional.

scholarly journals Combining QTL-seq and linkage mapping to uncover the genetic basis of single vs. paired spikelets in the advanced populations of two-ranked maize×teosinte

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhengjie Chen ◽  
Dengguo Tang ◽  
Kun Hu ◽  
Lei Zhang ◽  
Yong Yin ◽  
...  
Keyword(s):  
Fine Mapping ◽  
Linkage Mapping ◽  
Genetic Basis ◽  
Recurrent Selection ◽  
Epistatic Effect ◽  
Phenotypic Variance ◽  
Epistatic Qtl ◽  
Maize Domestication ◽  
Genomic Regions ◽  
Mapping Populations

Abstract Background Teosinte ear bears single spikelet, whereas maize ear bears paired spikelets, doubling the number of grains in each cupulate during maize domestication. In the past 20 years, genetic analysis of single vs. paired spikelets (PEDS) has been stagnant. A better understanding of genetic basis of PEDS could help fine mapping of quantitative trait loci (QTL) and cloning of genes. Results In this study, the advanced mapping populations (BC3F2 and BC4F2) of maize × teosinte were developed by phenotypic recurrent selection. Four genomic regions associated with PEDS were detected using QTL-seq, located on 194.64–299.52 Mb, 0–162.80 Mb, 12.82–97.17 Mb, and 125.06–157.01 Mb of chromosomes 1, 3, 6, and 8, respectively. Five QTL for PEDS were identified in the regions of QTL-seq using traditional QTL mapping. Each QTL explained 1.12–38.05% of the phenotypic variance (PVE); notably, QTL qPEDS3.1 with the average PVE of 35.29% was identified in all tests. Moreover, 14 epistatic QTL were detected, with the total PVE of 47.57–66.81% in each test. The QTL qPEDS3.1 overlapped with, or was close to, one locus of 7 epistatic QTL. Near-isogenic lines (NILs) of QTL qPEDS1.1, qPEDS3.1, qPEDS6.1, and qPEDS8.1 were constructed. All individuals of NIL-qPEDS6.1(MT1) and NIL-qPEDS8.1(MT1) showed paired spikelets (PEDS = 0), but the flowering time was 7 days shorter in the NIL-qPEDS8.1(MT1). The ratio of plants with PEDS > 0 was low (1/18 to 3/18) in the NIL-qPEDS1.1(MT1) and NIL-qPEDS3.1(MT1), maybe due to the epistatic effect. Conclusion Our results suggested that major QTL, minor QTL, epistasis and photoperiod were associated with the variation of PEDS, which help us better understand the genetic basis of PEDS and provide a genetic resource for fine mapping of QTL.

scholarly journals A genetic basis for the inviability of hybrids between sibling species of Drosophila.

Genetics ◽  
1990 ◽  
Vol 124 (4) ◽  
pp. 909-920 ◽  
Author(s):  
P Hutter ◽  
J Roote ◽  
M Ashburner
Keyword(s):  
Drosophila Melanogaster ◽  
Sibling Species ◽  
Interspecific Hybrids ◽  
Genetic Basis ◽  
P Element ◽  
Hybrid Inviability ◽  
Element Insertion ◽  
Complementary Genes ◽  
The Cross ◽  
Species Hybrids

Abstract A mutation of Drosophila melanogaster whose only known effect is the rescue of otherwise lethal interspecific hybrids has been characterized. This mutation, Hmr, maps to 1-31.84 (9D1-9E4). Hmr may be the consequence of a P element insertion. It rescues hybrid males from the cross of D. melanogaster females to males of its three sibling species, D. simulans, D. mauritiana and D. sechellia. This rescue is recessive, since hybrid males that carry both Hmr and a duplication expected to be Hmr+ are not rescued. Hmr also rescues the otherwise inviable female hybrids from the cross of compound-X D. melanogaster females to males of its sibling species. This rescue is also recessive, since a compound-X heterozygous for Hmr does not rescue. Another mutation, discovered on the In(1)AB chromosome of D. melanogaster, is also found to rescue normally inviable species hybrids: unlike Hmr, however, In(1)AB rescues hybrid females from the cross of In(1)AB/Y males to sibling females, as well as hybrid males from the cross of In(1)AB females to sibling males. These data are interpreted on the basis of a model for the genetic basis of hybrid inviability of complementary genes.

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