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Wednesday, May 2, 2012

Epigenetics and Speciation

Contributed by: Masafumi Nozawa

Epigenetic variation has recently been recognized as an additional layer of genetic changes. After the discovery of epigenetic variation, many researchers have studied its importance in adaptation and evolution. However, the role of epigenetic variation in speciation remains largely unexplored.
Durand et al. (1) recently showed that natural epigenetic variation in Arabidopsis thaliana contributes to the cause of genetic incompatibility responsible for post-zygotic reproductive isolation. When they crossed the Columbia-0 (col) strain with the Shahdara (sha) strain, some F2 hybrids showed reduced seed production by 80-90%. Linkage disequilibrium analysis identified two genomic regions, K4 and K5, that are responsible for the incompatibility. Further fine mapping revealed that K5 contains gene AtFOLT1, which encodes a folate transporter, and K4 contains a duplicate locus, AtFOLT2, only in sha. AtFOLT1 is expressed in col but not in sha, whereas AtFOLT2 exists only in sha. Interestingly, F2 hybrids become incompatible only when there is no AtFOLT transcript. Therefore, the lack of AtFOLT transcripts is responsible for the incompatibility (Fig. 1).

Fig. 1. Mechanism of the allelic incompatibility. In col, the promoter and the first part of the gene AtFOLT1 are totally unmethylated but they are in sha. The homologous region of AtFOLT2 is also methylated in sha, the gene being transcribed (black arrow) from the unmethylated upstream promoter (green box). Modified from Durand et al. (1).

Therefore, they examined SNPs that might be responsible for the suppression of AtFOLT1 in sha and identified 29 such SNPs between sha and col. However, another strain named Ishikawa was shown to express AtFOLT1 even if the nucleotide sequence of AtFOLT1 is exactly the same as that of sha. This indicates that epigenetic changes cause the silencing of AtFOLT1. Indeed, AtFOLT1 in sha was highly methylated.
They further investigated how the methylation is induced and found that AtFOLT2 in sha generates small RNAs which directly induce DNA methylation on promoter regions of AtFOLT1 and AtFOLT2. Yet, because AtFOLT2 in sha has an irregular promoter region which is not methylated, sha can express AtFOLT2 and therefore be fertile (Fig. 1). Interestingly, this small RNA is sufficient to induce de novo DNA methylation in the AtFOLT region, because after several generations the unmethylated AtFOLT1 region was methylated (Fig. 2).

Fig. 2. De novo DNA methylation of AtFOLT1 by small RNAs in the AtFOLT2 region. In F1, AtFOLT1 from col is expressed because the region is not methylated. However, small RNAs at the AtFOLT2 region derived from sha stochastically and progressively induce DNA methylation on the AtFOLT1 region. Consequently, AtFOLT1 is not expressed after seven generations.

In summary, this study represents the first case of a natural epiallele that has strong deleterious phenotypic consequences steadily maintained in the progenies of crosses between strains, which play roles in establishing reproductive isolation. I think this type of processes might be much more frequent than currently appreciated.

1. Durand S, Bouche N, Strand EP, Loudet O, and Camilleri C. (2012) Rapid establishment of genetic incompatibility through natural epigenetic variation. Curr Bio 22: 326-31.

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