Immune response during pathogen infection requires extensive transcription reprogramming. A fundamental mechanism of transcriptional regulation is histone acetylation. However, how pathogens interfere with this process to promote disease remains largely unknown. Here we demonstrate that the cytoplasmic effector PsAvh23 produced by the soybean pathogen Phytophthora sojae acts as a modulator of histone acetyltransferase (HAT) in plants. PsAvh23 binds to the ADA2 subunit of the HAT complex SAGA and disrupts its assembly by interfering with the association of ADA2 with the catalytic subunit GCN5. As such, PsAvh23 suppresses H3K9 acetylation mediated by the ADA2/GCN5 module and increases plant susceptibility. Expression of PsAvh23 or silencing of GmADA2/GmGCN5 resulted in misregulation of defense-related genes, most likely due to decreased H3K9 acetylation levels at the corresponding loci. This study highlights an effective counter-defense mechanism by which a pathogen effector suppresses the activation of defense genes by interfering with the function of the HAT complex during infection.

Different sizes of water clusters from a dimer to twenty water molecules are studied using density functional theory. The binding energies of water clusters are calculated, and a relationship in terms of a simple function has been found between binding energy and the size of the water clusters. The interpolation of this correlation function reproduces the binding energies for the other water clusters to an accuracy within 1 kcal/mol. The extrapolation of the function gives the binding energy, −11.38 kcal/mol, which agrees very well with the experimental binding energy of ice, −11.35 kcal/mol. We also find small water clusters composed of mainly planar four membered rings to be more stable, implying the existence of magic numbers for water clusters with sizes of 4, 8, and 12.

BackgroundFilamentous plant pathogen genomes often display a bipartite architecture with gene-sparse, repeat-rich compartments serving as a cradle for adaptive evolution. The extent to which this two-speed genome architecture is associated with genome-wide DNA modifications is unknown.ResultsWe show that the oomycetes Phytophthora infestans and Phytophthora sojae possess functional adenine N6-methylation (6mA) methyltransferases that modulate patterns of 6mA marks across the genome. In contrast, 5-methylcytosine could not be detected in these species. Methylated DNA IP sequencing (MeDIP-seq) of each species reveals 6mA is depleted around the transcription start sites (TSSs) and is associated with lowly expressed genes, particularly transposable elements. Genes occupying the gene-sparse regions have higher levels of 6mA in both genomes, possibly implicating the methylome in adaptive evolution. All six putative adenine methyltransferases from P. infestans and P. sojae, except PsDAMT2, display robust enzymatic activities. Surprisingly, single knockouts in P. sojae significantly reduce in vivo 6mA levels, indicating that the three enzymes are not fully redundant. MeDIP-seq of the psdamt3 mutant reveals uneven 6mA methylation reduction across genes, suggesting that PsDAMT3 may have a preference for gene body methylation after the TSS. Furthermore, transposable elements such as DNA elements are more active in the psdamt3 mutant. A large number of genes, particularly those from the adaptive genomic compartment, are differentially expressed.ConclusionsOur findings provide evidence that 6mA modification is potentially an epigenetic mark in Phytophthora genomes, and complex patterns of 6mA methylation may be associated with adaptive evolution in these important plant pathogens.Electronic supplementary materialThe online version of this article (10.1186/s13059-018-1564-4) contains supplementary material, which is available to authorized users.

We report a facile chemical vapor deposition (CVD) method to grow silicon/carbon (Si/C) microrods on the surface of commercial graphite microspheres (GMs) to prepare Si/C/GM composite materials as Li-ion battery anodes. Dimethyldichlorosilane and toluene were used as Si and C precursors, respectively. The CVD temperature and time, as well as the mechanism of materials growth were investigated. The samples were characterized by using X-ray diffraction, thermogravimetric analysis, X-ray photoelectron spectroscopy, Raman spectroscopy, scanning electron microscopy, and transmission electron microscopy.It was found that the obtained Si/C/GM composites with an urchin-like morphology are composed of Si particles, amorphous carbon, and graphite. The CVD conditions have a significant impact on the morphology and electrochemical performance of the composite materials. The composite prepared under the optimum CVD conditions, namely at 900 C for 5 h, displayed the best anode properties with a specific capacity of 562.0 mA h g À1 at a current density of 50 mA g À1 , much higher than that of GMs (361.0 mA h g À1 ), and a good cycling performance (i.e., a reversible capacity of 590.5 mA h g À1 after 50 cycles). The improved electrochemical performance is attributed to the incorporation of Si, together with the formation of a Si/C microrod network, which connects the GMs and buffers the volume change of Si during lithium ion insertion/extraction. The work provides a simple and low-cost route to enhance the performance of commercial graphite anode materials for Li-ion batteries.

The relentless adaptability of pathogen populations is a major obstacle to effective disease control measures. Increasing evidence suggests that gene transcriptional polymorphisms are a strategy deployed by pathogens to evade host immunity. However, the underlying mechanisms of transcriptional plasticity remain largely elusive. Here we found that the soybean root rot pathogen Phytophthora sojae evades the soybean Resistance gene Rps1b through transcriptional polymorphisms in the effector gene Avr1b that occur in the absence of any sequence variation. Elevated levels of histone H3 Lysine27 tri-methylation (H3K27me3) were observed at the Avr1b locus in a naturally occurring Avr1b-silenced strain but not in an Avr1b-expressing strain, suggesting a correlation between this epigenetic modification and silencing of Avr1b. To genetically test this hypothesis, we edited the gene, PsSu(z)12, encoding a core subunit of the H3K27me3 methyltransferase complex by using CRISPR/Cas9, and obtained three deletion mutants. H3K27me3 depletion within the Avr1b genomic region correlated with impaired Avr1b gene silencing in these mutants. Importantly, these mutants lost the ability to evade immune recognition by soybeans carrying Rps1b. These data support a model in which pathogen effector transcriptional polymorphisms are associated with changes in chromatin epigenetic marks, highlighting epigenetic variation as a mechanism of pathogen adaptive plasticity.