Natural variation for seed dormancy in Arabidopsis is regulated by additive genetic and molecular pathways

Abstract

Timing of germination is presumably under strong natural selection as it determines the environmental conditions in which a plant germinates and initiates its postembryonic life cycle. To investigate how seed dormancy is controlled, quantitative trait loci (QTL) analyses has been performed in six Arabidopsis thaliana recombinant inbred line populations by analyzing them simultaneously using a mixed model QTL approach. The recombinant inbred line populations were derived from crosses between the reference accession Landsberg erecta (Ler) and accessions from different world regions. In total, 11 delay of germination (DOG) QTL have been identified, and nine of them have been confirmed by near isogenic lines (NILs). The absence of strong epistatic interactions between the different DOG loci suggests that they affect dormancy mainly by distinct genetic pathways. This was confirmed by analyzing the transcriptome of freshly harvested dry seeds of five different DOG NILs. All five DOG NILs showed discernible and different expression patterns compared with the expression of their genetic background Ler. The genes identified in the different DOG NILs represent largely different gene ontology profiles. It is proposed that natural variation for seed dormancy in Arabidopsis is mainly controlled by different additive genetic and molecular pathways rather than epistatic interactions, indicating the involvement of several independent pathways.

Fig. 1.

Seed dormancy QTL identified in six RIL populations. Combined physical map of Ler/An-1, Ler/Cvi, Ler/Fei-0, Ler/Kond, Ler/Kas-2, and the Ler/Sha RIL populations. QTL are depicted as gray arrows along the chromosomes. Markers that were fixed as cofactors are indicated by the black horizontal bar in the gray arrows. The lengths of the arrows indicate the 1.5 [−log10(p)] unit dropoff intervals. –Log10(P) values that indicate the significance of the QTL are indicated below the DOG number. Allelic effects of the QTL in the different populations are indicated by the black arrows. Arrowheads pointing up represent Ler increasing the DSDS50 value; arrowheads pointing down represent the non-Ler allele increasing the DSDS50.

Fig. 2.

Average DSDS50 values and CIs representing dormancy behavior of Ler and DOG NILs (analysis was done on square root scale, back-transformed values are given). Asterisks indicate if the NILs differ significantly from Ler at P < 0.05 (on square root scale).

Fig. 3.

Changes in expression of differentially expressed genes do not correlate between DOG NILs. (A) Dormancy up-regulated (Dup) genes in DOG1 (n = 85), (B) Dup-regulated genes in DOG2 (n = 64), (C) Dup-regulated genes in DOG6 (n = 162), and (D) dormancy down-regulated genes in DOG6 (n = 188). Expression distribution of genes determined as differentially expressed in one genotype. The log2 expression level difference of each NILDOG compared with Ler is depicted. The reference is indicated in light gray; the circles indicate the outliers. All expression levels differences are depicted except some outliers used for the selection of genes, one gene repressed more than fourfold in NILDOG6 (B), and one gene induced more that fourfold in NILDOG2 (D).