Abstract

Hybrid lethality, a postzygotic mechanism of reproductive isolation, is a phenomenon that causes the death of F1 hybrid seedlings. Hybrid lethality is generally caused by the epistatic interaction of two or more loci. In the genus Nicotiana, N. debneyi has the dominant allele Hla1-1 at the HLA1 locus that causes hybrid lethality in F1 hybrid seedlings by interaction with N. tabacum allele(s). Here, we mapped the HLA1 locus using the F2 population segregating for the Hla1-1 allele derived from the interspecific cross between N. debneyi and N. fragrans. To map HLA1, several DNA markers including random amplified polymorphic DNA, amplified fragment length polymorphism, and simple sequence repeat markers, were used. Additionally, DNA markers were developed based on disease resistance gene homologs identified from the genome sequence of N. benthamiana. Linkage analysis revealed that HLA1 was located between two cleaved amplified polymorphic sequence markers Nb14-CAPS and NbRGH1-CAPS at a distance of 10.8 and 10.9 cM, respectively. The distance between these markers was equivalent to a 682 kb interval in the genome sequence of N. benthamiana.

Highlights

  • Species are often reproductively isolated from each other

  • Developmental defects of seedlings such as hybrid lethality, hybrid necrosis, and hybrid weakness are often observed in F1 [5,6,7] or later generations [8,9] in many plant species

  • After the test crosses with N. tabacum, crossed seeds were obtained from 81 of 125 F2 plants derived from the cross N. debneyi × N. fragrans; seeds could not be obtained in crosses using the remaining 44 F2 plants

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Summary

Introduction

Species are often reproductively isolated from each other. This mechanism, called reproductive isolation, has been an interesting theme in evolutionary biology because it plays an important role in preventing gene flow between species [1]. Many studies have reported the prevention or bypass of reproductive isolation [2,3,4], challenging cases are still often encountered. Developmental defects of seedlings such as hybrid lethality, hybrid necrosis, and hybrid weakness are often observed in F1 [5,6,7] or later generations (hybrid breakdown) [8,9] in many plant species. These phenomena are caused by epistatic interactions of two or more loci as explained by the Bateson–Dobzhansky–Muller model [10]. In other cases, seedling developmental defects were reported to be caused by duplicate genes such as histidinol-phosphate amino-transferase gene [15] or photosynthetic gene plastid transcriptionally active chromosome 14 [16]

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