Search bioRxivSearch

bioRxiv · 10.1101/2020.01.07.898106

Development of the yeast Saccharomyces cerevisiae as a biosensor for the toxicity detection of toxic substances

Abstract

A whole-cell biosensor developed with yeast Saccharomyces cerevisia to detect the toxicity of chlorothalonil has been developed. This biosensor relied on the inhibition effect for metabolism by toxicants to provide detection and the degree of toxicity to yeast cells. In order to further improve the toxic sensitivity of yeast cells biosensor, the effect of the action time, the initial pH value of the medium and the temperature on inhibiting cell growth were investigated. Response surface regression analysis was conducted to obtain optimal culture conditions. Th effects of treated yeast morphology, ROS, DNA, caspase 3 activity were analyzed. This optimized yeast as a biosensor was used to detect chlorothalonil and heavy metals. The results are as follows: at optimal culture conditions, EC50 values of chlorothalonil to yeast biosensor determined at incubation time 4 h increased from 0.25 {micro}g{middle dot}mL-1 in the control to 0.006 {micro}g{middle dot}mL-1, which increased by 41.67 times. Compared with the control yeast cells, the morphology of optimized yeast cells were more transparent, with significantly increased intracellular vesicle rate and cell membrane permeability, intracelluar ROS increased siginificantly, DNA bands extracted was ladder, and caspase 3 activity was stimulated. The yeast biosensor had a high sensitivity to heavy metals. After analysis, many treated cells were apoptosis which was the main reason for the increasing sensitivity to detect harmful substances. It was found that the method provides a new idea for the detection of harmful substances in the environment. Yeast cells biosensor could be used to detect harmful substances in the environment, sunch as chlorothalonil, heavy metals. Even through chemical analysis methods, such as ICP-MS and High Performance Liquid Choromatography (HPLC), have strengths in accuracy and limit of detection, it is impossible to evaluate the cytotoxicity and the biological effect of waste water by chemical result alone, and it is also expensive, prolix and complicated. However, the yeast cell biosensor is easy to operate, is sensitive to various toxicants, comparable to the other totxicity detection methods, is cheap in cost, and has. Therefore, the method which used yeast cells as biosensor will have great potential in the detection of the cytotoxicity of waste water in the future.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

GONG, L., Yang, G., Yang, B., Gu, J.. 2020-01-09. Development of the yeast Saccharomyces cerevisiae as a biosensor for the toxicity detection of toxic substances. https://doi.org/10.1101/2020.01.07.898106

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Functional characterization of Rho GTPase activating proteins SYDE1 and SYDE2

The human genome encodes more than 60 proteins containing Rho GTPase activating protein (RhoGAP) domains, many of which remain understudied with respect to their target specificity and biological roles. SYDE1 and SYDE2 are two such orphan RhoGAPs, for which there are few studies characterizing their biochemical and cellular functions and conflicting reports identifying their cognate GTPases. We previously identified SYDE1 and SYDE2 in a screen for substrates of the c-Jun N-terminal kinases. Here, we show that SYDE1 and SYDE2 are preferentially phosphorylated by JNK1 relative to other mitogen-activated protein kinases (MAPKs) at sites proximal to a kinase docking region. Purified SYDE1 and SYDE2 are shown to have significant catalytic GAP activity toward RhoA, Rac1, and Cdc42. However, neither up- nor down-regulation of SYDE1/2 expression leads to detectable changes in bulk GTP loading of any of these GTPases. Nevertheless, we demonstrate that SYDE1 and SYDE2, in a partially GAP-dependent manner, increase cell spreading and number of focal adhesions, and promote more directionally persistent migration in HEK293 cells. Together, these findings establish SYDE1 and SYDE2 as robust JNK substrates with catalytic activity toward a set of Rho GTPases and reveal basic functions of SYDE1 and SYDE2 in regulating cell morphology, adhesion, and migration.

cell biology

The filopodial scaffold polyphosphate dictates cell adhesion-versus-invasion decisions

Inorganic polyphosphate (polyP) is an ancient polymer conserved across all life, serving cell type and location specific functions in every major compartment. Yet its role at the plasma membrane, where it accumulates to peak levels in many primary cells, is largely unknown. Here we identify polyP as a stabilizing component of filopodia, actin based membrane protrusions that govern cell adhesion, contact inhibition, and chemotaxis. Elevating cellular polyP increases filopodial stability and enhances cell adhesion, whereas reducing polyP accelerates filopodial disassembly and promotes cell migration. Mechanistically, we find that polyP acts as a structural filopodial scaffold, recruiting and organizing IRSp53, a membrane curvature inducing protein. We show that metastatic fibroblasts and breast cancer organoids carry markedly reduced and intracellularly reorganized polyP levels relative to their non transformed counterparts. Restoring endogenous polyP via lipid nanoparticle delivery suppresses their invasive phenotypes and reverses prometastatic gene expression signatures, implicating polyP as a primordial tumor suppressor.

cell biology

Mitochondrial transfer mediates metabolic communication between beta cells and islet macrophages

Pancreatic islet macrophages support islet homeostasis and adapt their metabolic program in response to environmental cues, including beta cell released factors. Intercellular mitochondrial transfer is a biological process that modulates cellular responses. To test whether beta cells, which are strongly secretory, transfer mitochondria to islet macrophages, we generated mice with beta cell-specific expression of mitochondrial GFP (PhAMfloxIns1Cre). We demonstrate that beta cells transfer mitochondria to islet macrophages in vivo and in vitro. Diabetogenic stressors did not alter the frequency of mitochondrial transfer and macrophages containing beta cell-derived GFP exhibit increased protein synthesis rates. RNA-seq identified upregulation of activity-regulated cytoskeleton associated protein (Arc) in macrophages receiving beta cell-derived mitochondria, while disruption of actin cytoskeleton dynamics prevented mitochondrial transfer. Together, these findings identify mitochondrial transfer as a previously unrecognized mechanism of beta cell-macrophage communication that may contribute to islet homeostasis and immune regulation.

cell biology