Biology subjects

Ouyang, Y.

Publications and source records attributed to Ouyang, Y..

40 records · Page 3Linked to original sources

bioRxiv2020

Negative effects characterization and comparative transcriptomics elucidation on the lag phase of an industrial S. cerevisiae under the corn stover hydrolysate stress

During biofuels fermentation from pretreated lignocellulosic biomass, the strong toxicity of the lignocellulose hydrolysate is resulted from the synergistic effect of multiple lignocellulosic inhibitors, which far exceeds the sum of effects caused by every single inhibitor. Meanwhile, the synergistic effect is unclear and the underlying response mechanism of the industrial yeast towards the actual pretreated lignocellulose hydrolysate is still under exploration. Here, we employed an industrial S. cerevisiae for the transcriptomic analysis in two time points (early and late) of the lag phase under the corn stover hydrolysate stress. As investigation, the corn stover hydrolysate caused the accumulation of reactive oxygen species (ROS), damages of mitochondrial membrane and endoplasmic reticulum (ER) membrane in the industrial S. cerevisiae YBA_08 during the lag phase, especially these negative effects were more significant at the early lag phase. Based on the transcriptome profile, the industrial S. cerevisiae YBA_08 might recruit stress-related transcription factors (MSN4, STE12, SFL1, CIN5, COM2, MIG3, etc.) through the mitogen-activated protein kinase (MAPK)-signaling pathway to induce a transient G1/G2 arrest, and to activate defense bioprocesses like protectants metabolism, sulfur metabolism, glutaredoxin system, thioredoxin system, heat shock proteins chaperone and oxidoreductase detoxification, resisting those compounded stresses including oxidative stress, osmotic stress and structural stress. Surprisingly, this defense system might be accompanied with the transient repression of several bioprocesses like fatty acid metabolism, purine de novo biosynthesis and ergosterol biosynthesis. ImportanceThis research systematically demonstrated the lag phase response of an industrial yeast to the lignocellulosic hydrolysate in transcriptional level, providing a molecular fundament for understanding the synergistic effect of various lignocellulosic inhibitors and the regulatory mechanism of tolerance for industrial yeasts under this stress.

microbiology↗

bioRxiv2019

H. pylori infection inhibits autophagy to aggravate DNA damage by p62-mediated Rad51 ubiquitination

Helicobacter pylori (H. pylori) infection is the strongest known risk factor for gastric carcinogenesis. DNA damage response (DDR) and autophagy play key roles in tumorigenic transformation. However, it remains unclear how H. pylori infection modulate DNA damage and autophagy. Here we report that H. pylori infection promotes DNA damage via suppression of Rad51 expression through inhibition of autophagy and accumulation of p62 in gastric carcinogenesis. We find that H. pylori infection caused alteration of DDR pathway and autophagy in gastric cells and Mongolian gerbils in a CagA-dependent manner. Moreover, loss of autophagy led to promotion of DNA damage in H. pylori-infected cells. Furthermore, knockdown of autophagic substrate p62 upregulated Rad51 expression, and p62 promoted ubiquitination of Rad51 via the direct interaction of the UBA domain with Rad51. Finally, H. pylori infection was associated with elevated levels of p62 in gastric intestinal metaplasia and decreased levels of Rad51 in dysplasia compared to their H. pylori- counterparts. Our findings provide a novel mechanism into the linkage of H. pylori infection, autophagy, DNA damage and gastric tumorigenesis.

microbiology↗

bioRxiv2019

XPRESSyourself: Enhancing and Automating the Ribosome Profiling and RNA-Seq Analysis Toolkit

Ribosome profiling, an application of nucleic acid sequencing for monitoring ribosome activity, has revolutionized our understanding of protein translation dynamics. This technique has been available for a decade, yet the current state and standardization of publicly available computational tools for these data is bleak. We introduce XPRESSyourself, an analytical toolkit that eliminates barriers and bottlenecks associated with this specialized data type by filling gaps in the computational toolset for both experts and non-experts of ribosome profiling. XPRESSyourself automates and standardizes analysis procedures, decreasing time-to-discovery and increasing reproducibility. This toolkit acts as a reference implementation of current best practices in ribosome profiling analysis. We demonstrate this toolkits performance on publicly available ribosome profiling data by rapidly identifying hypothetical mechanisms related to neurodegenerative phenotypes and neuroprotective mechanisms of the small-molecule ISRIB during acute cellular stress. XPRESSyourself brings robust, rapid analysis of ribosome-profiling data to a broad and ever-expanding audience and will lead to more reproducible and accessible measurements of translation regulation. XPRESSyourself software is perpetually open-source under the GPL-3.0 license and is hosted at https://github.com/XPRESSyourself, where users can access additional documentation and report software issues.

bioinformatics↗

bioRxiv2019

CDC6 regulates both G2/M transition and metaphase-to-anaphase transition during the first meiosis of mouse oocytes

Cell division cycle protein CDC6 is essential for the initiation of DNA replication. CDC6 was recently shown to inhibit the microtubule-organizing activity of the centrosome. Here, we show that CDC6 is localized to the spindle from Pro-MI to MII stages of oocytes, and it plays important roles at two critical steps of oocyte meiotic maturation. CDC6 depletion facilitated the G2/M transition (GV breakdown, GVBD) through regulation of Cdh1 and cyclin B1 expression and CDK1 phosphorylation in a GVBD-inhibiting culture system containing milrinone. Furthermore, GVBD was significantly decreased after knockdown of cyclin B1 in CDC6-depleted oocytes, indicating that the effect of CDC6 loss on GVBD stimulation was mediated, at least in part, by raising cyclin B1. Knockdown of CDC6 also caused abnormal localization of {gamma}-tubulin, resulting in defective spindles, misaligned chromosomes, cyclin B1 accumulation and spindle assembly checkpoint (SAC) activation, leading to significant Pro-MI/MI arrest and PB1 extrusion failure. These phenotypes were also confirmed by time-lapse live cell imaging analysis. The results indicate that CDC6 is indispensable for maintaining G2 arrest of meiosis and functions in G2/M checkpoint regulation in mouse oocytes. Moreover, CDC6 is also a key player regulating meiotic spindle assembly and metaphase-to-anaphase transition in meiotic oocytes.\n\nSummary statementWe show that CDC6 is indispensable for maintaining G2 arrest of mouse oocytes. Moreover, CDC6 is also a key player regulating meiotic spindle assembly and metaphase-to-anaphase transition in meiotic oocytes.

developmental biology↗