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Frank Johannes

Publications and source records attributed to Frank Johannes.

3 recordsLinked to original sources

Epigenetic divergence is sufficient to trigger heterosis in Arabidopsis thaliana

Despite the importance and wide exploitation of heterosis in commercial crop breeding, the molecular mechanisms behind this phenomenon are not well understood. Interestingly, there is growing evidence that beside genetic also epigenetic factors contribute to heterosis. Here we used near-isogenic but epigenetically divergent parents to create epigenetic F1 hybrids (epiHybrids) in Arabidopsis, allowing us to quantify the contribution of epigenetics to heterosis. We measured traits such as leaf area (LA), growth rate (GR), flowering time (FT), main stem branching (MSB), rosette branching (RB) and final plant height (HT) and observed several strong positive and negative heterotic phenotypes among the epiHybrids. For LA and HT mainly positive heterosis was observed, while FT and MSB mostly displayed negative heterosis. Heterosis for FT, LA and HT could be associated with several heritable, differentially methylated regions (DMRs) in the parental genomes. These DMRs contain 35 (FT and LA) and 14 (HT) genes, which may underlie the heterotic phenotypes observed. In conclusion, our study indicates that epigenetic divergence can be sufficient to cause heterosis.\n\nAuthor SummaryCrossing two genetically distinct parents generates hybrid offspring. Sometimes hybrids are performing better than their parents in particular traits and this is referred to as heterosis. Hybridization and heterosis are naturally occurring processes and crop breeders intentionally cross genetically different parental lines in order to generate hybrids with maximized traits such as yield or stress tolerance. So far, the mechanisms behind heterosis are not well understood. In this study we focused on the effect of epigenetic variation onto heterosis in hybrids, and for this purpose we created epigenetic hybrids (epiHybrids) by crossing wildtype plants with a selection of genetically very similar but epigenetically divergent lines. An extensive phenotypic analysis of the epiHybrids and their parental lines showed that epigenetic divergence between parental genomes can be a major determinant of heterosis. Importantly, multiple heterotic phenotypes could be associated with meiotically heritable differentially methylated regions (DMRs) in the parental genomes, allowing us to map epigenetic quantitative trait loci (QTLs) for heterosis. Our results indicate that epigenetic variation can contribute to heterosis and suggests that heritable epigenetic variation could be exploited for the improvement of crop traits.

Plant Biology

chromstaR: Tracking combinatorial chromatin state dynamics in space and time

BackgroundPost-translational modifications of histone residue tails are an important component of genome regulation. It is becoming increasingly clear that the combinatorial presence and absence of various modifications define discrete chromatin states which determine the functional properties of a locus. An emerging experimental goal is to track changes in chromatin state maps across different conditions, such as experimental treatments, cell-types or developmental time points.\n\nResultsHere we present chromstaR, an algorithm for the computational inference of combinatorial chromatin state dynamics across an arbitrary number of conditions. ChromstaR uses a multivariate Hidden Markov Model to determine the number of discrete combinatorial chromatin states using multiple ChIP-seq experiments as input and assigns every genomic region to a state based on the presence/absence of each modification in every condition. We demonstrate the advantages of chromstaR in the context of three common experimental data scenarios. First, we study how different histone modifications combine to form combinatorial chromatin states in a single tissue. Second, we infer genome-wide patterns of combinatorial state differences between two cell types or conditions. Finally, we study the dynamics of combinatorial chromatin states during tissue differentiation involving up to six differentiation points. Our findings reveal a striking sparcity in the combinatorial organization and temporal dynamics of chromatin state maps.\n\nConclusionschromstaR is a versatile computational tool that facilitates a deeper biological understanding of chromatin organization and dynamics. The algorithm is implemented as an R-package and freely available from http://bioconductor.org/packages/chromstaR/.

Bioinformatics

Signatures of Dobzhansky-Muller Incompatibilities in the Genomes of Recombinant Inbred Lines

In the construction of Recombinant Inbred Lines (RILs) from two divergent inbred parents certain genotype (or epigenotype) combinations may be functionally \"incompatible\" when brought together in the genomes of the progeny, thus resulting in sterility or lower fertility. Natural selection against these epistatic combinations during inbreeding can change haplotype frequencies and distort linkage disequilibrium (LD) relations between loci within and across chromosomes. These LD distortions have received increased experimental attention, because they point to genomic regions that may drive Dobzhansky-Muller-type of reproductive isolation and, ultimately, speciation in the wild. Here we study the selection signatures of two-locus epistatic incompatibility models and quantify their impact on the genetic composition of the genomes of 2-way RILs obtained by selfing. We also consider the biases introduced by breeders when trying to counteract the loss of lines by selectively propagating only viable seeds. Building on our theoretical results, we develop model-based maximum likelihood (ML) tests which can be employed in pairwise genome scans for incompatibility loci using multi-locus genotype data. We illustrate this ML approach in the context of two published A.thaliana RIL panels. Our work lays the theoretical foundation for studying more complex systems such as RILs obtained by sibling mating and/or from multi-parental crosses.

Genetics