Genome-wide patterns of segregation and linkage disequilibrium: The construction of a linkage genetic map of the poplar rust fungus Melampsora larici-populina

Summary

This research focused on creating a genetic map of the fungus that causes rust disease in poplar trees. Understanding the genetic makeup of this pathogen is crucial for developing better disease-resistant trees. The study provides a foundation for identifying genes that make the fungus more aggressive and helps improve strategies to protect poplar plantations. Impacts on everyday life: – Helps protect poplar trees used in wood production and bioenergy – Contributes to more sustainable forestry practices – Supports development of disease-resistant trees for commercial plantations – Reduces economic losses in timber industry – Advances methods for studying plant diseases that affect other crops

Background

The poplar rust fungus Melampsora larici-populina causes significant yield reduction and economic losses in commercial poplar plantations. After decades of breeding for qualitative resistance and subsequent breakdown of resistance genes, breeders now focus on quantitative resistance, perceived to be more durable. However, quantitative resistance can also be challenged by increased pathogen aggressiveness. Understanding the genetic architecture of aggressiveness traits is therefore crucial for developing durable resistance.

Objective

To construct a genetic linkage map for M. larici-populina to enable mapping of quantitative trait loci related to aggressiveness. This required generating a large progeny through selfing of the reference strain 98AG31 on larch plants and validating the progeny’s meiotic origin through segregation analysis.

Results

Twelve out of 14 microsatellite loci exhibited expected Mendelian segregation ratios. Two pairs of microsatellite loci showed significant linkage disequilibrium, allowing identification of one linkage group. Analysis of SNP-based markers identified 23 putative linkage groups comprising 81 scaffolds, representing 65% of the genome. Linkage disequilibrium was detectable at distances up to 1 Mbp. The analysis revealed potential genome assembly issues requiring scaffold reorganization.

Conclusion

The study demonstrated that a high-density genetic linkage map could be constructed using SNPs from low-coverage resequencing of M. larici-populina offspring. The preliminary results identified 23 linkage groups and highlighted areas for genome assembly improvement. This genetic map will enable future QTL mapping of aggressiveness traits and assist genome assembly refinement.
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