Construction of a genetic linkage map of the banana fungal pathogen, Mycosphaerella fijiensis, causal agent of Black Sigatoka disease

The haploid, hemibiotrophic ascomycete fungus Mycosphaerella fijiensis (Morelet) is the causal agent of black Sigatoka, the most economically important disease of banana (Musa spp.). A genetic linkage map of M. fijiensis was constructed from a cross between isolates CIRAD86 (from Cameroon) and CIRAD139A (from Colombia). Sixty one of the progeny were analyzed using molecular markers and the Mating Type (MAT) locus. The genetic linkage map consists of 298 AFLP and 16 SSR markers with twenty three linkage groups, containing 5 or more markers, covering 1879 cM. Markers are separated on average by around 5.9 cM. The MAT locus was shown to segregate in a 1:1 ratio but could not be successfully mapped. The relation between physical size and genetic distance was approximately 40.9 kb/cM. The estimated total haploid genome size was calculated using the genetic mapping data, to be 4303.5 cM. This is the first genetic linkage map reported for this important foliar pathogen of banana (Texte intégral

Diversity, genetic mapping, and signatures of domestication in the carrot (Daucus carota L.) genome, as revealed by Diversity Arrays Technology (DArT) markers

Carrot is one of the most economically important vegetables worldwide, but genetic and genomic resources supporting carrot breeding remain limited. We developed a Diversity Arrays Technology (DArT) platform for wild and cultivated carrot and used it to investigate genetic diversity and to develop a saturated genetic linkage map of carrot. We analyzed a set of 900 DArT markers in a collection of plant materials comprising 94 cultivated and 65 wild carrot accessions. The accessions were attributed to three separate groups: wild, Eastern cultivated and Western cultivated. Twenty-seven markers showing signatures for selection were identified. They showed a directional shift in frequency from the wild to the cultivated, likely reflecting diversifying selection imposed in the course of domestication. A genetic linkage map constructed using 188 F2 plants comprised 431 markers with an average distance of 1.1 cM, divided into nine linkage groups. Using previously anchored single nucleotide polymorphisms, the linkage groups were physically attributed to the nine carrot chromosomes. A cluster of markers mapping to chromosome 8 showed significant segregation distortion. Two of the 27 DArT markers with signatures for selection were segregating in the mapping population and were localized on chromosomes 2 and 6. Chromosome 2 was previously shown to carry the Vrn1 gene governing the biennial growth habit essential for cultivated carrot. The results reported here provide background for further research on the history of carrot domestication and identify genomic regions potentially important for modern carrot breeding

Genome-wide linkage scan for loci associated with epilepsy in Belgian shepherd dogs.

BackgroundIdiopathic epilepsy in the Belgian shepherd dog is known to have a substantial genetic component. The objective of this study was to identify genomic regions associated with the expression of generalized seizures in the Belgian Tervuren and Sheepdog.ResultsDNA from 366 dogs, of which 74 were classified as epileptic, representing two extended families were subjected to a genome-wide linkage scan using 410 microsatellite markers yielding informative coverage averaging 5.95 +/- 0.21 Mb. Though previous studies based on pedigree analyses proposed a major gene of influence, the present study demonstrated the trait to be highly polygenic. Studies of complex disorders in humans indicate that a liberal composite evaluation of genetic linkage is needed to identify underlying quantitative trait loci (QTLs). Four chromosomes yielded tentative linkage based upon LOD scores in excess of 1.0. Possible QTLs within these regions were supported also by analyses of multipoint linkage, allele frequency, TDT, and transmission of haplotype blocks.ConclusionsTaken together the data tentatively indicate six QTLs, three on CFA 2, and one on each of CFA 6, 12, and 37, that support fine mapping for mutations associated with epilepsy in the Belgian shepherd. The study also underscores the complexity of genomic linkage studies for polygenic disorders

What does it take to evolve behaviorally complex organisms?

What genotypic features explain the evolvability of organisms that have to accomplish many different tasks? The genotype of behaviorally complex organisms may be more likely to encode modular neural architectures because neural modules dedicated to distinct tasks avoid neural interference, i.e., the arrival of conflicting messages for changing the value of connection weights during learning. However, if the connection weights for the various modules are genetically inherited, this raises the problem of genetic linkage: favorable mutations may fall on one portion of the genotype encoding one neural module and unfavorable mutations on another portion encoding another module. We show that this can prevent the genotype from reaching an adaptive optimum. This effect is different from other linkage effects described in the literature and we argue that it represents a new class of genetic constraints. Using simulations we show that sexual reproduction can alleviate the problem of genetic linkage by recombining separate modules all of which incorporate either favorable or unfavorable mutations. We speculate that this effect may contribute to the taxonomic prevalence of sexual reproduction among higher organisms. In addition to sexual recombination, the problem of genetic linkage for behaviorally complex organisms may be mitigated by entrusting evolution with the task of finding appropriate modular architectures and learning with the task of finding the appropriate connection weights for these architectures

Tapasin gene polymorphism in systemic onset juvenile rheumatoid arthritis: a family-based case-control study

Juvenile rheumatoid arthritis (JRA) comprises a group of chronic systemic inflammatory disorders that primarily affect joints and can cause long-term disability. JRA is likely to be a complex genetic trait, or a series of such traits, with both genetic and environmental factors contributing to the risk for developing the disease and to its progression. The HLA region on the short arm of chromosome 6 has been intensively evaluated for genetic contributors to JRA, and multiple associations, and more recently linkage, has been detected. Other genes involved in innate and acquired immunity also map to near the HLA cluster on 6p, and it is possible that variation within these genes also confers risk for developing JRA. We examined the TPSN gene, which encodes tapasin, an endoplasmic reticulum chaperone that is involved in antigen processing, to elucidate its involvement, if any, in JRA. We employed both a case-control approach and the transmission disequilibrium test, and found linkage and association between the TPSN allele (Arg260) and the systemic onset subtype of JRA. Two independent JRA cohorts were used, one recruited from the Rheumatology Clinic at Cincinnati Children's Hospital Medical Center (82 simplex families) and one collected by the British Paediatric Rheumatology Group in London, England (74 simplex families). The transmission disequilibrium test for these cohorts combined was statistically significant (chi(2) = 4.2, one degree of freedom; P = 0.04). Linkage disequilibrium testing between the HLA alleles that are known to be associated with systemic onset JRA did not reveal linkage disequilibrium with the Arg260 allele, either in the Cincinnati systemic onset JRA cohort or in 113 Caucasian healthy individuals. These results suggest that there is a weak association between systemic onset JRA and the TPSN polymorphism, possibly due to linkage disequilibrium with an as yet unknown susceptibility allele in the centromeric part of chromosome 6

Genome-Wide Association and Linkage Analysis of Quantitative Traits: Comparison pf Likelihood-Ratio Test and Conditional Score Statistic

Over the past decade, genetic analysis has shifted from linkage studies, which identify broad regions containing putative trait loci, to genome-wide association studies, which detect the association of a marker with a specific phenotype. Because linkage and association analysis provide complementary information, developing a method to combine these analyses may increase the power to detect a true association. In this paper we compare a linkage score and association score test as well as a newly proposed combination of these two scores with traditional linkage and association methods.National Institutes of Health (National Institute of General Medical Sciences R01 GM031575, National Center for Research Resources Shared Instrumentation grant 1S10RR163736-01A1

A saturated genetic linkage map of autotetraploid alfalfa (Medicago sativa L.) developed using genotyping-by-sequencing is highly syntenous with the Medicago truncatula genome.

A genetic linkage map is a valuable tool for quantitative trait locus mapping, map-based gene cloning, comparative mapping, and whole-genome assembly. Alfalfa, one of the most important forage crops in the world, is autotetraploid, allogamous, and highly heterozygous, characteristics that have impeded the construction of a high-density linkage map using traditional genetic marker systems. Using genotyping-by-sequencing (GBS), we constructed low-cost, reasonably high-density linkage maps for both maternal and paternal parental genomes of an autotetraploid alfalfa F1 population. The resulting maps contain 3591 single-nucleotide polymorphism markers on 64 linkage groups across both parents, with an average density of one marker per 1.5 and 1.0 cM for the maternal and paternal haplotype maps, respectively. Chromosome assignments were made based on homology of markers to the M. truncatula genome. Four linkage groups representing the four haplotypes of each alfalfa chromosome were assigned to each of the eight Medicago chromosomes in both the maternal and paternal parents. The alfalfa linkage groups were highly syntenous with M. truncatula, and clearly identified the known translocation between Chromosomes 4 and 8. In addition, a small inversion on Chromosome 1 was identified between M. truncatula and M. sativa. GBS enabled us to develop a saturated linkage map for alfalfa that greatly improved genome coverage relative to previous maps and that will facilitate investigation of genome structure. GBS could be used in breeding populations to accelerate molecular breeding in alfalfa

A Genetic Linkage Map Using an F1 Population in Rubber Tree (Hevea brasiliensis) based on microsatellite markers. P0527

The construction of molecular gene linkage map in Hevea requires specific methodology because of high heterozygosity. Unlike annual crops, a cross between two heterozygous parents in Hevea can yield information up to four alleles, which are segregated further. The mapping population was a full-sib progeny (F1 progeny) derived from a cross between the cultivars PB217 and PR255. A set of 603 microsatellite primer pairs was tested for polymorphism the two parents and six F1 progenies genotypes. Linkage map was obtained using OneMap (Margarido et al., 2007). LOD Score 4.5 and recombination fraction of 0.40 was considered to determine linkage between markers. In total, 288 marks were genotyped (230 SSR genomic loci and 58 EST-SSR). The map consists of 288 markers, distributed in 23 linkage groups (LG) and 2833.8 cM in length with an average genetic distance of 9.8 cM between adjacent markers. The largest group has 228.7 cM (29 markers) and the smallest has 10.3 cM (4 markers). SSRs provide powerful tool for genetic linkage map construction that can be applied for identification of QTL. Importantly, the marker linked to the QTL can be further applied to MAS in rubber tree breeding program for selecting plant that contains desirable phenotype. The map is not saturated enough and some chromosome regions could not be linked. The chromosome number accepted today, for most Hevea species, is 18 (2n=36). The present map will be used for yield rubber QTL mapping and other important economical characteristics. (Texte integral

High-density SNP association study of the 17q21 chromosomal region linked to autism identifies CACNA1G as a novel candidate gene.

Chromosome 17q11-q21 is a region of the genome likely to harbor susceptibility to autism (MIM(209850)) based on earlier evidence of linkage to the disorder. This linkage is specific to multiplex pedigrees containing only male probands (MO) within the Autism Genetic Resource Exchange (AGRE). Earlier, Stone et al.(1) completed a high-density single nucleotide polymorphism association study of 13.7 Mb within this interval, but common variant association was not sufficient to account for the linkage signal. Here, we extend this single nucleotide polymorphism-based association study to complete the coverage of the two-LOD support interval around the chromosome 17q linkage peak by testing the majority of common alleles in 284 MO trios. Markers within an interval containing the gene, CACNA1G, were found to be associated with Autism Spectrum Disorder at a locally significant level (P=1.9 × 10(-5)). While establishing CACNA1G as a novel candidate gene for autism, these alleles do not contribute a sufficient genetic effect to explain the observed linkage, indicating that there is substantial genetic heterogeneity despite the clear linkage signal. The region thus likely harbors a combination of multiple common and rare alleles contributing to the genetic risk. These data, along with earlier studies of chromosomes 5 and 7q3, suggest few if any major common risk alleles account for Autism Spectrum Disorder risk under major linkage peaks in the AGRE sample. This provides important evidence for strategies to identify Autism Spectrum Disorder genes, suggesting that they should focus on identifying rare variants and common variants of small effect