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Garcia, C.

Publications and source records attributed to Garcia, C..

At least 37 records · Page 2Linked to original sources

Supervised Automation of Cell Counting in Confocal Microscopic Cochlear Imaging Datasets Using Macro in Imaris

Analyzing confocal microscopic data of biological samples using the Imaris software poses challenges due to its time-consuming nature involving tedious multiple steps and possibility of human errors. Here, we developed a supervised automation protocol to minimize manual input in cell and spot counting on confocal images obtained from mouse cochlear sections. The protocol increases efficiency by incorporating image recognition and object-oriented macros. Moreover, the protocol being adaptable allows scientists in diverse other fields to customize it for their specific needs. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=196 SRC="FIGDIR/small/604970v1_ufig1.gif" ALT="Figure 1"> View larger version (64K): org.highwire.dtl.DTLVardef@11b4aa0org.highwire.dtl.DTLVardef@c08c7dorg.highwire.dtl.DTLVardef@1479b59org.highwire.dtl.DTLVardef@280227_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

A comparison among EL-FAME, PLFA, and quantitative PCR methods to detect changes in the abundance of soil bacteria and fungi

EL-FAME (ester-linked fatty acid methyl ester), PLFA (phospholipid fatty acid) and qPCR (quantitative PCR) of ribosomal genes are three of the most common methods used to quantify soil microbial communities. The reliability of these three methods has not been simultaneously compared in situations of rapid changes in soil microbial abundances. For this purpose, we (i) incubated badland, cropland, and forest soils with nutrients or antibiotics for 2, 7, 14, and 28 days, (ii) quantified total, bacterial, and fungal abundances through EL-FAME, PLFA, and qPCR methods, and (iii) measured soil basal respiration. The general dynamic patterns of the three soil microbial fractions in response to soil addition of nutrients and antibiotics were captured by the three methods, which led to strong and positive associations between the abundances of total microorganisms, bacteria, and fungi measured by the three techniques. However, these relationships were found to be stronger between the EL-FAME and PLFA results, indicating that reliability of the fatty-acid based methods is higher than that of the qPCR. Further, soil basal respiration was associated to a higher extent with total, bacterial, and fungal abundances captured by EL-FAME and PLFA analyses than with those measured by qPCR, which suggests that the first two methods are most closely related to the soil living microbial community. In general, dynamics in the abundance of total and bacterial communities were better captured than those of fungi. The PLFA analysis seems to perform better than the EL-FAME method in forest soil and in detecting the small antibiotic-induced decreases in microbial abundances. Since the EL-FAME method is cheaper and allows a much faster processing of samples than the PLFA method, and the reliability of both methods is similar in detecting rapid changes of soil microbial abundances, choosing EL-FAME over PLFA may be advantageous in most cases.

microbiology↗

Tissue-resident regulatory T cells exert dualistic anti-tumour and pro-repair function in the exocrine pancreas

Regulatory T cells are fundamentally important for maintaining immune homeostasis, and their potent immune-suppressive roles make them attractive immunotherapeutic targets in cancer. Recent work suggests potential functions of tissue-resident Tregs (trTregs) in tissue-repair and epithelial cell homeostasis. Here, we describe a rare population of trTreg in the exocrine pancreas. We show that these cells share common features of trTregs, including expression of the IL-33 receptor ST2 and production of the epithelial growth factor Amphiregulin, and display an oligoclonal T cell receptor repertoire. Using a mouse model of acute pancreatitis, we show that pancreatic Tregs rapidly expand upon release of IL-33 by fibroblasts. Moreover, depletion of Tregs after initiation of pancreatic injury impairs the regeneration of the exocrine parenchyma. This effect is due, in part, through a direct effect of Tregs on acinar cell proliferation. Finally, we show that transient Treg depletion in established orthotopic pancreatic tumours leads to tumour rejection yet provokes long-lasting damages to surrounding exocrine parenchyma. In all, our results demonstrate the tissue-repair capacity of pancreatic Tregs, and highlight a dualistic role of these cells in the pancreatic tumour ecosystem, with their harmful immune-suppressive function in the tumour coupled to a beneficial tissue-repair function in the surrounding tissue.

immunology↗

When paleontology meets genomics: complete mitochondrial genomes of two saber-toothed cats' species (Felidae: Machairodontinae)

Within the Machairodontinae subfamily, commonly referred as saber-toothed cats, it is worth noting that only two species, namely Homotherium latidens, recognized as the scimitar-toothed cat, and Smilodon populator, renowned as the saber-toothed tiger, possess partial mitochondrial genomes accessible in the NCBI database. These sequences, however, do not include the mitogenome control region (D-loop) and have several gaps in their genes, including protein-coding genes (PCGs) that are widely used in phylogenetic analysis. In this study, we aimed to obtain a complete assembly of the mitogenomes of these two species from next-generation sequencing data available at NCBIs SRA. The de novo assemblies showed complete mitogenomes with 17,323bp (H. latidens) and 16,769 bp (S. populator), both with 13 PCGs, 22tRNAs, two rRNAs and the D-loop (Control region), with all genes following the standard order and position of most vertebrate mitogenomes. Our phylogeny and molecular dating, despite being generally very similar to previous studies, reveals an earliest divergence between North American and North Sea H. latidens specimens which may be related to an Early Pleistocene migration across Beringia.

genomics↗

Genetic differentiation and host specialization among OsHV-1 infecting two oyster species in France

AbstractCross-species transmission is a major driver of disease emergence in humans and animals. The Ostreavirus ostreidmalaco1 (OsHV-1) is mainly associated with mortality in the Pacific oyster Magallana gigas, but has also been found in other mollusks, including the European flat oyster Ostrea edulis. This raises questions about OsHV-1 host specificity. This study explored the genetic differentiation of OsHV-1 in M. gigas and O. edulis and the underlying mechanisms. Using high-throughput sequencing, 40 OsHV-1 genomes were obtained from both O. edulis and M. gigas and were analyzed to assess viral diversity, lineage isolation, and cross-species transmission. Comparative genomics, population genetics, phylogenetic and phylodynamic methods revealed that host species significantly influence viral genetic structure. The data suggest that OsHV-1 was introduced in Europe with M. gigas, followed by a cross-species transmission event and divergence into two distinct lineages. Selection signals were identified in genomic regions involved in key viral functions, including host binding, DNA replication, and membrane-associated proteins, indicating possible adaptation to different hosts. Future research should investigate coevolution between OsHV-1 and a broader range of host species using phylogenetic approaches to better understand host-virus dynamics.

evolutionary biology↗

Impairment of autophagy-lysosomal activity near the chronically implanted microelectrodes

Intracortical microelectrodes that can record and stimulate brain activity have become a valuable technique for basic science research and clinical applications. However, long-term implantation of these microelectrodes can lead to progressive neurodegeneration in the surrounding microenvironment, characterized by elevation in disease-associated markers. Dysregulation of autophagy-lysosomal degradation, a major intracellular waste removal process, is considered a key factor in the onset and progression of neurodegenerative diseases. It is plausible that similar dysfunctions in autophagy-lysosomal degradation contribute to tissue degeneration following implantation-induced focal brain injury, ultimately impacting recording performance. To understand how the focal, persistent brain injury caused by long-term microelectrode implantation impairs the autophagy-lysosomal pathway, we employed two-photon microscopy and immunohistology. This investigation focused on the spatiotemporal characterization of autophagy-lysosomal activity near the chronically implanted microelectrode. We observed an aberrant accumulation of immature autophagy vesicles near the microelectrode over the chronic implantation period. Additionally, we found deficits in autophagy-lysosomal clearance proximal to the chronic implant, which was associated with an accumulation of autophagy cargo and a reduction in lysosomal protease level during the chronic period. Furthermore, our evidence suggests astrocytes contribute to the clearance of myelin debris via autophagy-lysosomal degradation near the implanted microelectrode. Together, this study sheds light on the process of brain tissue degeneration caused by long-term microelectrode implantation, with a specific focus on impaired intracellular waste degradation.

bioengineering↗

Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia

Cardiac macrophages are heterogenous in phenotype and functions, which has been associated with differences in their ontogeny. Despite extensive research, our understanding of the precise role of different subsets of macrophages in ischemia/reperfusion injury remains incomplete. We here investigated macrophage lineages and ablated tissue macrophages in homeostasis and after I/R injury in a CSF1R-dependent manner. Genomic deletion of a fms-intronic regulatory element (FIRE) in the Csf1r locus resulted in specific absence of resident homeostatic and antigen-presenting macrophages, without affecting the recruitment of monocyte-derived macrophages to the infarcted heart. Specific absence of homeostatic, monocyte-independent macrophages altered the immune cell crosstalk in response to injury and induced proinflammatory neutrophil polarization, resulting in impaired cardiac remodelling without influencing infarct size. In contrast, continuous CSF1R inhibition led to depletion of both resident and recruited macrophage populations. This augmented adverse remodelling after I/R and led to an increased infarct size and deterioration of cardiac function. In summary, resident macrophages orchestrate inflammatory responses improving cardiac remodelling, while recruited macrophages determine infarct size after I/R injury. These findings attribute distinct beneficial effects to different macrophage populations in the context of myocardial infarction. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=88 SRC="FIGDIR/small/539799v4_ufig1.gif" ALT="Figure 1"> View larger version (34K): org.highwire.dtl.DTLVardef@14fa4bcorg.highwire.dtl.DTLVardef@1c86bbborg.highwire.dtl.DTLVardef@118edfcorg.highwire.dtl.DTLVardef@1b06916_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Linking the evolution of two prefrontal brain regions to social and foraging challenges in primates

The diversity of cognitive skills across primates remains both a fascinating and a controversial issue. Recent comparative studies provided conflicting results regarding the contribution of social vs ecological constraints to the evolution of cognition. Here, we used an interdisciplinary approach combining comparative cognitive neurosciences and behavioral ecology. Using brain imaging data from 16 primate species, we measured the size of two prefrontal brain regions, the frontal pole (FP) and the dorso-lateral prefrontal cortex (DLPFC), respectively involved in metacognition and working memory, and examined their relation to a combination of socio-ecological variables. The size of these prefrontal regions, as well as the whole brain, was best explained by three variables: body mass, daily traveled distance (an index of ecological constraints) and population density (an index of social constraints). The strong influence of ecological constraints on FP and DLPFC volumes suggests that both metacognition and working memory are critical for foraging in primates. Interestingly, FP volume was much more sensitive to social constraints than DLPFC volume, in line with laboratory studies showing an implication of FP in complex social interactions. Thus, our data highlights the relative weight of social vs ecological constraints on the evolution of specific prefrontal brain regions and their associated cognitive operations in primates. FundingThis work was supported by recurrent funding from CNRS to SB, SP and CG. It was also supported by the ANR-17-CE27-0005 (HOMTECH).

neuroscience↗

Insights into mammalian TE diversity via the curation of 248 mammalian genome assemblies

We examined transposable element (TE) content of 248 placental mammal genome assemblies, the largest de novo TE curation effort in eukaryotes to date. We find that while mammals resemble one another in total TE content and diversity, they show substantial differences with regard to recent TE accumulation. This includes multiple recent expansion and quiescence events across the mammalian tree. Young TEs, particularly LINEs, drive increases in genome size while DNA transposons are associated with smaller genomes. Mammals tend to accumulate only a few types of TE at any given time, with one TE type dominating. We also found association between dietary habit and the presence of DNA transposon invasions. These detailed annotations will serve as a benchmark for future comparative TE analyses among placental mammals. One-Sentence SummaryA de novo assessment of TE content in 248 mammals finds informative trends in mammalian genome evolution.

genomics↗

DNA primase large subunit is an essential plant gene for geminiviruses, putatively priming viral ss-DNA replication

The family of Geminiviridae consists of more than 500 circular single-stranded (ss) DNA viral species that can infect numerous dicot and monocot plants. Geminiviruses replicate their genome in the nucleus of a plant cell, taking advantage of the hosts DNA replication machinery. For converting their DNA into double-stranded DNA, and subsequent replication, these viruses rely on host DNA polymerases. However, the priming of the very first step of this process, i.e. the conversion of incoming circular ssDNA into a dsDNA molecule, has remained elusive for almost 30 years. In this study, sequencing of melon (Cucumis melo) accession K18 carrying the Tomato leaf curl New Delhi virus (ToLCNDV) recessive resistance quantitative trait locus (QTL) in chromosome 11, and analyses of DNA sequence data from 100 melon genomes, showed a conservation of a shared mutation in the DNA Primase Large subunit (PRiL) of all accessions that exhibited resistance upon a challenge with ToLCNDV. Silencing of (native) Nicotiana benthamiana PriL and subsequent challenging with three different geminiviruses showed a severe reduction in titers of all three viruses, altogether emphasizing an important role of PRiL in geminiviral replication. A model is presented explaining the role of PriL during initiation of geminiviral DNA replication, i.e. as a regulatory subunit of primase that generates an RNA primer at the onset of DNA replication in analogy to DNA Primase-mediated initiation of DNA replication in all living organisms.

plant biology↗

Genomic accordions may hold the key to Monkeypox Clade IIb's increased transmissibility

The currently expanding monkeypox epidemic is caused by a subclade IIb descendant of a monkeypox virus (MPXV) lineage traced back to Nigeria in 1971. In contrast to monkeypox cases caused by clade I and subclade IIa MPXV, the prognosis of current cases is generally favorable, but person-to-person transmission is much more efficient. MPXV evolution is driven by selective pressure from hosts and loss of virus-host interacting genes. However, there is no satisfactory genetic explanation using single-nucleotide polymorphisms (SNPs) for the observed increased MPXV transmissibility. We hypothesized that key genomic changes may occur in the genomes low-complexity regions (LCRs), which are highly challenging to sequence and have been dismissed as uninformative. Using a combination of highly sensitive techniques, we determined a first high-quality MPXV genome sequence of a representative of the current epidemic with LCRs resolved at unprecedented accuracy. This effort revealed significant variation in short-tandem repeats within LCRs. We demonstrate that LCR entropy in the MPXV genome is significantly higher than that of SNPs and that LCRs are not randomly distributed. In silico analyses indicate that expression, translation, stability, or function of MPXV orthologous poxvirus genes (OPGs) 153, 204, and 208 could be affected in a manner consistent with the established "genomic accordion" evolutionary strategies of orthopoxviruses. Consequently, we posit that genomic studies focusing on phenotypic MPXV clade-/subclade-/lineage-/strain differences should change their focus to the study of LCR variability instead of SNP variability.

genomics↗

Identification of leukemia-associated immunophenotypes by database-guided flow cytometry provides a highly sensitive and reproduciblestrategy for the study of measurable residual disease in acutemyeloblastic leukemia

BackgroundMultiparametric Flow Cytometry (MFC) is an essential tool to study the involved cell lineages, the aberrant differentiation/maturation patterns and the expression of aberrant antigens in acute myeloid leukemia (AML). The characterization of leukemia-associated immunophenotypes (LAIPs) at the moment of diagnosis is critical to establish reproducible strategies for the study of measurable residual disease using MFC (MFC-MRD). MethodsIn this study, we identified and characterized LAIPs by comparing the leukemic populations of 145 AML patients, using the EuroFlow AML/ MDS MFC panel, with 6 databases of normal myeloid progenitors (MPCs). Principal component analysis was used to identify and characterize the LAIPs, which were then used to generate individual profiles for MFC-MRD monitoring. Furthermore, we investigated the relationship between the expression patterns of LAIPs and the different subtypes of AML. The MFC-MRD study was performed by identifying residual AML populations that matched with the LAIPs at diagnosis. To further validate this approach, the presence of MRD was also assessed by qPCR (qPCR-MRD). Finally, we studied the association between MFC-MRD and progression-free survival (PFS). ResultsThe strategy used in this study allowed us to describe more than 300 different LAIPs and facilitated the association of specific phenotypes with certain subtypes of AML. The MFC-MRD monitoring based on LAIPs with good/strong specificity was applicable to virtually all patients and showed a good correlation with qPCR-MRD and PFS. ConclusionsThe described methodology provides an objective method to identify and characterize LAIPs. Furthermore, it provides a theoretical basis to develop highly sensitive MFC-MRD strategies.

cancer biology↗

Calibration of crop phenology models: Going beyond recommendations

A major effect of environment on crops is through crop phenology, and therefore, the capacity to predict phenology for new environments is important. Mechanistic crop models are a major tool for such predictions, but calibration of crop phenology models is difficult and there is no consensus on the best approach. Here we propose an original, detailed approach, a protocol, for calibration of such models. The protocol covers all the steps in the calibration work-flow, namely choice of default parameter values, choice of objective function, choice of parameters to estimate from the data, calculation of optimal parameter values and diagnostics. The major innovation is in the choice of which parameters to estimate from the data, which combines expert knowledge and data-based model selection. First, almost additive parameters are identified and estimated. This should make bias (average difference between observed and simulated values) nearly zero. These are "obligatory" parameters, that will definitely be estimated. Then candidate parameters are identified, which are parameters likely to explain the remaining discrepancies between simulated and observed values. A candidate is only added to the list of parameters to estimate if it leads to a reduction in BIC (Bayesian Information Criterion), which is a model selection criterion. A second original aspect of the protocol is the specification of documentation for each stage of the protocol. The protocol was applied by 19 modeling teams to three data sets for wheat phenology. All teams first calibrated their model using their "usual" calibration approach, so it was possible to compare usual and protocol calibration. Evaluation of prediction error was based on data from sites and years not represented in the training data. Compared to usual calibration, calibration following the new protocol reduced the variability between modeling teams by 22% and significantly reduced prediction error.

plant biology↗

Emergence and clonal expansion in Europe of Vibrio aestuarianus lineages pathogenic for oysters

Crassostrea gigas oysters represent a significant global food source, with 4.7 million tons harvested per year. In 2001, the bacterium V. aesturianus francensis emerged as a pathogen that causes adult oyster mortality in France and Ireland. Its impact on oyster aquaculture has increased in Europe since its reemergence in 2012. To better understand the evolutionary mechanisms leading to the emergence and persistence over time of this pathogen, we conducted a survey of mollusk diseases through national reference laboratories (NRLs) across Europe. We analyzed 54 new genomes of V. aestuarianus (Va) isolated from multiple environmental compartments since 2001, in areas with and without bivalve mortalities. We used a combination of comparative genomics and population genetics approaches to show that Va francensis lineages have undergone clonal expansion in Europe, likely after a recent selective bottleneck. Low mutation and recombination rates may have selected particular virulent genotypes. Furthermore, we identified a specific cus-cop-containing island conferring copper resistance to Va francensis whose acquisition may have favored the emergence of pathogenic lineages adapted to oysters.

microbiology↗

Heparins enhance C1 esterase inhibitor activity: a promising remedy for acute hereditary angioedema

RationaleHereditary angioedema (HAE) is a potentially life-threatening illness most commonly due to deficiency or dysfunction of C1-esterase inhibitor (C1-INH). While specific treatments are available to thwart acute exacerbations, they are extremely costly and some can be associated with rare but serious side effects. The heparins are long known to augment C1-INH activity and case reports / series have documented their efficacy in treating HAE. Objectiveto determine if unfractionated heparin and two low-molecular weight heparins (enoxaparin and nadroparin) can augment C1-INH activity ex vivo in the sera of patients with HAE and in an in vitro biochemical assay. MethodsC1-INH activity in the absence or presence of the heparin formulations were analyzed by two different methods. To measure C1-INH activity ex vivo, a commercially available assay was utilized with patient sera, excess amounts of C1s, and a substrate of C1s which, upon cleavage by C1s, produces a chromogenic product. To determine biochemically the C1-INH activity in vitro, a pharmacologic grade C1-INH, recombinant C1s (C1s-CCP12SP), and a peptide substrate of C1s were employed. Microscale thermophoresis was used to determine whether C1-INH binds to heparin. Main resultsin patient sera, nadroparin was superior to enoxaparin and unfractionated heparin in augmenting C1-INH activity, followed by enoxaparin and then unfractionated heparin. In the in vitro biochemical assay, all three heparins augmented C1-INH-C1s binding linearly in a dose-dependent fashion. Microscale thermophoresis assay demonstrated that nadroparin binds to C1-INH, providing a mechanism by which heparin facilitates the interaction between C1-INH and the proteases known to produce bradykinin, the mediator of HAE. Conclusionlow-molecular weight heparin augments C1-INH activity and should be studied as a potential treatment for acute HAE.

pharmacology and toxicology↗

Ex vivo and in vivo evidence that cigarette smoke-exposed T regulatory cells impair host immunity against Mycobacterium tuberculosis

A strong epidemiologic link exists between exposure to cigarette smoke (CS) and increased susceptibility to tuberculosis (TB). In vitro macrophage and in vivo murine studies showed that CS and nicotine impair host-protective immune cells against Mycobacterium tuberculosis (MTB) infection. However, little is known about how CS may affect immunosuppressive cells in the context of MTB infection. Thus, we investigated whether CS-exposed T regulatory cells (Tregs) could exacerbate MTB infection in co-culture with human macrophages and in the adoptive transfer of Tregs from air- and CS-exposed mice. We found that exposure of primary human Tregs to CS extract impaired the ability of human monocyte-derived macrophages to control an MTB infection by inhibiting phagosome-lysosome fusion and autophagosome formation. Neutralization of CTLA-4 on the CS extract-exposed Tregs abrogated the impaired control of MTB infection in macrophage and Treg co-cultures. In Foxp3+GFP+DTR+ (Thy1.2) mice depleted of endogenous Tregs, adoptive transfer of Tregs from donor CS-exposed B6.PL(Thy1.1) mice with subsequent MTB infection of the recipient Thy1.2 mice resulted in a greater burden of MTB in the lungs and spleens than those that received Tregs from airexposed mice. Mice that received Tregs from CS-exposed mice and then infected with MTB had modest but significantly reduced numbers of interleukin-12-positive dendritic cells and interferon-gamma-positive CD4+ T cells in the lungs and increased number of programmed cell death protein-1 positive CD4+ T cells in both the lungs and spleens.

immunology↗

Microglia-secreted TNF-α affects differentiation efficiency and viability of pluripotent stem cell-derived human dopaminergic precursors

Parkinsons Disease is a neurodegenerative disorder characterized by the progressive loss of dopaminergic cells of the substantia nigra pars compacta. Even though successful transplantation of dopamine-producing cells into the striatum exhibits favourable effects in animal models and clinical trials; transplanted cell survival is low. Since every transplant elicits an inflammatory response which can affect cell survival and differentiation, we aimed to study in vivo and in vitro the impact of the pro-inflammatory environment on human dopaminergic precursors. We first observed that transplanted human dopaminergic precursors into the striatum of immunosuppressed rats elicited an early and sustained activation of astroglial and microglial cells after 15 days post-transplant. This long-lasting response was associated with Tumor necrosis factor alpha expression in microglial cells. In vitro conditioned media from activated BV2 microglial cells increased cell death, decreased Tyrosine hydroxylase -positive cells and induced morphological alterations on human neural stem cells-derived dopaminergic precursors at two differentiation stages: 19 days and 28 days. Those effects were ameliorated by inhibition of Tumor necrosis factor alpha, a cytokine which was previously detected in vivo and in conditioned media from activated BV-2 cells. Our results suggest that a pro-inflammatory environment is sustained after transplantation under immunosuppression, providing a window of opportunity to modify this response to increase transplant survival and differentiation. In addition, our data show that the microglia-derived pro-inflammatory microenvironment has a negative impact on survival and differentiation of dopaminergic precursors. Finally, Tumor necrosis factor alpha plays a key role in these effects, suggesting that this cytokine could be an interesting target to increase the efficacy of human dopaminergic precursors transplantation in Parkinsons Disease.

neuroscience↗

Insight in the quorum sensing-driven lifestyle of the non-pathogenic Agrobacterium tumefaciens 6N2 and the interactions with the yeast Meyerozyma guilliermondii

Agrobacterium tumefaciens is considered a prominent phytopathogen, though most isolates are nonpathogenic. Agrobacteria can inhabit plant tissues interacting with other microorganisms. Yeasts are likewise part of these communities. We analyzed the quorum sensing (QS) systems of A. tumefaciens strain 6N2, and its relevance for the interaction with the yeast Meyerozyma guilliermondii, both sugarcane endophytes. We show that strain 6N2 is nonpathogenic, produces OHC8-HSL, OHC10-HSL, OC12-HSL and OHC12-HSL as QS signals, and possesses a complex QS architecture, with one truncated, two complete systems, and three additional QS-signal receptors. A proteomic approach showed differences in QS-regulated proteins between pure (64 proteins) and dual (33 proteins) cultures. Seven proteins were consistently regulated by quorum sensing in pure and dual cultures. M. guilliermondii proteins influenced by QS activity were also evaluated. Several up- and down- regulated proteins differed depending on the bacterial QS. These results show the importance of the QS regulation in the bacteria-yeast interactions. HighlightsThe avirulent A. tumefaciens 6N2 has two replicons and a complex QS architecture The profile of QS-regulated proteins is modified in dual cultures with Pa. laurentii The bacterial QS activity alters the proteome of the yeast Pa. laurentii

microbiology↗