A CRY-BIC negative-feedback circuitry regulating blue light sensitivity of Arabidopsis.

Cryptochromes are blue light receptors that regulate various light responses in plants. Arabidopsis cryptochrome 1 (CRY1) and cryptochrome 2 (CRY2) mediate blue light inhibition of hypocotyl elongation and long-day (LD) promotion of floral initiation. It has been reported recently that two negative regulators of Arabidopsis cryptochromes, Blue light Inhibitors of Cryptochromes 1 and 2 (BIC1 and BIC2), inhibit cryptochrome function by blocking blue light-dependent cryptochrome dimerization. However, it remained unclear how cryptochromes regulate the BIC gene activity. Here we show that cryptochromes mediate light activation of transcription of the BIC genes, by suppressing the activity of CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), resulting in activation of the transcription activator ELONGATED HYPOCOTYL 5 (HY5) that is associated with chromatins of the BIC promoters. These results demonstrate a CRY-BIC negative-feedback circuitry that regulates the activity of each other. Surprisingly, phytochromes also mediate light activation of BIC transcription, suggesting a novel photoreceptor co-action mechanism to sustain blue light sensitivity of plants under the broad spectra of solar radiation in nature

Effects of Temperature on Development and Voltinism of Chaetodactylus krombeini (Acari: Chaetodactylidae): Implications for Climate Change Impacts

Temperature plays an important role in the growth and development of arthropods, and thus the current trend of climate change will alter their biology and species distribution. We used Chaetodactylus krombeini (Acari: Chaetodactylidae), a cleptoparasitic mite associated with Osmia bees (Hymenoptera: Megachilidae), as a model organism to investigate how temperature affects the development and voltinism of C. krombeini in the eastern United States. The effects of temperature on the stage-specific development of C. krombeini were determined at seven constant temperatures (16.1, 20.2, 24.1, 27.5, 30.0, 32.4 and 37.8°C). Parameters for stage-specific development, such as threshold temperatures and thermal constant, were determined by using empirical models. Results of this study showed that C. krombeini eggs developed successfully to adult at all temperatures tested except 37.8°C. The nonlinear and linear empirical models were applied to describe quantitatively the relationship between temperature and development of each C. krombeini stage. The nonlinear Lactin model estimated optimal temperatures as 31.4, 32.9, 32.6 and 32.5°C for egg, larva, nymph, and egg to adult, respectively. In the linear model, the lower threshold temperatures were estimated to be 9.9, 14.7, 13.0 and 12.4°C for egg, larva, nymph, and egg to adult, respectively. The thermal constant for each stage completion were 61.5, 28.1, 64.8 and 171.1 degree days for egg, larva, nymph, and egg to adult, respectively. Under the future climate scenarios, the number of generations (i.e., voltinism) would increase more likely by 1.5 to 2.0 times by the year of 2100 according to simulation. The findings herein firstly provided comprehensive data on thermal development of C. krombeini and implications for the management of C. krombeini populations under global warming were discussed

Loss of androgen signaling in mesenchymal sonic hedgehog responsive cells diminishes prostate development, growth, and regeneration.

Prostate embryonic development, pubertal and adult growth, maintenance, and regeneration are regulated through androgen signaling-mediated mesenchymal-epithelial interactions. Specifically, the essential role of mesenchymal androgen signaling in the development of prostate epithelium has been observed for over 30 years. However, the identity of the mesenchymal cells responsible for this paracrine regulation and related mechanisms are still unknown. Here, we provide the first demonstration of an indispensable role of the androgen receptor (AR) in sonic hedgehog (SHH) responsive Gli1-expressing cells, in regulating prostate development, growth, and regeneration. Selective deletion of AR expression in Gli1-expressing cells during embryogenesis disrupts prostatic budding and impairs prostate development and formation. Tissue recombination assays showed that urogenital mesenchyme (UGM) containing AR-deficient mesenchymal Gli1-expressing cells combined with wildtype urogenital epithelium (UGE) failed to develop normal prostate tissue in the presence of androgens, revealing the decisive role of AR in mesenchymal SHH responsive cells in prostate development. Prepubescent deletion of AR expression in Gli1-expressing cells resulted in severe impairment of androgen-induced prostate growth and regeneration. RNA-sequencing analysis showed significant alterations in signaling pathways related to prostate development, stem cells, and organ morphogenesis in AR-deficient Gli1-expressing cells. Among these altered pathways, the transforming growth factor β1 (TGFβ1) pathway was up-regulated in AR-deficient Gli1-expressing cells. We further demonstrated the activation of TGFβ1 signaling in AR-deleted prostatic Gli1-expressing cells, which inhibits prostate epithelium growth through paracrine regulation. These data demonstrate a novel role of the AR in the Gli1-expressing cellular niche for regulating prostatic cell fate, morphogenesis, and renewal, and elucidate the mechanism by which mesenchymal androgen-signaling through SHH-responsive cells elicits the growth and regeneration of prostate epithelium

Genome-Scale Promoter Engineering by Coselection MAGE

Multiplex Automated Genome Engineering (MAGE) employs short oligonucleotides to scarlessly modify genomes. However, insertions of >10 bases are still inefficient, but can be improved substantially by selection of highly modified chromosomes. Here, we describe Co-Selection MAGE (CoS-MAGE) to optimize biosynthesis of aromatic amino acid derivatives by combinatorially inserting multiple T7 promoters simultaneously into 12 genomic operons. Promoter libraries can be quickly generated to study gain-of-function epistatic interactions in gene networks

DNS study of a pipe flow following a step increase in flow rate

Direct numerical simulation (DNS) is conducted to study the transient flow in a pipe following a near-step increase of flow rate from an initial turbulent flow. The results are compared with those of the transient flow in a channel reported in He and Seddighi (2013). It is shown that the flow again exhibits a laminar–turbulent transition, similar to that in a channel. The behaviours of the flow in a pipe and a channel are the same in the near-wall region, but there are significant differences in the centre of the flow. The correlation between the critical Reynolds number and free stream turbulence previously established for a channel flow has been shown to be applicable to the pipe flow. The responses of turbulent viscosity, vorticity Reynolds number, and budget terms are analysed. Some significant differences have been found to exist between the developments of the vorticity Reynolds number in the pipe and channel flows

Loss of the tumor suppressor, Tp53, enhances the androgen receptor-mediated oncogenic transformation and tumor development in the mouse prostate.

Recent genome analysis of human prostate cancers demonstrated that both AR gene amplification and TP53 mutation are among the most frequently observed alterations in advanced prostate cancer. However, the biological role of these dual genetic alterations in prostate tumorigenesis is largely unknown. In addition, there are no biologically relevant models that can be used to assess the molecular mechanisms for these genetic abnormalities. Here, we report a novel mouse model, in which elevated transgenic AR expression and Trp53 deletion occur simultaneously in mouse prostatic epithelium to mimic human prostate cancer cells. These compound mice developed an earlier onset of high-grade prostatic intraepithelial neoplasia and accelerated prostate tumors in comparison with mice harboring only the AR transgene. Histological analysis showed prostatic sarcomatoid and basaloid carcinomas with massive squamous differentiation in the above compound mice. RNA-sequencing analyses identified a robust enrichment of the signature genes for human prostatic basal cell carcinomas in the above prostate tumors. Master regulator analysis revealed SOX2 as a transcriptional regulator in prostatic basal cell tumors. Elevated expression of SOX2 and its downstream target genes were detected in prostatic tumors of the compound mice. Chromatin immunoprecipitation analyses implicate a coregulatory role of AR and SOX2 in the expression of prostatic basal cell signature genes. Our data demonstrate a critical role of SOX2 in prostate tumorigenesis and provide mechanistic insight into prostate tumor aggressiveness and progression mediated by aberrant AR and p53 signaling pathways