VLBI Technology Development at SHAO

VLBI technology development made significant progress at SHAO in the last few years. The development status of the Chinese DBBC, the software and FPGA-based correlators, and the new VLBI antenna, as well as VLBI applications are summarized in this paper

Analyses of the yeast Rad51 recombinase A265V mutant reveal different in vivo roles of Swi2-like factors

The Saccharomyces cerevisiae Swi2-like factors Rad54 and Rdh54 play multifaceted roles in homologous recombination via their DNA translocase activity. Aside from promoting Rad51-mediated DNA strand invasion of a partner chromatid, Rad54 and Rdh54 can remove Rad51 from duplex DNA for intracellular recycling. Although the in vitro properties of the two proteins are similar, differences between the phenotypes of the null allele mutants suggest that they play different roles in vivo. Through the isolation of a novel RAD51 allele encoding a protein with reduced affinity for DNA, we provide evidence that Rad54 and Rdh54 have different in vivo interactions with Rad51. The mutant Rad51 forms a complex on duplex DNA that is more susceptible to dissociation by Rdh54. This Rad51 variant distinguishes the in vivo functions of Rad54 and Rdh54, leading to the conclusion that two translocases remove Rad51 from different substrates in vivo. Additionally, we show that a third Swi2-like factor, Uls1, contributes toward Rad51 clearance from chromatin in the absence of Rad54 and Rdh54, and define a hierarchy of action of the Swi2-like translocases for chromosome damage repair

Cdk1 Targets Srs2 to Complete Synthesis-Dependent Strand Annealing and to Promote Recombinational Repair

Cdk1 kinase phosphorylates budding yeast Srs2, a member of UvrD protein family, displays both DNA translocation and DNA unwinding activities in vitro. Srs2 prevents homologous recombination by dismantling Rad51 filaments and is also required for double-strand break (DSB) repair. Here we examine the biological significance of Cdk1-dependent phosphorylation of Srs2, using mutants that constitutively express the phosphorylated or unphosphorylated protein isoforms. We found that Cdk1 targets Srs2 to repair DSB and, in particular, to complete synthesis-dependent strand annealing, likely controlling the disassembly of a D-loop intermediate. Cdk1-dependent phosphorylation controls turnover of Srs2 at the invading strand; and, in absence of this modification, the turnover of Rad51 is not affected. Further analysis of the recombination phenotypes of the srs2 phospho-mutants showed that Srs2 phosphorylation is not required for the removal of toxic Rad51 nucleofilaments, although it is essential for cell survival, when DNA breaks are channeled into homologous recombinational repair. Cdk1-targeted Srs2 displays a PCNA–independent role and appears to have an attenuated ability to inhibit recombination. Finally, the recombination defects of unphosphorylatable Srs2 are primarily due to unscheduled accumulation of the Srs2 protein in a sumoylated form. Thus, the Srs2 anti-recombination function in removing toxic Rad51 filaments is genetically separable from its role in promoting recombinational repair, which depends exclusively on Cdk1-dependent phosphorylation. We suggest that Cdk1 kinase counteracts unscheduled sumoylation of Srs2 and targets Srs2 to dismantle specific DNA structures, such as the D-loops, in a helicase-dependent manner during homologous recombinational repair

Photoluminescence excitation spectroscopy of InGaN epilayers

Abstract Background The fungal pathogen Candida albicans is frequently seen in immune suppressed patients, and resistance to one of the most widely used antifungals, fluconazole (FLC), can evolve rapidly. In recent years it has become clear that plasticity of the Candida albicans genome contributes to drug resistance through loss of heterozygosity (LOH) at resistance genes and gross chromosomal rearrangements that amplify gene copy number of resistance associated genes. This study addresses the role of the homologous recombination factors Rad54 and Rdh54 in cell growth, DNA damage and FLC resistance in Candida albicans. Results The data presented here support a role for homologous recombination in cell growth and DNA damage sensitivity, as Candida albicans rad54Δ/rad54Δ mutants were hypersensitive to MMS and menadione, and had an aberrant cell and nuclear morphology. The Candida albicans rad54Δ/rad54Δ mutant was defective in invasion of Spider agar, presumably due to the altered cellular morphology. In contrast, mutation of the related gene RDH54 did not contribute significantly to DNA damage resistance and cell growth, and deletion of either Candida albicans RAD54 or Candida albicans RDH54 did not alter FLC susceptibility. Conclusions Together, these results support a role for homologous recombination in genome stability under nondamaging conditions. The nuclear morphology defects in the rad54Δ/rad54Δ mutants show that Rad54 performs an essential role during mitotic growth and that in its absence, cells arrest in G2. The viability of the single mutant rad54Δ/rad54Δ and the inability to construct the double mutant rad54Δ/rad54Δ rdh54Δ/rdh54Δ suggests that Rdh54 can partially compensate for Rad54 during mitotic growth.Peer Reviewe

Improvement of Winter Wheat Aboveground Biomass Estimation Using Digital Surface Model Information Extracted from Unmanned-Aerial-Vehicle-Based Multispectral Images

Aboveground biomass (AGB) is an important indicator for characterizing crop growth conditions. A rapid and accurate estimation of AGB is critical for guiding the management of farmland and achieving production potential, and it can also provide vital data for ensuring food security. In this study, by applying different water and nitrogen treatments, an unmanned aerial vehicle (UAV) equipped with a multispectral imaging spectrometer was used to acquire images of winter wheat during critical growth stages. Then, the plant height (Hdsm) extracted from the digital surface model (DSM) information was used to establish and improve the estimation model of AGB, using the backpropagation (BP) neural network, a machine learning method. The results show that (1) the R2, root-mean-square error (RMSE), and relative predictive deviation (RPD) of the AGB estimation model, constructed directly using the Hdsm, are 0.58, 4528.23 kg/hm2, and 1.25, respectively. The estimated mean AGB (16,198.27 kg/hm2) is slightly smaller than the measured mean AGB (16,960.23 kg/hm2). (2) The R2, RMSE, and RPD of the improved AGB estimation model, based on AGB/Hdsm, are 0.88, 2291.90 kg/hm2, and 2.75, respectively, and the estimated mean AGB (17,478.21 kg/hm2) is more similar to the measured mean AGB (17,222.59 kg/hm2). The improved AGB estimation model boosts the accuracy by 51.72% compared with the AGB directly estimated using the Hdsm. Moreover, the improved AGB estimation model shows strong transferability in regard to different water treatments and different year scenarios, but there are differences in the transferability for different N-level scenarios. (3) Differences in the characteristics of the data are the key factors that lead to the different transferability of the AGB estimation model. This study provides an antecedent in regard to model construction and transferability estimation of AGB for winter wheat. We confirm that, when different datasets have similar histogram characteristics, the model is applicable to new scenarios

Identification of novel immune and barrier genes in atopic dermatitis by means of laser capture microdissection

BACKGROUND: The molecular signature of atopic dermatitis/AD lesions is associated with Th2 and Th22 activation, and epidermal alterations. However, the epidermal and dermal AD transcriptomes and their respective contributions to abnormalities in respective immune and barrier phenotypes are unknown. OBJECTIVE: To establish the genomic profile of the epidermal and dermal compartments of lesional/LS and non-lesional/NL AD, as compared with normal skin. METHODS: Laser capture micro-dissection/LCM was performed to separate epidermis and dermis of LS and NL skin from AD patients and normal skin from healthy volunteers followed by gene expression (microarrays and RT-PCR) and immunostaining studies. RESULTS: Our study identified novel immune and barrier genes, including the IL-34 cytokine and claudins 4 and 8, and showed increased detection of key AD genes usually undetectable on arrays (i.e. IL-22, TSLP, CCL22, and CCL26). Overall, the combined epidermal and dermal transcriptomes enlarged the AD transcriptome adding 674 up-regulated and 405 down-regulated differentially expressed genes between LS and NL skin to the AD transcriptome. We were also able to localize individual transcripts as primarily epidermal (DEFB4A) or dermal (IL-22, CTLA4, and CCR7), and link their expressions to possible cellular sources. CONCLUSIONS: This is the first report that establishes robust epidermal and dermal genomic signatures of LS, NL AD and normal/N skin, as compared with whole tissues. These data establish the utility of LCM to separate different compartments and cellular subsets in AD, allowing localization of key barrier or immune molecules, and enable detection of gene products usually not detected on arrays