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International audience; Quantitative disease resistance, often influenced by environmental factors, is thought to be the result of DNA sequence variants segregating at multiple loci. However, heritable differences in DNA methylation, so-called transgenerational epigenetic variants, also could contribute to quantitative traits. Here, we tested this possibility using the well-characterized quantitative resistance of Arabidopsis to clubroot, a Brassica major disease caused by Plasmodiophora brassicae. For that, we used the epigenetic recombinant inbred lines (epiRIL) derived from the cross ddm1-2 9 Col-0, which show extensive epigenetic variation but limited DNA sequence variation. Quantitative loci under epigenetic control (QTL epi) mapping was carried out on 123 epiRIL infected with P. brassicae and using various disease-related traits. EpiRIL displayed a wide range of continuous phenotypic responses. Twenty QTL epi were detected across the five chromosomes, with a bona fide epigenetic origin for 16 of them. The effect of five QTL epi was dependent on temperature conditions. Six QTL epi co-localized with previously identified clubroot resistance genes and QTL in Arabidopsis. Co-localization of clubroot resistance QTL epi with previously detected DNA-based QTL reveals a complex model in which a combination of allelic and epiallelic variations interacts with the environment to lead to variation in clubroot quantitative resistance.

Variation in DNA methylation enables plants to inherit traits independently of changes to DNA sequence. Here, we have screened an Arabidopsis population of epigenetic recombinant inbred lines (epiRILs) for resistance against Hyaloperonospora arabidopsidis (Hpa). These lines share the same genetic background, but show variation in heritable patterns of DNA methylation. We identified four epigenetic quantitative trait loci (epiQTLs) that provide quantitative resistance without reducing plant growth or resistance to other (a)biotic stresses. Phenotypic characterisation and RNA-sequencing analysis revealed that Hpa-resistant epiRILs are primed to activate defence responses at the relatively early stages of infection. Collectively, our results show that hypomethylation at selected pericentromeric regions is sufficient to provide quantitative disease resistance, which is associated with genome-wide priming of defence-related genes. Based on comparisons of global gene expression and DNA methylation between the wild-type and resistant epiRILs, we discuss mechanisms by which the pericentromeric epiQTLs could regulate the defence-related transcriptome., eLife digest In plants, animals and microbes genetic information is encoded by DNA, which are made up of sequences of building blocks, called nucleotide bases. These sequences can be separated into sections known as genes that each encode specific traits. It was previously thought that only changes to the sequence of bases in a DNA molecule could alter the traits passed on to future generations. However, it has recently become clear that some traits can also be inherited through modifications to the DNA that do not alter its sequence. One such modification is to attach a tag, known as a methyl group, to a nucleotide base known as cytosine. These methyl tags can be added to, or removed from, DNA to create different patterns of methylation. Previous studies have shown that plants whose DNA is less methylated than normal (‘hypo-methylated’) are more resistant to plant diseases. However, the location and identity of the hypo-methylated DNA regions controlling this resistance remained unknown. To address this problem, Furci, Jain et al. studied how DNA methylation in a small weed known as Arabidopsis thaliana affects how well the plants can resist a disease known as downy mildew. Furci, Jain et al. studied a population of over 100 A. thaliana lines that have the same DNA sequences but different patterns of DNA methylation. The experiments identified four DNA locations that were less methylated in lines with enhanced resistance to downy mildew. Importantly, this form of resistance did not appear to reduce how well the plants grew, or make them less able to resist other diseases or environmental stresses. The results of further experiments suggested that reduced methylation at the four DNA regions prime the plant’s immune system, enabling a faster and stronger activation of a multitude of defence genes across the genome after attack by downy mildew. The next steps following on from this work are to investigate exactly how the four DNA regions with reduced methylation can prime so many different defence genes in the plant. Further research is also needed to determine whether it is possible to breed crop plants with lower levels of methylation at specific DNA locations to improve disease resistance, but without decreasing the amount and quality of food produced.

Endocytosis is essential for uptake of many substances into the cell, but how it links to nutritional signalling is poorly understood. Here, we show a new role for endocytosis in regulating the response to low phosphate in Schizosaccharomyces pombe. Loss of function of myosin I (Myo1), Sla2/End4 or Arp2, proteins involved in the early steps of endocytosis, led to increased proliferation in low-phosphate medium compared to controls. We show that once cells are deprived of phosphate they undergo a quiescence response that is dependent on the endocytic function of Myo1. Transcriptomic analysis revealed a wide perturbation of gene expression with induction of stress-regulated genes upon phosphate starvation in wild-type but not Δmyo1 cells. Thus, endocytosis plays a pivotal role in mediating the cellular response to nutrients, bridging the external environment and internal molecular functions of the cell., Highlighted Article: The endocytic machinery, including the type 1 myosin Myo1, is required to establish a quiescence response to low-phosphate stress in fission yeast.

We present ePeak, a Snakemake-based pipeline for the identification and quantification of reproducible peaks from raw ChIP-seq, CUT&RUN and CUT&Tag epigenomic profiling techniques. It also includes a statistical module to perform tailored differential marking and binding analysis with state of the art methods. ePeak streamlines critical steps like the quality assessment of the immunoprecipitation, spike-in calibration and the selection of reproducible peaks between replicates for both narrow and broad peaks. It generates complete reports for data quality control assessment and optimal interpretation of the results. We advocate for a differential analysis that accounts for the biological dynamics of each chromatin factor. Thus, ePeak provides linear and nonlinear methods for normalisation as well as conservative and stringent models for variance estimation and significance testing of the observed marking/binding differences. Using a published ChIP-seq dataset, we show that distinct populations of differentially marked/bound peaks can be identified. We study their dynamics in terms of read coverage and summit position, as well as the expression of the neighbouring genes. We propose that ePeak can be used to measure the richness of the epigenomic landscape underlying a biological process by identifying diverse regulatory regimes.