Abstract
Seed death resulting from hybridization between Arabidopsis thaliana and Arabidopsis arenosa has complex genetic determination and involves deregulation 5 to 8 d after pollination (DAP) of agamous-like genes and retroelements. To identify causal mechanisms, we compared transcriptomes of compatible and incompatible hybrids and parents at 3 DAP. Hybrids misexpressed endosperm and seed coat regulators and hyperactivated genes encoding ribosomal, photosynthetic, stress-related, and immune response proteins. Regulatory disruption was more severe in Columbia-0 hybrids than in C24 hybrids, consistent with the degree of incompatibility. Maternal loss-of-function alleles for endosperm growth factor transparent testa glabra2 and HAIKU1 and defense response regulators non-expressor of pathogenesis related1 and salicylic acid induction-deficient2 increased hybrid seed survival. The activation of presumed polycomb repressive complex (PRC) targets, together with a 20-fold reduction in expression of fertilization independent seed2, indicated a PRC role. Proximity to transposable elements affected natural variation for gene regulation, but transposon activation did not differ from controls. Collectively, this investigation provides candidates for multigenic orchestration of the incompatibility response through disruption of endosperm development, a novel role for communication between endosperm and maternal tissues and for pathways previously connected to immunity, but, surprisingly, does not identify a role for transposons.
Highlights
Parental combination as well as the genotype of each parent determines hybrid phenotype suggests that the outcome of hybridization depends on the balance of positive and negative interactions between parental genomes
Compared with A. thaliana seeds, interspecies hybrid embryos from both ecotypes were similar at 2 d after pollination (DAP), but a few C24 hybrids advanced to higher stages (Figure 1)
Endosperm of Col-0 3 A. arenosa hybrid seed was delayed at 3 DAP, as shown in Supplemental Figures 3A and 3B online (74.0 nuclei 6 SE 3.8; t test, P = 0.001 versus 95.6 nuclei 6 SE 4.1 in selfed Col-0), but C24 interspecific hybrid embryos appeared nearly normal at 3 DAP (82.0 6 SE 9.2; t test, P = 0.12 versus 94.5 6 SE 4.2 in selfed C24)
Summary
Parental combination as well as the genotype of each parent determines hybrid phenotype suggests that the outcome of hybridization depends on the balance of positive and negative interactions between parental genomes. Heterosis has been attributed to positive gene interactions (reviewed in Hochholdinger and Hoecker, 2007; Chen, 2010) ranging from genome-wide effects to single-locus effects (Lippman and Zamir, 2007; Krieger et al, 2010). Hybridization can lead to reduced hybrid fitness, including seed failure, germination defects, hybrid necrosis, and sterility. Manifestation of these traits is thought to result from the interaction of diverged parental genes and result in hybrid incompatibly (Dobzhansky, 1936; Muller, 1942; Orr, 1995; reviewed in Bomblies et al, 2007; Rieseberg and Blackman, 2010; Maheshwari and Barbash, 2011). The molecular basis of hybrid incompatibility has been variously attributed to cis-
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