Mutagenesis and selection of enzymatic catalysts for biotechnological applications: development of an integrated in vivo method

Due to their properties as catalysts producing highly enantio- and regioselective compounds from target substrates under mild reaction conditions, the use of enzymes in biotechnological processes is rising. However, their often insufficient activity on non-natural compounds and narrow substrate ranges still limit their use in industrial setups. To obtain enzymes with enhanced activities, methods of directed evolution are available, involving mutant gene library generation and high throughput testing of individual variants in a cellular context. Linking of the targeted enzymatic activity to cell growth by constructing strains conditionally auxotrophic for essential metabolites or for energy carriers have significantly enlarged the application range of directed evolution (Chen et al., 2022). To achieve spatial and temporal connection between mutagenesis and variant screening, in vivo mutagenesis approaches have recently been developed. Among them are inducible systems employing different deaminase base editors tethered to T7 RNA polymerase (T7 RNAP), provoking base substitutions concomitant to transcription depending on the deaminase used (Cravens et al., 2021; (https://2021.igem.org/ Team:Evry_Paris-Saclay). However, these techniques have not yet been applied for the amelioration of industrial biocatalysts.
The components of the systems, i.e. target genes, T7 RNAP-deaminase fusion proteins and regulatory modules, are plasmid borne. The PhD student will further develop this method by inserting the T7 RNAP editor and the target gene into the E. coli chromosome, thus stabilizing the system and opening the possibility of multiple rounds of mutagenesis and selection steps in GM3 automated continuous culture devices available in the laboratory. He/she will establish a mutagenesis and selection protocol, using a native gene enabling conditional metabolic selection as reporter. The validated protocol will subsequently be applied to heterologous NADPH-dependent dehydrogenases using a generic NADPH sensor selection strain constructed and used in the lab (Lindner et al., 2018). These will include the screening for alcohol and amine dehydrogenases, activities already studied by our group (Ducrot et al., 2020), to obtain variants with broadened substrate specificity. Their potential for synthetic applications will be assessed in laboratory scale, using targets chosen in collaboration with national and international partners. In vitro characterization of the enzymatic activity of enhanced variants will also be undertaken. The PhD student will benefit from multiple expertise and equipment of the UMR Génomique Métabolique, covering molecular genetics, synthetic biology, directed evolution, chemical analytics and enzymology.

Elucidation of the homarine degradation pathway in the oceans

Context:
Primary biological production in the oceans exerts significant control over atmospheric CO2. Every day, phytoplankton transform 100 million tonnes of CO2 into thousands of different organic compounds (1). Most of these molecules (as metabolites) are biologically labile and converted back into CO2 within a few hours or days. The climate-carbon feedback loops mediated by this reservoir of labile dissolved organic carbon (DOC) depend on this network of microbes and metabolites. In other words, the resilience of the ocean to global changes(such as temperature rise and acidification) will depend on how this network responds to these perturbations.
Because of its short lifespan, this pool of labile DOC is difficult to observe. Yet these microbial metabolites are the most important carbon transport pathways in the ocean and are assimilated by marine bacteria as sources of carbon and energy. Knowledge of the main metabolic pathways (from genes to metabolites) is therefore essential for modelling carbon flows in the oceans. However, the diversity of these molecules remains largely unexplored and many of them have no annotated biosynthetic and/or catabolic pathways. This is the case for homarin (N-methylpicolinate), an abundant compound in the oceans. Homarine content can reach 400 mM in the marine cyanobacterium Synechococchus (2) and this ubiquitous organism contributes between 10 and 20% of global net primary production (3).Because of its abundance, homarine is probably an important metabolite in the carbon cycle.

Project:
In this thesis project, we aim to elucidate the homarine degradation pathway in the oceans.
Ruegeria pomeroyi DSS-3 is a Gram-negative aerobic bacterium and a member of the marine Roseobacter clade. Its close relatives account for around 10-20% of the bacterial plankton in the mixed coastal and oceanic layer (4). In the laboratory, DSS-3 can use homarine as its sole carbon source but to date, there is no information on the genes and catabolites involved in this process.
Comparative analysis of RNAseq experiments conducted on DSS-3 cultures grown with homarine or glucose (control) as a carbon source will enable us to identify the candidate genes involved in the degradation pathway. This pathway will also be studied using a metabolomic approach based on liquid chromatography coupled with very high resolution mass spectrometry. The difference in profile between DSS-3 metabolomes from cells grown on glucose as a carbon source and those from cells grown on homarine will help to detect catabolites in the pathway. Finally, the candidate genes will be cloned for recombinant expression in E. coli, the corresponding proteins purified and their activity characterized in order to reconstruct the entire homarine degradation pathway in vitro.
Analysis of the expression of these genes in data from the Tara Oceans project (5) will be the first step towards a better understanding of the role of homarine in the carbon cycle.

References :
(1) doi.org/10.1038/358741a0
(2) doi.org/10.1128/mSystems.01334-20
(3) doi.org/10.1073/pnas.1307701110
(4) doi.10.1038/nature03170
(5) https://fondationtaraocean.org/expedition/tara-oceans/

Effects of the combination of ionizing radiation and radio-enhancing molecules in breast cancer models

The proposed program aims to evaluate the efficacy of molecules enhancing the effects of radiotherapy, in in vitro and in vivo models of breast cancer. Two types of molecules, namely an inhibitor of mitochondrial genome maintenance and an inhibitor of the Base Excision Repair pathway, will be tested for radiopotentiation efficacy in the models.
The proposed inhibitors, whether targeting mitochondrial genome maintenance or the BER pathway, are already being investigated in vitro, both in the laboratory and by collaborators. We have shown that inhibition of the mechanisms targeted leads to an impairment in DNA damage repair following genotoxic stress. During this project, we will evaluate the effects of inhibitors on DNA damage repair induced by irradiation of different types (conventional, ultra-high dose rate, even extreme dose rate) and the associated mechanisms.
Variability in response to therapeutic combinations is frequently observed when moving from in vitro to in vivo models. We will therefore evaluate the inhibitors on cell line models well characterized in the laboratory, and corresponding to different breast cancer subtypes. On the other hand, the studies will be completed by a validation of the effects observed in vitro on a murine model of breast cancer. This xenograft model, developed in immunocompetent animals, will enable us to monitor the clinical, histological and immune response of the animals and their tumors, in order to confirm the interest of the molecules for therapeutic application in support of radiotherapy.
The proposed program will benefit from the laboratory's collaborations with physicists and chemists, and IRCM's experimental facilities and platforms (irradiation, animal experimentation, microscopy, cytometry, etc.).

Dynamic interplay of Rad51 nucleoprotein filament-associated proteins - Involvement in the regulation of homologous recombination

Homologous recombination (HR) is an important repair mechanism for DNA double-strand breaks induced by ionizing radiation. A key step in HR is the formation of Rad51 nucleoprotein filaments on the single-stranded DNA that is generated from these breaks. We were the first to show, using yeast as a model, that a tight control of the formation of these filaments is essential for HR not to induce chromosomal rearrangements by itself (eLife 2018, Cells 2021). In humans, the functional homologs of the yeast control proteins are tumor suppressors. Thus, the control of HR seems to be as important as the mechanism of HR itself. Our project involves the use of new molecular tools that allow a breakthrough in the study of these controls. We will use a functional fluorescent version of the Rad51 protein, first developed by our collaborators A. Taddei (Institut Curie), R. Guérois and F. Ochsenbein (I2BC, Joliot, CEA). This major advance will allow us to observe the influence of regulatory proteins on DNA repair by microscopy in living cells. We have also developed highly accurate structural models of control protein complexes associated with Rad51 filaments. We will adopt a multidisciplinary approach based on genetics, molecular biology, biochemistry, and protein structure in collaboration with W.D. Heyer (University of California, Davis, USA), to understand the function of the regulators of Rad51 filament formation. The description of the organization of these proteins with Rad51 filaments will allow us to develop new therapeutic approaches.

DNA METHYLATION AND THE 3D GENOME ORGANIZATION OF BACTERIA

DNA methylation in bacteria has been traditionally studied in the context of antiparasitic defense and as part of the innate immune discrimination between self and non-self DNA. However, sequencing advances that allow genome-wide analysis of DNA methylation at the single-base resolution are nowadays expanding and have propelled a modern epigenomic revolution in our understanding of the extent, evolution, and physiological relevance of methylation. Typically, the first step in studying the functional impacts of bacterial DNA methylation is to compare global gene expression between wild-type (WT) and methyltransferase (MTase) mutant strains. Several studies using RNA-seq for such comparisons have shown that perturbation of a single DNA MTase often results in tens, hundreds, and sometimes thousands of differentially expressed (DE) genes. According to the local competition model, competitive binding between an MTase and other DNA-binding proteins (e.g.: transcription factors) at specific motif sites affects transcription of a nearby gene, leading to phenotypic variation within the bacterial population. However, while in some cases the regulatory effects of MTases can be conclusively traced to methylation at the promoters of target genes, the large majority (>90%) of DE genes do not have methylated sites in their promoter regions, which implies that the local competition model does not apply to most DE genes. Another possibility is that the methylation status at individual motif sites might regulate the expression of a transcription factor, causing a broad downstream shift in the expression of its target genes. Yet, the latter is also not sufficiently explanatory for such a large number of DE genes. One hypothesis relates to the effect of DNA methylation on the chromosome topology whereby methylation induces structural changes that alter the repertoire of genes exposed to the cellular transcriptional machinery. We have recently identified CamA, a core MTase of Clostridioides difficile methylating at CAAAAA, with a
role in biofilm formation, sporulation, and in-vivo transmission. Moreover, in a subsequent large-scale analysis, we found that CamA was just the tip of the iceberg, with 45% of Genbank’s bacterial species containing at least one core or quasi-core MTase, which shows that the latter are abundant and suggests that their epigenetic modifications are likely important and frequent. On top of this, S-adenosyl-l-methionine (SAM) analogues were found to successfully inhibit CamA, in what represents a substantial first step in generating potent and selective epigenetically targeted therapeutics that can be exploited as new antimicrobials.
In this PhD project proposal, the successful candidate is asked to decipher the interplay between bacterial methylation, spatial genome organization and gene expression by answering the following questions: i) does methylation alter chromosomal interaction domains? ii) are DE genes and/or target methylation motifs enriched in changeable chromosomal interaction domain boundaries? iii) Can we tinker the methylome (globally or locally) to repress certain human pathogens? He / she will use Hi-C and long-read sequencing technologies combined with microbial genetics, and comparative genomics to broadly leverage the field of microbial epigenomics.

Crosstalk between adipocytes and T lymphocytes, key players in immunity in adipose tissue

The metabolic and endocrine role of adipose tissue (AT) is established. The AT is composed mainly of adipocytes but also of immune cells, best known for controlling the metabolic homeostasis of the tissue. The immune activity of TA is associated with the secretion of cytokines and metabolites that modulate its immune function. Obesity, characterized by an accumulation of AT at the subcutaneous or visceral level, is associated with the local inflammation of AT. However, the AT can be infected by different pathogens and it constitutes a site of accumulation of CD8 T lymphocytes (TL) specific for them, which protect against reinfection. These data therefore encourage us to investigate the interactions between adipocytes and CD8-TL in the AT.
The project will be carried out in the CoVir team, which is developing various projects aimed at deciphering the anti-infectious properties of adipose tissue. It is part of a consortium established for an ANR project (INSERM, CNRS, Institut Pasteur de Lille). The objective of the team's project is to study the local contribution of adipocytes and CD8-TL residing in the TA during influenza virus infection in a non-human primate (NHP) model. The NHP presents metabolic and immune responses similar to humans. In addition to in-vivo approaches in NHP, we will develop a 3D co-culture model to target the interaction between adipocytes and CD8-TL, without interference from inflammatory and metabolic signals external to TA. This project benefits from the historical expertise developed in the institute (IMVA-HB UMR 1184/I IDMIT, directed by R. Le Grand) concerning the study of viral infections in the preclinical model of PNH. IDMIT platforms provide equipment and expertise in histology, cytometry (LFC), cytokine/chemokine detection (L2I) and animal welfare (ASW).
The thesis project will focus on in vitro approaches. We will compare the interactions between adipocytes and LT, by studying the metabolic and immune response of each of these fractions. Indeed, adipocyte cells exhibit strong metabolic activity but exert their own immune activity (through the production of microbicidal peptides) and immunomodulatory activity. Concerning immune cells, their functional activity is dependent on their metabolic functions and it is crucial to evaluate the immune-metabolic modifications of immune cells in the presence of adipocytes. The organoid model will allow us to evaluate : (i) the impact of the context of obesity to those in a context of metabolic normality, (ii) the impact of viral pathogens on each of these two fractions. In the medium term, this model will make it possible to test strategies for modulating TA functions during metabolic pathologies or viral infections.

ROLE OF UNFOLDED PROTEIN RESPONSE IN MAINTAINING THE SPERMATOGONIAL STEM CELL POOL IN THE ADULT MOUSE

Adverse conditions (oxidative stress, imbalanced lipid, glucose or calcium levels, or inflammation) induce the accumulation of abnormal proteins resulting in ER stress. The Unfolded Stress Response (UPR) is activated to restore cellular homeostasis, but severe or chronic stress results in apoptotic cell death. Uncontrolled UPR signaling promotes many human diseases (diabetes, Parkinson's, Alzheimer's, liver disease, cancer...), but nothing is known about its implication in adult male sterility. Spermatozoa production relies on Spermatogonial Stem Cells (SSC) which are maintained by self-renewal throughout life. We have shown that the clonogenic activity of SSC is drastically impaired after ER stress through differentiation entry. An HTS screen has highlighted 2 of the 3 UPR branches as being involved in the clonogenic activity of SSC in vitro. The role of these 2 UPR pathways will be further investigated in SSC cultures of mice to determine whether they are involved in the induction of cell death or in the balance between self renewal and differentiation. In treated SSC cultures, cell death, cell cycle, induction of differentiation and synergy between UPR pathways will be analyzed. As the effect of each pathway is mediated by transcriptional factors, the target genes will be characterized by RNAseq in order to identify the gene networks controlled by UPR effectors and involved in the fate of SSC. For the most relevant pathway, an in vivo study will confirm the role of the UPR effector in CSS property.

Complex brain organoid model reproducing the glioblastoma tumor niche and its immune component for the development of personalized medicine

Glioblastoma, responsible for 3,500 annual deaths in France, is an extremely aggressive brain tumor that is resistant to current treatments. Clinical trials in immunotherapy have shown only transient effects, underscoring the importance of understanding resistance mechanisms and developing more targeted therapeutic strategies.

We have developed an innovative model of glioma stem cell invasion in immunocompetent and vascularized brain organoids derived from induced pluripotent stem cells (iPSCs) (Raguin et al., submitted). This model faithfully reproduces the glioblastoma tumor niche, including vascular co-option, reprogramming of microglia into tumor-associated macrophages, and tumor recurrence following radiotherapy.

The aim of this PhD project is to derive a universal brain organoid model for the transfer of glioma cells from patients and lymphocytes to optimize the immunotherapy approach (CAR-T cells).

The project involves creating a universal model of human brain organoids that are immunologically "silent" by suppressing the expression of the HLA class I/II system in iPSCs (CRISPR/CAS9 for the ß2M and CIITA genes). Additionally, it aims to elucidate the mechanisms of immunosuppression induced by irradiation, such as the reprogramming of microglial/macrophage cells and the involvement of senescence. Various approaches to make the tumor microenvironment more conducive to immunotherapy will be explored, including activating the type I interferon pathway through genetic modification or with cGAS/STING pathway agonists. Subsequently, the use of CAR-T cells targeting an antigen overexpressed by glioblastoma cells (CD276/B7-H3) will be studied. This model could be used in personalized medicine by co-cultivating patients' tumor cells, monocytes, and CAR-T cells.

This project offers innovative perspectives for the personalized treatment of glioblastoma via immunotherapy and could represent a major advancement in this therapeutic approach.

Multiplexed whole-body in vivo imaging monitoring of pathogen dissemination and immune responses dynamics in tuberculosis

This thesis is dedicated to set up a multiplexed medical imaging monitoring of pathogen colonization and associated immune responses dynamics at the whole body scale for various infectious diseases. This could provide an innovative and non-invasive tool to better understand dynamics links between immune responses and pathogen distribution throughout the body and potentially provide new biomarkers associated to several diseases. To tackle this issue this thesis would implement such strategy in tuberculosis disease. The main aim is to determine the relationship between Mycobacterium tuberculosis dissemination and associated immune responses across the whole body during the course of tuberculosis infection from early infection to latent or active tuberculosis thanks to innovative multiplexed imaging protocols. The goal of this study is to provide correlations in time and space between local bacterial burden and several immune cell infiltrations (activated macrophages and T lymphocytes subsets) occurring following infection and detected over time by imaging. These findings could then provide, with minimal invasiveness, predictive biomarkers on disease or local granuloma progression and may provide also valuable insight on potential immune targets for future preventive or curative strategies based on modulation of the immune system. To do so, this thesis would take advantage of the preclinical Non-human primate model of tuberculosis developed in France and on our in vivo imaging of pathogens and immune cells expertise in NHPs. Of note, deeper immune cell profiling in samples of interest (imaging guided) will be assessed by spatial or single-cell transcripomic technologies in tissue samples to provide additional readouts on TB pathophysiology and potential treatment efficacy.

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