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Abstract
Arachis hypogaea (peanut) is a very important crop cultivated worldwide. It is an allotetraploid species with low genetic diversity and high susceptibility to root-knot nematode (RKN) Meloidogyne arenaria. Most commercial cultivars harbor a single RKN resistance locus derived from the wild species A. cardenasii. There is, however, a risk that this resistance could breakdown and could lead to devastating consequences for peanut production, therefore, additional sources of resistance are urgently needed.
Strong resistant to RKN is present in the peanut wild relative A. stenosperma. Previously, three QTLs were mapped in the A. stenosperma genome (A02, A04 and A09). Here, to validate these chromosome segments within the genetic background of tetraploid peanut, an F2 population was developed from a cross between A. hypogaea with the induced allotetraploid BatSten1 ([A. batizocoi x A. stenosperma]4x). This population was genotyped using a SNP array and phenotyped for nematode resistance. QTL analysis allowed us to verify the major-effect QTL on chromosome A02, where an R-gene cluster is co-located, and a secondary QTL on A09, the two QTL providing a disease reduction up to 98.2%.
To incorporate RKN resistance from A. stenosperma into peanut cultivars, selected F2:3 lines were crossed and backcrossed with advanced peanut breeding lines. Later, phenotypic screening for resistance and genotypic characterization of BC2F1 lines allowed us to validate and refine the genomic regions that confer resistance. Furthermore, we performed genome-wide genotyping of advanced backcrossed lines (BC3F1s); and lines harboring the resistance alleles and that had a high recurrent genome recovery were selected. In the future, further selection and advancement will be needed for eventual germplasm release. These genotypes that incorporate strong RKN resistance and the markers linked to this trait, represent a valuable tool for introgression of a new nematode resistance into agronomically adapted peanuts and can significantly impact peanut production in RKN-affected areas.
Finally, due to the synthetic origin of the allotetraploid BatSten1, there was the possibility of inter-genomic interactions at the transcriptome level (‘genomics shock’) between the A and K subgenomes genomes of the synthetic BatSten1. Therefore, we started the exploration of changes in expression of homeologous genes pairs.
Strong resistant to RKN is present in the peanut wild relative A. stenosperma. Previously, three QTLs were mapped in the A. stenosperma genome (A02, A04 and A09). Here, to validate these chromosome segments within the genetic background of tetraploid peanut, an F2 population was developed from a cross between A. hypogaea with the induced allotetraploid BatSten1 ([A. batizocoi x A. stenosperma]4x). This population was genotyped using a SNP array and phenotyped for nematode resistance. QTL analysis allowed us to verify the major-effect QTL on chromosome A02, where an R-gene cluster is co-located, and a secondary QTL on A09, the two QTL providing a disease reduction up to 98.2%.
To incorporate RKN resistance from A. stenosperma into peanut cultivars, selected F2:3 lines were crossed and backcrossed with advanced peanut breeding lines. Later, phenotypic screening for resistance and genotypic characterization of BC2F1 lines allowed us to validate and refine the genomic regions that confer resistance. Furthermore, we performed genome-wide genotyping of advanced backcrossed lines (BC3F1s); and lines harboring the resistance alleles and that had a high recurrent genome recovery were selected. In the future, further selection and advancement will be needed for eventual germplasm release. These genotypes that incorporate strong RKN resistance and the markers linked to this trait, represent a valuable tool for introgression of a new nematode resistance into agronomically adapted peanuts and can significantly impact peanut production in RKN-affected areas.
Finally, due to the synthetic origin of the allotetraploid BatSten1, there was the possibility of inter-genomic interactions at the transcriptome level (‘genomics shock’) between the A and K subgenomes genomes of the synthetic BatSten1. Therefore, we started the exploration of changes in expression of homeologous genes pairs.