RESUMEN
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 × Col-0, which show extensive epigenetic variation but limited DNA sequence variation. Quantitative loci under epigenetic control (QTLepi ) 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 QTLepi were detected across the five chromosomes, with a bona fide epigenetic origin for 16 of them. The effect of five QTLepi was dependent on temperature conditions. Six QTLepi co-localized with previously identified clubroot resistance genes and QTL in Arabidopsis. Co-localization of clubroot resistance QTLepi 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.
Asunto(s)
Arabidopsis/genética , Arabidopsis/inmunología , Resistencia a la Enfermedad/genética , Epigénesis Genética , Variación Genética , Enfermedades de las Plantas/genética , Enfermedades de las Plantas/microbiología , Arabidopsis/crecimiento & desarrollo , Arabidopsis/microbiología , Secuencia de Bases , Metilación de ADN/genética , Patrón de Herencia/genética , Mutación/genética , Fenotipo , Plasmodiophorida/fisiología , Sitios de Carácter Cuantitativo/genética , TemperaturaRESUMEN
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.
Asunto(s)
Endocitosis/fisiología , Regulación Fúngica de la Expresión Génica/fisiología , Cadenas Pesadas de Miosina/metabolismo , Fosfatos/metabolismo , Proteínas de Schizosaccharomyces pombe/metabolismo , Schizosaccharomyces/metabolismo , Transducción de Señal/fisiología , Proteína 2 Relacionada con la Actina/genética , Proteína 2 Relacionada con la Actina/metabolismo , Eliminación de Gen , Cadenas Pesadas de Miosina/genética , Schizosaccharomyces/genética , Proteínas de Schizosaccharomyces pombe/genética , TranscriptomaRESUMEN
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.
Asunto(s)
Arabidopsis/genética , Metilación de ADN , ADN de Plantas/química , Resistencia a la Enfermedad/genética , Enfermedades de las Plantas/genética , Centrómero/ultraestructura , Análisis por Conglomerados , Epigénesis Genética , Epigenómica , Perfilación de la Expresión Génica , Regulación de la Expresión Génica de las Plantas , Genes de Plantas , Haplotipos , Oomicetos/patogenicidad , Fenotipo , Enfermedades de las Plantas/microbiología , Sitios de Carácter Cuantitativo , Carácter Cuantitativo Heredable , Análisis de Secuencia de ARNRESUMEN
Transposable elements (TEs) are mobile parasitic sequences that have been repeatedly coopted during evolution to generate new functions and rewire gene regulatory networks. Yet, the contribution of active TEs to the creation of heritable mutations remains unknown. Using TE accumulation lines in Arabidopsis thaliana we show that once initiated, transposition produces an exponential spread of TE copies, which rapidly leads to high mutation rates. Most insertions occur near or within genes and targets differ between TE families. Furthermore, we uncover an essential role of the histone variant H2A.Z in the preferential integration of Ty1/copia retrotransposons within environmentally responsive genes and away from essential genes. We also show that epigenetic silencing of new Ty1/copia copies can affect their impact on major fitness-related traits, including flowering time. Our findings demonstrate that TEs are potent episodic (epi)mutagens that, thanks to marked chromatin tropisms, limit the mutation load and increase the potential for rapid adaptation.