Genome-wide association analysis identifies resistance loci for bacterial blight in a diverse collection of indica rice germplasm

Bacterial blight, which is caused by Xanthomonas oryzae pv. oryzae (Xoo), is one of the most devastating rice diseases worldwide. The development and use of disease-resistant cultivars have been the most effective strategy to control bacterial blight. Identifying the genes mediating bacterial blight resistance is a prerequisite for breeding cultivars with broad-spectrum and durable resistance. We herein describe a genome-wide association study involving 172 diverse Oryza sativa ssp. indica accessions to identify loci influencing the resistance to representative strains of six Xoo races. Twelve resistance loci containing 121 significantly associated signals were identified using 317,894 single nucleotide polymorphisms, which explained 13.3–59.9% of the variability in lesion length caused by Xoo races P1, P6, and P9a. Two hotspot regions (L11 and L12) were located within or nearby two cloned R genes (xa25 and Xa26) and one fine-mapped R gene (Xa4). Our results confirmed the relatively high resolution of genome-wide association studies. Moreover, we detected novel significant associations on chromosomes 2, 3, and 6–10. Haplotype analyses of xa25, the Xa26 paralog (MRKc; LOC_Os11g47290), and a Xa4 candidate gene (LOC_11g46870) revealed differences in bacterial blight resistance among indica subgroups. These differences were responsible for the observed variations in lesion lengths resulting from infections by Xoo races P1 and P9a. Our findings may be relevant for future studies involving bacterial blight resistance gene cloning, and provide insights into the genetic basis for bacterial blight resistance in indica rice, which may be useful for knowledge-based crop improvement. (Résumé d'auteur

Toward a direct measurement of the cosmic acceleration: The first observation of HI 21cm absorption line at FAST

In this work, we report the first result from the investgation of Neutral atomic hydrogen(HI) 21cm absorption line in spectrum of PKS1413+135 as a associated type at redshift $z\approx 0.24670041$ observed by FAST using the observing time of 10 minutes for the absorber and the spectral resolution of the raw data was setted to 10 Hz. The full spectral profile is analysed by fitting the absorption line with single Gaussian function as the resolution of 10kHz in 2MHz bandwidth, eventually intending to illustrate the latest cosmic acceleration by the direct measurement of time evolution of the redshift of HI 21cm absorption line with Hubble flow toward a same background Quasar in the time interval of more than a decade or many years as a detectable signal that produced by the accelerated expansion of the Universe in the era of FAST at low redshift space,namely redshift drift $\dot{z}$ or SL effect. The obtained HI gas column density $\rm N_{HI} \approx 2.2867\times 10^{22}/cm^2$ of this DLA system, much equivalent to the originally observed value $\rm N_{HI} \approx 1.3\times 10^{19}\times(T_s/f)/cm^2$ within the uncertainties of the spin temperature of a spiral host galaxy, and the signal to noise ratio SNR highly reaching 57.4357 for the resolution of 10kHz evidently validates the opportunities of the HI 21cm absorption lines of DLA systems to enforce the awareness of the physical motivation of dark energy by the probe of $\rm\dot{z}$ with the enhancement of accuracy in the level of $\sim 10^{-10}$ per decade.Comment: 26 pages,8 figures, 3 tables, submitted to JCA

MicroRNA-221 and microRNA-222 regulate gastric carcinoma cell proliferation and radioresistance by targeting PTEN

<p>Abstract</p> <p>Background</p> <p>MicroRNAs (miRNAs) can function as either oncogenes or tumor suppressor genes via regulation of cell proliferation and/or apoptosis. MiR-221 and miR-222 were discovered to induce cell growth and cell cycle progression via direct targeting of p27 and p57 in various human malignancies. However, the roles of miR-221 and miR-222 have not been reported in human gastric cancer. In this study, we examined the impact of miR-221 and miR-222 on human gastric cancer cells, and identified target genes for miR-221 and miR-222 that might mediate their biology.</p> <p>Methods</p> <p>The human gastric cancer cell line SGC7901 was transfected with AS-miR-221/222 or transduced with pMSCV-miR-221/222 to knockdown or restore expression of miR-221 and miR-222, respectively. The effects of miR-221 and miR-222 were then assessed by cell viability, cell cycle analysis, apoptosis, transwell, and clonogenic assay. Potential target genes were identified by Western blot and luciferase reporter assay.</p> <p>Results</p> <p>Upregulation of miR-221 and miR-222 induced the malignant phenotype of SGC7901 cells, whereas knockdown of miR-221 and miR-222 reversed this phenotype via induction of PTEN expression. In addition, knockdonwn of miR-221 and miR-222 inhibited cell growth and invasion and increased the radiosensitivity of SGC7901 cells. Notably, the seed sequence of miR-221 and miR-222 matched the 3'UTR of PTEN, and introducing a PTEN cDNA without the 3'UTR into SGC7901 cells abrogated the miR-221 and miR-222-induced malignant phenotype. PTEN-3'UTR luciferase reporter assay confirmed PTEN as a direct target of miR-221 and miR-222.</p> <p>Conclusion</p> <p>These results demonstrate that miR-221 and miR-222 regulate radiosensitivity, and cell growth and invasion of SGC7901 cells, possibly via direct modulation of PTEN expression. Our study suggests that inhibition of miR-221 and miR-222 might form a novel therapeutic strategy for human gastric cancer.</p

One-to-Multiple Clean-Label Image Camouflage (OmClic) based Backdoor Attack on Deep Learning

Image camouflage has been utilized to create clean-label poisoned images for implanting backdoor into a DL model. But there exists a crucial limitation that one attack/poisoned image can only fit a single input size of the DL model, which greatly increases its attack budget when attacking multiple commonly adopted input sizes of DL models. This work proposes to constructively craft an attack image through camouflaging but can fit multiple DL models' input sizes simultaneously, namely OmClic. Thus, through OmClic, we are able to always implant a backdoor regardless of which common input size is chosen by the user to train the DL model given the same attack budget (i.e., a fraction of the poisoning rate). With our camouflaging algorithm formulated as a multi-objective optimization, M=5 input sizes can be concurrently targeted with one attack image, which artifact is retained to be almost visually imperceptible at the same time. Extensive evaluations validate the proposed OmClic can reliably succeed in various settings using diverse types of images. Further experiments on OmClic based backdoor insertion to DL models show that high backdoor performances (i.e., attack success rate and clean data accuracy) are achievable no matter which common input size is randomly chosen by the user to train the model. So that the OmClic based backdoor attack budget is reduced by M$\times$ compared to the state-of-the-art camouflage based backdoor attack as a baseline. Significantly, the same set of OmClic based poisonous attack images is transferable to different model architectures for backdoor implant

X-ray Emission of Baryonic Gas in the Universe: Luminosity-Temperature Relationship and Soft-Band Background

We study the X-ray emission of baryon fluid in the universe using the WIGEON cosmological hydrodynamic simulations. It has been revealed that cosmic baryon fluid in the nonlinear regime behaves like Burgers turbulence, i.e. the fluid field consists of shocks. Like turbulence in incompressible fluid, the Burgers turbulence plays an important role in converting the kinetic energy of the fluid to thermal energy and heats the gas. We show that the simulation sample of the $\Lambda$CDM model without adding extra heating sources can fit well the observed distributions of X-ray luminosity versus temperature ($L_{\rm x}$ vs. $T$) of galaxy groups and is also consistent with the distributions of X-ray luminosity versus velocity dispersion ($L_{\rm x}$ vs. $\sigma$). Because the baryonic gas is multiphase, the $L_{\rm x}-T$ and $L_{\rm x}-\sigma$ distributions are significantly scattered. If we describe the relationships by power laws $L_{\rm x}\propto T^{\alpha_{LT}}$ and $L_{\rm x}\propto \sigma^{\alpha_{LV}}$, we find $\alpha_{LT}>2.5$ and $\alpha_{LV}>2.1$. The X-ray background in the soft $0.5-2$ keV band emitted by the baryonic gas in the temperature range $10^5<T<10^7$ K has also been calculated. We show that of the total background, (1) no more than 2% comes from the region with temperature less than $10^{6.5}$ K, and (2) no more than 7% is from the region of dark matter with mass density $\rho_{\rm dm}<50 \bar{\rho}_{\rm dm}$. The region of $\rho_{\rm dm}>50\bar{\rho}_{\rm dm}$ is generally clustered and discretely distributed. Therefore, almost all of the soft X-ray background comes from clustered sources, and the contribution from truly diffuse gas is probably negligible. This point agrees with current X-ray observations.Comment: 32 pages including 14 figures and 2 tables. Final version for publication in Ap

Bis[3-(pyrazin-2-yl)-5-(pyridin-2-yl-κN)-1,2,4-triazol-1-ido-κN 1]copper(II)

In the mononuclear title complex, [Cu(C11H7N6)2], the CuII atom lies on a crystallographic inversion centre and is coordinated by four N atoms from two bidentate chelate monoanionic 3-(pyrazin-2-yl)-5-(pyridin-2-yl-1,2,4-triazol-1-ido ligands, two from the triazolide rings [Cu—N = 1.969 (2) Å] and two from the pyridine rings [Cu—N = 2.027 (2) Å], giving a slightly distorted square-planar geometry

MiR-221 and miR-222 target PUMA to induce cell survival in glioblastoma

<p>Abstract</p> <p>Background</p> <p>MiR-221 and miR-222 (miR-221/222) are frequently up-regulated in various types of human malignancy including glioblastoma. Recent studies have reported that miR-221/222 regulate cell growth and cell cycle progression by targeting p27 and p57. However the underlying mechanism involved in cell survival modulation of miR-221/222 remains elusive.</p> <p>Results</p> <p>Here we showed that miR-221/222 inhibited cell apoptosis by targeting pro-apoptotic gene PUMA in human glioma cells. Enforced expression of miR-22/222 induced cell survival whereas knockdown of miR-221/222 rendered cells to apoptosis. Further, miR-221/222 reduced PUMA protein levels by targeting PUMA-3'UTR. Introducing PUMA cDNA without 3'UTR abrogated miR-221/222-induced cell survival. Notably, knockdown of miR-221/222 induces PUMA expression and cell apoptosis and considerably decreases tumor growth in xenograft model. Finally, there was an inverse relationship between PUMA and miR-221/222 expression in glioma tissues.</p> <p>Conclusion</p> <p>To our knowledge, these data indicate for the first time that miR-221/222 directly regulate apoptosis by targeting PUMA in glioblastoma and that miR-221/222 could be potential therapeutic targets for glioblastoma intervention.</p