Chitin is the major component of fungal cell wall and serves as a molecular pattern that can be recognized by the receptor OsCEBiP in rice, a lysine motif (LysM) receptor-like protein (RLP), to trigger immune responses. The molecular mechanisms underlying chitin recognition remain elusive. Here we report the crystal structures of the ectodomain of OsCEBiP (OsCEBiP-ECD) in free and chitin-bound forms. The structures reveal that OsCEBiP-ECD contains three tandem LysMs followed by a novel structure fold of cysteine-rich domain. The structures showed that chitin binding induces no striking conformational changes in OsCEBiP. Structural comparison among N-acetylglucosamine (NAG) oligomer-bound LysMs revealed a highly conserved recognition mechanism, which is expected to facilitate study of other LysM-containing proteins for their NAG binding. Modeling study showed that chitin induces OsCEBiP homodimerization in a "sliding mode". Our data provide insights into rice chitin receptor-mediated immunity triggered by fungal cell wall.
Identifying influential spreaders in complex networks is crucial in understanding, controlling and accelerating spreading processes for diseases, information, innovations, behaviors, and so on. Inspired by the gravity law, we propose a gravity model that utilizes both neighborhood information and path information to measure a node’s importance in spreading dynamics. In order to reduce the accumulated errors caused by interactions at distance and to lower the computational complexity, a local version of the gravity model is further proposed by introducing a truncation radius. Empirical analyses of the Susceptible-Infected-Recovered (SIR) spreading dynamics on fourteen real networks show that the gravity model and the local gravity model perform very competitively in comparison with well-known state-of-the-art methods. For the local gravity model, the empirical results suggest an approximately linear relation between the optimal truncation radius and the average distance of the network.
Strigolactones (SLs) are the latest confirmed phytohormones that regulate shoot branching by inhibiting bud outgrowth in higher plants. Perception of SLs depends on a novel mechanism employing an enzyme-receptor DWARF14 (D14) that hydrolyzes SLs and becomes covalently modified. This stimulates the interaction between D14 and D3, leading to the ubiquitination and degradation of the transcriptional repressor protein D53. However, the regulation of SL perception in rice remains elusive. In this study, we provide evidences that D14 is ubiquitinated after SL treatment and degraded through the 26S proteasome system. The Lys280 site of the D14 amino acid sequence was important for SL-induced D14 degradation, but did not change the subcellular localization of D14 nor disturbed the interaction between D14 and D3, nor D53 degradation. Biochemical and genetic analysis indicated that the key amino acids in the catalytic center of D14 were essential for D14 degradation. We further showed that D14 degradation is dependent on D3 and is tightly correlated with protein levels of D53. These findings revealed that D14 degradation takes place following D53 degradation and functions as an important feedback regulation mechanism of SL perception in rice.
Background:Thin endometrium is associated with poor reproductive outcomes; estrogen treatment can increase endometrial thickness (EMT). The aim of this retrospective cohort study was to investigate the factors influencing the effectiveness of estrogen treatment and reproductive outcomes after the treatment in patients with thin endometrium.Methods:Relevant clinical data of 101 patients with thin endometrium who had undergone estrogen treatment were collected. Possible factors influencing the effectiveness of treatment were analyzed retrospectively by logistic regression analysis. Eighty-seven infertile women without thin endometrium who had undergone assisted reproduction served as controls. The cases and controls were matched for age, assisted reproduction method, and number of embryos transferred. Reproductive outcomes of study and control groups were compared using Student's t-test and the Chi-square test.Results:At the end of estrogen treatment, EMT was ≥8 mm in 93/101 patients (92.1%). Effectiveness of treatment was significantly associated with maximal pretreatment EMT (P = 0.017) and treatment duration (P = 0.004). The outcomes of assisted reproduction were similar in patients whose treatment was successful in increasing EMT to ≥8 mm and the control group. The rate of clinical pregnancy in patients was associated with the number of good-quality embryos transferred in both fresh (P = 0.005) and frozen-thawed (P = 0.000) embryo transfer cycles.Conclusions:Thinner EMT before estrogen treatment requires longer treatment duration and predicts poorer treatment outcomes. The effectiveness of treatment depends on the duration of estrogen administration. Assisted reproductive outcomes of patients whose treatment is successful (i.e., achieves an EMT ≥8 mm) are similar to those of controls. The quality of embryos transferred is an important predictor of assisted reproductive outcomes in patients treated successfully with exogenous estrogen.
BackgroundOvarian cancer is the most lethal of gynecological malignancies. Fourier Transform Infrared (FTIR) spectroscopy has gradually developed as a convenient, inexpensive and non-destructive technique for the study of many diseases. In this study, FTIR spectra of normal and several heterogeneous ovarian cancer cell lines as well as ovarian cancer tissue samples were compared in the spectral region of 4000 cm− 1 - 600 cm− 1.MethodsCell samples were collected from human ovarian surface epithelial cell line (HOSEpiC) and five ovarian cancer cell lines (ES2, A2780, OVCAR3, SKOV3 and IGROV1). Validation spectra were performed on normal and cancerous tissue samples from 12 ovarian cancer patients. FTIR spectra were collected from a NICOLET iN10 MX spectrometer and the spectral data were analyzed by OMNIC 8.0 software.ResultsSpectral features discriminating malignant tissues from normal tissues were integrated by cell line data and tissue data. In particular changes in cancerous tissues, the decrease in the amount of lipids and nucleic acids were observed. Protein conformation and composition were also altered in some cancer cells. The band intensity ratio of 1454/1400 was higher in normal cells/tissues and lower in cancer cells/tissues.ConclusionThe spectral features revealed the important molecular characteristics about ovarian cancer cells/tissues. These findings demonstrate the possible diagnostic use of FTIR spectroscopy, providing the research model and evidences, and supporting the future study on more tissue samples to establish a data bank of spectra features for the possible discrimination of ovarian cancers.
The aim of the present study was to determine the influence of stress on the colonic mucosa and immune system and to further investigate the association between stress and development and pathogenesis of ulcerative colitis (UC). Mice were treated with 2,4,6-trinitrobenzenesulfonic acid to induce an animal model of UC, and stress was induced by water immersion and restraint. Subsequently, the disease activity index (DAI), secretory immunoglobulin A (sIgA), IgA, interleukin (IL)-6 and-8, tumor necrosis factor-α (TNF-α), complement component (C)3 and C4, and alterations in the colonic mucosa were observed. The DAI scores and the expression levels of IL-6, IL-8 and TNF-α significantly increased in the experimental UC mice compared with the control mice, while the expression levels of IgA and sIgA decreased (all P<0.01). DAI and colonic mucosa damage scores increased in the stress-treated mouse models of UC compared with the untreated mouse models of UC (P<0.05). Expression levels of IgA and sIgA decreased, while IL-6, IL-8 and TNF-α further increased in the stress-treated UC mice (P<0.05). The expression levels of C3 and C4 were not affected by stress or UC (P>0.05). These results indicated that UC may be associated with an immune disorder and that stress can aggravate colonic mucosa injury and alter the immune response. Furthermore, stress and immunity may serve roles in the pathogenesis of UC.
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