Characterization of the complete mitochondrial genome of the Reeves’ muntjac Muntiacus reevesi (Artiodactyla, Ruminantia, Cervidae) and its phylogeny

We present the complete mitogenome of Muntiacus reevesi. We found that the mitogenome of this circle is 16,535 bp in size and includs 13 protein-coding genes, 22 transfer RNA genes, two ribosomal RNA genes, and one noncoding control region (D-loop) that are conserved in most Cervidae mitogenomes. The total base composition of the Muntiacus reevesi mitogenome is 33.18% A, 28.99 % T, 24.43% C, and 13.40% G, which is typical for mammalian mitogenomes. Phylogenetic analyses. Phylogenetic analyses showed that M. reevesi clustered with M. vuquangensis and M. putaoensis as a branch and that they are closely genetically related

QseBC is involved in the biofilm formation and antibiotic resistance in Escherichia coli isolated from bovine mastitis

Background Mastitis is one of the most common infectious diseases in dairy cattle and causes significant financial losses in the dairy industry worldwide. Antibiotic therapy has been used as the most effective strategy for clinical mastitis treatment. However, due to the extensive use of antibacterial agents, antimicrobial resistance (AMR) is considered to be one of the reasons for low cure rates in bovine mastitis. In addition, biofilms could protect bacteria by restricting antibiotic access and shielding the bacterial pathogen from mammary gland immune defences. The functional mechanisms of quorum sensing E. coli regulators B an d C (QseBC) have been well studied in E. coli model strains; however, whether QseBC regulates antibiotic susceptibility and biofilm formation in clinical E. coli strain has not been reported. Methods In this study, we performed construction of the qseBC gene mutant, complementation of the qseBC mutant, antimicrobial susceptibility testing, antibacterial activity assays, biofilm formation assays, real-time reverse transcription PCR (RT-PCR) experiments and electrophoretic mobility shift assays (EMSAs) to investigate the role of qseBC in regulating biofilm formation and antibiotic susceptibility in the clinical E. coli strain ECDCM2. Results We reported that inactivation of QseBC led to a decrease in biofilm formation capacity and an increase in antibiotic susceptibility of an E. coli strain isolated from a dairy cow that suffered from mastitis. In addition, this study indicated that QseBC increased biofilm formation by upregulating the transcription of the biofilm-associated genes bcsA, csgA, fliC, motA, wcaF and fimA and decreased antibiotic susceptibility by upregulating the transcription of the efflux-pump-associated genes marA, acrA, acrB, acrD, emrD and mdtH. We also performed EMSA assays, and the results showed that QseB can directly bind to the marA promoter. Conclusions The QseBC two-component system affects antibiotic sensitivity by regulating the transcription of efflux-pump-associated genes. Further, biofilm-formation-associated genes were also regulated by QseBC TCS in E. coli ECDCM2. Hence, this study might provide new clues to the prevention and treatment of infections caused by the clinical E. coli strains

TRPS1 Suppresses Breast Cancer Epithelial-mesenchymal Transition Program as a Negative Regulator of SUZ12

Breast cancer (BC) is among the most common malignant diseases and metastasis is the handcuff of treatment. Cancer metastasis is a multistep process associated with the epithelial-mesenchymal transition (EMT) program. Several studies have demonstrated that transcriptional repressor GATA binding 1 (TRPS1) played important roles in development and progression of primary BC. In this study we sought to identify the mechanisms responsible for this function of TRPS1 in the continuum of the metastatic cascade. Here we described that TRPS1 was significantly associated with BC metastasis using public assessable datasets. Clinically, loss of TRPS1 expression in BC was related to higher histological grade. In vitro functional study and bioinformatics analysis revealed that TRPS1 inhibited cell migration and EMT in BC. Importantly, we identified SUZ12 as a novel target of TRPS1 related to EMT program. ChIP assay demonstrated TRPS1 directly inhibited SUZ12 transcription by binding to the SUZ12 promoter. Loss of TRPS1 resulted in increased SUZ12 binding and H3K27 tri-methylation at the CDH1 promoter and repression of E-cadherin. In all, our data indicated that TRPS1 maintained the expression of E-cadherin by inhibiting SUZ12, which might provide novel insight into how loss of TRPS1 contributed to BC progression

Great Disparity in Photoluminesence Quantum Yields of Colloidal CsPbBr₃ Nanocrystals with Varied Shape: The Effect of Crystal Lattice Strain

Understanding the big discrepancy in the photoluminesence quantum yields (PLQYs) of nanoscale colloidal materials with varied morphologies is of great significance to its property optimization and functional application. Using different shaped CsPbBr₃ nanocrystals with the same fabrication processes as model, quantitative synchrotron radiation X-ray diffraction analysis reveals the increasing trend in lattice strain values of the nanocrystals: nanocube, nanoplate, nanowire. Furthermore, transient spectroscopic measurements reveal the same trend in the defect quantities of these nanocrystals. These experimental results unambiguously point out that large lattice strain existing in CsPbBr₃ nanoparticles induces more crystal defects and thus decreases the PLQY, implying that lattice strain is a key factor other than the surface defect to dominate the PLQY of colloidal photoluminesence materials