The evolution of the genetic architecture of an allopolyploid and the genetic basis of the selfing syndrome

Polyploidization, the increase in genome size caused by the inheritance of an additional set (or sets) of chromosomes is a major force in evolution.

Allopolyploidy corresponds to two processes altering fundamentally the hereditary material: whole genome duplication (WGD) and hybridization. Transition to allopolyploidy is also often accompanied by a mating system shift, from outcrossing to selfing. Three major transitions at once seem a tall order.

Yet, our recent genomic studies in natural sheperd’s purse (Capsella bursa-pastoris) as well as with resynthetized allopolyploids, together with studies in other allopolyploid species, have demonstrated the absence of genomic shocks. Instead, there is a strong parental legacy and a gradual evolution of both alloploidy and the selfing syndrome.

Hence, understanding the evolution of these two transitions implies understanding more subtle processes, in particular, how the genetic architecture of quantitative traits is altered by the joint effect of WGD, hybridization and mating system shift.

We propose here (i) to leverage recent progress in the analysis of the architecture of complex traits and carry out genomewide association studies (GWAS) in C. bursa-pastoris and its parental diploid species (ii) to take advantage of our series of resynthetized Capsella polyploids to cross these resynthetized polyploids with established C. bursa-pastoris to identify genes associated with the progressive evolution of the selfing syndrome.