bioRxiv Science⌕ Search

Biology subjects

Beyaert, R.

Publications and source records attributed to Beyaert, R..

6 recordsLinked to original sources

Multi-Step Pathway Engineering in Probiotic Saccharomyces boulardii for Abscisic Acid Production in the Gut

The plant hormone abscisic acid (ABA) has gained attention for its role in animals and humans, particularly due to its protective effects in various immune and inflammatory disorders. Given its high concentrations in fruits like figs, bilberries and apricots, ABA shows promise as a nutraceutical. However scalability, short half-life and cost limit the use of ABA-enriched fruit extracts and synthetic supplements. In this study, we propose an alternative ABA administration method to overcome these challenges. We genetically engineered a strain of the probiotic Saccharomyces boulardii to produce and deliver ABA directly to the gut of mice. Using the biosynthesis pathway from Botrytis cinerea, four genes (bcaba1-4) were integrated into S. boulardii, enabling ABA production at 30{degrees}C, as previously described in Saccharomyces cerevisiae. Introducing an additional cytochrome P450 reductase gene resulted in a 7-fold increase in ABA titers, surpassing previous ABA-producing S. cerevisiae strains. Supplementation of the ABA-producing S. boulardii in the diet of mice (at a concentration of 5 x 108 CFU/g) led to effective gut colonization but resulted in low serum ABA levels (approximately 1.8 ng/mL). The absence of detectable serum ABA after administration of the ABA-producing probiotic through oral gavage, prompted further investigation to determine the underlying cause. The physiological body temperature (37{degrees}C) was identified as a major bottleneck for ABA production. Modifications to enhance the mevalonate pathway flux improved ABA levels at 37{degrees}C. However, additional modifications are needed to optimize ABA production before testing this probiotic in disease contexts in mice.

synthetic biology↗

CREB determines the expression of ST2 in Tregs and mediates the balance between type 1 and type 2 immune responses

Regulatory T cells (Tregs) are gatekeepers of immune homeostasis and characterized by expression of Foxp3, which maintains Treg identity. Here we demonstrate that in mice with a Foxp3-specific knockout of CREB, enhanced numbers of Tregs are found in vivo in spleen, lung and colon. These Tregs display a reduced Foxp3 expression, but enhanced expression of the IL-33 receptor (ST-2), IL-10, IL-13, and CREM. CREB deficient Tregs were highly suppressive in vitro and prevented disease activity in CD4 T cell mediated transfer colitis in an IL-10 dependent way. Mechanistically CREB fulfils dual roles in Tregs. First it downregulates Foxp3 expression, however in cooperation with CREM, CREB expression in Tregs alters chromatin accessibility to the ST-2 region and thereby influences T cell specific immune responses mediated by IL-10. Brief summary: Mice with a Foxp3-specific knockout of CREB display enhanced expression of IL-13, IL-10, ST-2 and CREM, which prevents gut inflammation GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=140 SRC="FIGDIR/small/601312v2_ufig1.gif" ALT="Figure 1"> View larger version (22K): org.highwire.dtl.DTLVardef@a2d341org.highwire.dtl.DTLVardef@1db6852org.highwire.dtl.DTLVardef@19e024borg.highwire.dtl.DTLVardef@a8c84d_HPS_FORMAT_FIGEXP M_FIG C_FIG Created by Biorender

immunology↗

Extreme miniaturization in plasmid design: generation of the 903 bp cloning vector pICOt2

Inspired by the size optimizations in the recently published pUdO series of plasmids, we set out to break our previous world record (pICOz, 1185 bp) in designing the smallest possible self-replicating high copy cloning vector. By replacing the zeocin resistance marker with trimethoprim resistance, deleting the parts upstream of -35 in the ampicilin resistance promoter and replacing the extended multiple cloning site with a single SpeI site, we managed to reduce the plasmid size to 903 bp, almost a 24% reduction in size compared to our previous accomplishments.

synthetic biology↗

"Franken-CARD9": chimeric proteins for high-resolution studies of activating mutations in CARD10, CARD11 and CARD14

CARD9, -10, -11 and -14 all belong to the CARD-coiled coil (CC) protein family and originated from a single common ancestral protein early in vertebrate evolution. All four proteins form CARD-CC/BCL10/MALT1 (CBM) complexes leading to NF-{kappa}B activation after upstream phosphorylation by various protein kinase C (PKC) isoforms. CBM complex signaling is critical for innate and adaptive immunity, but aberrant activation can cause autoimmune or autoinflammatory diseases, or be oncogenic. CARD9 shows a superior auto-inhibition with very low spontaneous activity when overexpressed in HEK293T cells. In contrast, the poor auto-inhibition of other CARD-CC family proteins, especially CARD10 (CARMA3) and CARD14 (CARMA2), is hampering characterization of upstream activators or activating mutations in overexpression studies. We grafted different domains from CARD10, -11 and 14 on CARD9 to generate chimeric CARD9 backbones for functional characterization of activating mutants using NF-{kappa}B reporter gene activation in HEK293T cells as readout. CARD11 (CARMA1) activity was not further reduced by grafting on CARD9 backbones. The chimeric CARD9 approach was subsequently validated by using several known disease-associated mutations in CARD10 and CARD14, and additional screening allowed us to identify several novel activating natural variants in human CARD9 and CARD10. Using Genebass as a resource of exome-based disease association statistics, we found that activated alleles of CARD9 correlate with irritable bowel syndrome (IBS), constipation, osteoarthritis, fibromyalgia, insomnia, anxiety and depression, which can occur as comorbidities.

genetics↗

IRG1 controls immunometabolic host response and restricts intracellular Mycobacterium tuberculosis infection

Mycobacterium tuberculosis (Mtb), the pathogen causing human tuberculosis, has evolved multiple strategies to successfully prevent clearance by immune cells and to establish dissemination and long-term survival in the host. The modulation of host immunity to maximize pathogen elimination while minimizing inflammation-mediated tissue damage may provide another tool to fight drug-resistant Mtb strains. Metabolic reprogramming of phagocytes can dramatically influence the intracellular colonization by Mtb and the key players involved in this process remain a matter of debate. Here, we demonstrate that aconitate decarboxylase 1 (Acod1; also known as immune-responsive gene 1, IRG1), which converts cis-aconitate into the metabolite itaconate, is a major player in controlling the acute phase of Mtb infection. Exposure of IRG1-deficient mice to a virulent Mtb strain (H37Rv) was lethal, while M. bovis BCG and the H37Ra attenuated Mtb strain induced neither lethality nor severe lung immunopathology. Lungs of IRG1-deficient mice infected by Mtb H37Rv displayed large areas of necrotizing granulomatous inflammation and neutrophil infiltration, accompanied by reduced levels of B and T lymphocytes and increased levels of alveolar and interstitial macrophage populations, compared to their wild type counterparts. Next, we show that IRG1, beyond its recruitment to Mtb-containing vacuoles, restricts Mtb replication and lipid droplets accumulation in phagocytes, hallmarks of a tight interplay between the bacillus and the host. Altogether, IRG1 confines the host response to create a favourable phagocytic environment for Mtb controlled intracellular replication.

immunology↗

Defining the relevant combinatorial space of the PKC/CARD-CC signal transduction nodes

Biological signal transduction typically display a so-called bow-tie or hour glass topology: Multiple receptors lead to multiple cellular responses but the signals all pass through a narrow waist of central signaling nodes. One such critical signaling node for several inflammatory and oncogenic signaling pathways in humans are the CARD-CC / Bcl10 / MALT1 (CBM) complexes, which get activated by upstream protein kinase C (PKC). In humans, there are four phylogenetically distinct CARD-CC family (CARD9, -10, -11 and -14) proteins and 9 true PKC isozymes ( to {iota}). At this moment, less than a handful of PKC/CARD-CC relationships are known from experimental evidence. In order to explore the biologically relevant combinatorial space out of all 36 potential permutations in this two-component signaling event, we made use of CRISPR/Cas9 genome-edited HEK293T cells to mutate CARD10 for subsequent pairwise cotransfections of all CARD-CC family members and activated mutants of all true PKCs. By quantitative reporter gene expression readout, we could define specific strong and weak PKC/CARD-CC relationships. Surprisingly as many as 21 PKC/CARD-CC combinations were found to have synergistic effects. We also discovered heterodimerization between different CARD-CC proteins, and that this can influence their PKC response profile. This information will be valuable for future studies of novel signaling pathways dependent on the CBM complex signaling nodes.

systems biology↗