348 research outputs found

    Genome-wide analysis of the nucleotide binding site leucine-rich repeat genes of four orchids revealed extremely low numbers of disease resistance genes

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    Orchids are one of the most diverse flowering plant families, yet possibly maintain the smallest number of the nucleotide-binding site-leucine-rich repeat (NBS-LRR) type plant resistance (R) genes among the angiosperms. In this study, a genome-wide search in four orchid taxa identified 186 NBS-LRR genes. Furthermore, 214 NBS-LRR genes were identified from seven orchid transcriptomes. A phylogenetic analysis recovered 30 ancestral lineages (29 CNL and one RNL), far fewer than other angiosperm families. From the genetics aspect, the relatively low number of ancestral R genes is unlikely to explain the low number of R genes in orchids alone, as historical gene loss and scarce gene duplication has continuously occurred, which also contributes to the low number of R genes. Due to recent sharp expansions, Phalaenopsis equestris and Dendrobium catenatum having 52 and 115 genes, respectively, and exhibited an "early shrinking to recent expanding" evolutionary pattern, while Gastrodia elata and Apostasia shenzhenica both exhibit a "consistently shrinking" evolutionary pattern and have retained only five and 14 NBS-LRR genes, respectively. RNL genes remain in extremely low numbers with only one or two copies per genome. Notably, all of the orchid RNL genes belong to the ADR1 lineage. A separate lineage, NRG1, was entirely absent and was likely lost in the common ancestor of all monocots. All of the TNL genes were absent as well, coincident with the RNL NRG1 lineage, which supports the previously proposed notion that a potential functional association between the TNL and RNL NRG1 genes

    DNA-PK-Dependent RPA2 Hyperphosphorylation Facilitates DNA Repair and Suppresses Sister Chromatid Exchange

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    Hyperphosphorylation of RPA2 at serine 4 and serine 8 (S4, S8) has been used as a marker for activation of the DNA damage response. What types of DNA lesions cause RPA2 hyperphosphorylation, which kinase(s) are responsible for them, and what is the biological outcome of these phosphorylations, however, have not been fully investigated. In this study we demonstrate that RPA2 hyperphosphorylation occurs primarily in response to genotoxic stresses that cause high levels of DNA double-strand breaks (DSBs) and that the DNA-dependent protein kinase complex (DNA-PK) is responsible for the modifications in vivo. Alteration of S4, S8 of RPA2 to alanines, which prevent phosphorylations at these sites, caused increased mitotic entry with concomitant increases in RAD51 foci and homologous recombination. Taken together, our results demonstrate that RPA2 hyperphosphorylation by DNA-PK in response to DSBs blocks unscheduled homologous recombination and delays mitotic entry. This pathway thus permits cells to repair DNA damage properly and increase cell viability

    Genome-Wide Identification of Polycomb Target Genes Reveals a Functional Association of Pho with Scm in Bombyx mori

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    Polycomb group (PcG) proteins are evolutionarily conserved chromatin modifiers and act together in three multimeric complexes, Polycomb repressive complex 1 (PRC1), Polycomb repressive complex 2 (PRC2), and Pleiohomeotic repressive complex (PhoRC), to repress transcription of the target genes. Here, we identified Polycomb target genes in Bombyx mori with holocentric centromere using genome-wide expression screening based on the knockdown of BmSCE, BmESC, BmPHO, or BmSCM gene, which represent the distinct complexes. As a result, the expressions of 29 genes were up-regulated after knocking down 4 PcG genes. Particularly, there is a significant overlap between targets of BmPho (331 out of 524) and BmScm (331 out of 532), and among these, 190 genes function as regulator factors playing important roles in development. We also found that BmPho, as well as BmScm, can interact with other Polycomb components examined in this study. Further detailed analysis revealed that the C-terminus of BmPho containing zinc finger domain is involved in the interaction between BmPho and BmScm. Moreover, the zinc finger domain in BmPho contributes to its inhibitory function and ectopic overexpression of BmScm is able to promote transcriptional repression by Gal4-Pho fusions including BmScm-interacting domain. Loss of BmPho expression causes relocalization of BmScm into the cytoplasm. Collectively, we provide evidence of a functional link between BmPho and BmScm, and propose two Polycomb-related repression mechanisms requiring only BmPho associated with BmScm or a whole set of PcG complexes

    Myosin Light Chain Kinase Mediates Intestinal Barrier Disruption following Burn Injury

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    Background: Severe burn injury results in the loss of intestinal barrier function, however, the underlying mechanism remains unclear. Myosin light chain (MLC) phosphorylation mediated by MLC kinase (MLCK) is critical to the pathophysiological regulation of intestinal barrier function. We hypothesized that the MLCK-dependent MLC phosphorylation mediates the regulation of intestinal barrier function following burn injury, and that MLCK inhibition attenuates the burn-induced intestinal barrier disfunction. Methodology/Principal Findings: Male balb/c mice were assigned randomly to either sham burn (control) or 30 % total body surface area (TBSA) full thickness burn without or with intraperitoneal injection of ML-9 (2 mg/kg), an MLCK inhibitor. In vivo intestinal permeability to fluorescein isothiocyanate (FITC)-dextran was measured. Intestinal mucosa injury was assessed histologically. Tight junction proteins ZO-1, occludin and claudin-1 was analyzed by immunofluorescent assay. Expression of MLCK and phosphorylated MLC in ileal mucosa was assessed by Western blot. Intestinal permeability was increased significantly after burn injury, which was accompanied by mucosa injury, tight junction protein alterations, and increase of both MLCK and MLC phosphorylation. Treatment with ML-9 attenuated the burn-caused increase of intestinal permeability, mucosa injury, tight junction protein alterations, and decreased MLC phosphorylation, but not MLCK expression

    Network Properties of Robust Immunity in Plants

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    Two modes of plant immunity against biotrophic pathogens, Effector Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI), are triggered by recognition of pathogen effectors and Microbe-Associated Molecular Patterns (MAMPs), respectively. Although the jasmonic acid (JA)/ethylene (ET) and salicylic acid (SA) signaling sectors are generally antagonistic and important for immunity against necrotrophic and biotrophic pathogens, respectively, their precise roles and interactions in ETI and PTI have not been clear. We constructed an Arabidopsis dde2/ein2/pad4/sid2-quadruple mutant. DDE2, EIN2, and SID2 are essential components of the JA, ET, and SA sectors, respectively. The pad4 mutation affects the SA sector and a poorly characterized sector. Although the ETI triggered by the bacterial effector AvrRpt2 (AvrRpt2-ETI) and the PTI triggered by the bacterial MAMP flg22 (flg22-PTI) were largely intact in plants with mutations in any one of these genes, they were mostly abolished in the quadruple mutant. For the purposes of this study, AvrRpt2-ETI and flg22-PTI were measured as relative growth of Pseudomonas syringae bacteria within leaves. Immunity to the necrotrophic fungal pathogen Alternaria brassicicola was also severely compromised in the quadruple mutant. Quantitative measurements of the immunity levels in all combinatorial mutants and wild type allowed us to estimate the effects of the wild-type genes and their interactions on the immunity by fitting a mixed general linear model. This signaling allocation analysis showed that, contrary to current ideas, each of the JA, ET, and SA signaling sectors can positively contribute to immunity against both biotrophic and necrotrophic pathogens. The analysis also revealed that while flg22-PTI and AvrRpt2-ETI use a highly overlapping signaling network, the way they use the common network is very different: synergistic relationships among the signaling sectors are evident in PTI, which may amplify the signal; compensatory relationships among the sectors dominate in ETI, explaining the robustness of ETI against genetic and pathogenic perturbations

    Understanding of sub-band gap absorption of femtosecond-laser sulfur hyperdoped silicon using synchrotron-based techniques

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    [[abstract]]The correlation between sub-band gap absorption and the chemical states and electronic and atomic structures of S-hyperdoped Si have been extensively studied, using synchrotron-based x-ray photoelectron spectroscopy (XPS), x-ray absorption near-edge spectroscopy (XANES), extended x-ray absorption fine structure (EXAFS), valence-band photoemission spectroscopy (VB-PES) and first-principles calculation. S 2p XPS spectra reveal that the S-hyperdoped Si with the greatest (~87%) sub-band gap absorption contains the highest concentration of S2โˆ’ (monosulfide) species. Annealing S-hyperdoped Si reduces the sub-band gap absorptance and the concentration of S2โˆ’ species, but significantly increases the concentration of larger S clusters [polysulfides (Sn2โˆ’, nโ€‰>โ€‰2)]. The Si K-edge XANES spectra show that S hyperdoping in Si increases (decreased) the occupied (unoccupied) electronic density of states at/above the conduction-band-minimum. VB-PES spectra evidently reveal that the S-dopants not only form an impurity band deep within the band gap, giving rise to the sub-band gap absorption, but also cause the insulator-to-metal transition in S-hyperdoped Si samples. Based on the experimental results and the calculations by density functional theory, the chemical state of the S species and the formation of the S-dopant states in the band gap of Si are critical in determining the sub-band gap absorptance of hyperdoped Si samples.[[notice]]่ฃœๆญฃๅฎŒ็•ข[[journaltype]]ๅœ‹ๅค–[[incitationindex]]SCI[[ispeerreviewed]]Y[[booktype]]้›ปๅญ็‰ˆ[[countrycodes]]GB
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