Polyploidization has provided much genetic variation for plant adaptive evolution, but the mechanisms by which the molecular evolution of polyploid genomes establishes genetic architecture underlying species differentiation are unclear. Brassica is an ideal model to increase knowledge of polyploid evolution. Here we describe a draft genome sequence of Brassica oleracea, comparing it with that of its sister species B. rapa to reveal numerous chromosome rearrangements and asymmetrical gene loss in duplicated genomic blocks, asymmetrical amplification of transposable elements, differential gene co-retention for specific pathways and variation in gene expression, including alternative splicing, among a large number of paralogous and orthologous genes. Genes related to the production of anticancer phytochemicals and morphological variations illustrate consequences of genome duplication and gene divergence, imparting biochemical and morphological variation to B. oleracea. This study provides insights into Brassica genome evolution and will underpin research into the many important crops in this genus.

BackgroundPlant disease resistance (R) genes with the nucleotide binding site (NBS) play an important role in offering resistance to pathogens. The availability of complete genome sequences of Brassica oleracea and Brassica rapa provides an important opportunity for researchers to identify and characterize NBS-encoding R genes in Brassica species and to compare with analogues in Arabidopsis thaliana based on a comparative genomics approach. However, little is known about the evolutionary fate of NBS-encoding genes in the Brassica lineage after split from A. thaliana.ResultsHere we present genome-wide analysis of NBS-encoding genes in B. oleracea, B. rapa and A. thaliana. Through the employment of HMM search and manual curation, we identified 157, 206 and 167 NBS-encoding genes in B. oleracea, B. rapa and A. thaliana genomes, respectively. Phylogenetic analysis among 3 species classified NBS-encoding genes into 6 subgroups. Tandem duplication and whole genome triplication (WGT) analyses revealed that after WGT of the Brassica ancestor, NBS-encoding homologous gene pairs on triplicated regions in Brassica ancestor were deleted or lost quickly, but NBS-encoding genes in Brassica species experienced species-specific gene amplification by tandem duplication after divergence of B. rapa and B. oleracea. Expression profiling of NBS-encoding orthologous gene pairs indicated the differential expression pattern of retained orthologous gene copies in B. oleracea and B. rapa. Furthermore, evolutionary analysis of CNL type NBS-encoding orthologous gene pairs among 3 species suggested that orthologous genes in B. rapa species have undergone stronger negative selection than those in B .oleracea species. But for TNL type, there are no significant differences in the orthologous gene pairs between the two species.ConclusionThis study is first identification and characterization of NBS-encoding genes in B. rapa and B. oleracea based on whole genome sequences. Through tandem duplication and whole genome triplication analysis in B. oleracea, B. rapa and A. thaliana genomes, our study provides insight into the evolutionary history of NBS-encoding genes after divergence of A. thaliana and the Brassica lineage. These results together with expression pattern analysis of NBS-encoding orthologous genes provide useful resource for functional characterization of these genes and genetic improvement of relevant crops.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-3) contains supplementary material, which is available to authorized users.

Generally, self-healing research based on commercial rubber is of great significance in sustainable development by extending the lifetime of materials. However, it is still a great challenge so far to prepare recyclable rubber that combine excellent self-healing properties with good mechanical strength and is also recyclable. Herein, we report the use of epoxidized natural rubber (ENR), a reactive polymer presenting dual functional groups (unsaturated double bonds and epoxy sites) available for cross-linking, to prepare a dual cross-linked self-healing ENR based on dynamic disulfide metathesis and thermoreversible hydrogen bonding. Specifically, different structures of aromatic disulfide compounds are introduced into the same system to promote the disulfide metathesis and thus improving the self-healing efficiency of the material. As a result, the dual cross-linked ENR shows high mechanical strength (9.3 ± 0.3 MPa), high self-healing efficiency (up to 98%), and ideal recyclability. In addition, cyclic fatigue tensile test shows that the self-healing properties of the present material are not affected by the damage forms, whether it is complete fracture or cyclic fatigue damage. These outcomes are expected to promote the development of self-healing technology in the sustainable application of cross-linked rubber materials.

The programmed cell death pathway, necroptosis, relies on the pseudokinase, Mixed Lineage Kinase domain-Like (MLKL), for cellular execution downstream of death receptor or Toll-like receptor ligation. Receptor-interacting protein kinase-3 (RIPK3)-mediated phosphorylation of MLKL's pseudokinase domain leads to MLKL switching from an inert to activated state, where exposure of the N-terminal four-helix bundle (4HB) 'executioner' domain leads to cell death. The precise molecular details of MLKL activation, including the stoichiometry of oligomer assemblies, mechanisms of membrane translocation and permeabilisation, remain a matter of debate. Here, we dissect the function of the two 'brace' helices that connect the 4HB to the pseudokinase domain of MLKL. In addition to establishing that the integrity of the second brace helix is crucial for the assembly of mouse MLKL homotrimers and cell death, we implicate the brace helices as a device to communicate pseudokinase domain phosphorylation event(s) to the N-terminal executioner 4HB domain. Using mouse:human MLKL chimeras, we defined the first brace helix and adjacent loop as key elements of the molecular switch mechanism that relay pseudokinase domain phosphorylation to the activation of the 4HB domain killing activity. In addition, our chimera data revealed the importance of the pseudokinase domain in conferring host specificity on MLKL killing function, where fusion of the mouse pseudokinase domain converted the human 4HB + brace from inactive to a constitutive killer of mouse fibroblasts. These findings illustrate that the brace helices play an active role in MLKL regulation, rather than simply acting as a tether between the 4HB and pseudokinase domains.

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Summary Despite the great agricultural and ecological importance of efficient use of urea‐containing nitrogen fertilizers by crops, molecular and physiological identities of urea transport in higher plants have been investigated only in Arabidopsis. We performed short‐time urea‐influx assays which have identified a low‐affinity and high‐affinity (Km of 7.55 μM) transport system for urea‐uptake by rice roots (Oryza sativa). A high‐affinity urea transporter OsDUR3 from rice was functionally characterized here for the first time among crops. OsDUR3 encodes an integral membrane‐protein with 721 amino acid residues and 15 predicted transmembrane domains. Heterologous expression demonstrated that OsDUR3 restored yeast dur3‐mutant growth on urea and facilitated urea import with a Km of c. 10 μM in Xenopus oocytes. Quantitative reverse‐transcription polymerase chain reaction (qPCR) analysis revealed upregulation of OsDUR3 in rice roots under nitrogen‐deficiency and urea‐resupply after nitrogen‐starvation. Importantly, overexpression of OsDUR3 complemented the Arabidopsis atdur3‐1 mutant, improving growth on low urea and increasing root urea‐uptake markedly. Together with its plasma membrane localization detected by green fluorescent protein (GFP)‐tagging and with findings that disruption of OsDUR3 by T‐DNA reduces rice growth on urea and urea uptake, we suggest that OsDUR3 is an active urea transporter that plays a significant role in effective urea acquisition and utilisation in rice.

The leucine-rich repeat kinase 2 (LRRK2) gene and α-synuclein gene (SNCA) are the key influencing factors of Parkinson's disease (PD). It is reported that dysfunction of LRRK2 may influence the accumulation of α-synuclein and its pathology to alter cellular functions and signaling pathways by the kinase activation of LRRK2. The accumulation of α-synuclein is one of the main stimulants of microglial activation. Microglia are macrophages that reside in the brain, and activation of microglia is believed to contribute to neuroinflammation and neuronal death in PD. Therefore, clarifying the complex relationship among LRRK2, α-synuclein and microglials could offer targeted clinical therapies for PD. Here, we provide an updated review focused on the discussion of the evidence supporting some of the key mechanisms that are important for LRRK2-dependent neurodegeneration in PD.

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