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Szigeti, A.

Publications and source records attributed to Szigeti, A..

3 recordsLinked to original sources

Host and microbial factors influence bacterial colonization of the honey bee gut

The guts of many animals are colonized by host-specific microbes, yet the extent to which host filtering (host-derived constraints) shapes microbial colonization and host specificity remains poorly understood. Here, we used gnotobiotic honey bees (Apis mellifera) as a model system to systematically assess the colonization potential of a phylogenetically and ecologically diverse panel of 56 bacterial strains, spanning native symbionts, opportunistic bee-associated taxa, gut microbes from other bee species, and non-bee environmental isolates. Bacterial load and colonization frequency were quantified by strain-specific qPCR seven days post-inoculation, in monocolonization and in the presence of a synthetic community composed of native honeybee core bacteria. Bacterial load was highest for native strains and declined with increasing phylogenetic distance from native symbionts. Co-colonization with the synthetic community reduces load across all groups, but native strains were least affected. Across strains, completeness of KEGG metabolic pathways correlated with bacterial load in some ecological groups; however, metabolic capacity alone did not fully explain colonization patterns, either in monocolonization or under competitive conditions. A key finding was that in vitro sensitivity to antimicrobial peptide (AMPs; apidaecin, abaecin, defensins, hymenoptaecin) varied widely among strains and was highest in closely related bee-associated bacteria. Notably, even highly successful colonizers such as Gilliamella and Snodgrassella were AMP-sensitive. AMP sensitivity showed a negative correlation with bacterial load, but not with the frequency of host colonization. These findings suggest that AMPs modulate symbiont abundance rather than acting as strict barriers to colonization. Overall, our results reveal that host filtering in the bee gut is multifaceted, integrating immune-mediated barriers, microbial traits, and competitive interactions.

microbiology↗

Unveiling the Origins and Genetic Makeup of the 'Forgotten People': A Study of the Sarmatian-Period Population in the Carpathian Basin

SO_SCPLOWUMMARYC_SCPLOWThe nomadic Sarmatians dominated the Pontic Steppe from 3rd century BCE and the Great Hungarian Plain from 50 CE until the Huns 4th-century expansion. In this study, we present the first large-scale genetic analysis of 156 genomes from 1st- to 5th-century Hungary and the Carpathian foothills. Our findings reveal minor East Asian ancestry in the Carpathian Basin (CB) Sarmatians, distinguishing them from other regional populations. Using F4-statistics, qpAdm, and IBD analysis, we show that CB Sarmatians descended from Steppe Sarmatians originating in the Ural and Kazakhstan regions, with Romanian Sarmatians serving as a genetic bridge between the two groups. We also identify two previously unknown migration waves during the Sarmatian era and a notable continuity of the Sarmatian population into the Hunnic period, despite a smaller influx of Asian-origin individuals. These results shed new light on Sarmatian migrations and the genetic history of a key population neighbouring the Roman Empire.

genetics↗

Epigenetic Regulation Explains The Functionality Behind Colon Cancer Specific Biomarker Septin9

Despite advancements in early cancer detection and prevention methods, colorectal cancer (CRC) remains a significant global health problem. It is the third most common cancer and the second leading cause of cancer-related deaths worldwide. Additionally, there has been a marked increase of incidence in young adults, and the reasons for this tendency are not fully understood. Therefore, the need for more effective diagnostic methods of assessing disease risk at early stage is crucial. One of the newly developed blood-based circulating biomarkers with promising potential is the short hypermethylated region located at the Septin9 intronic region. Several clinical studies have proven its performance and applicability. However, the molecular mechanism behind this consistent and recurrent feature present in most of the CRC and related precancerous stages and why it is specific and advantageous for CRC development are poorly understood. Here, we used comprehensive epigenetic and gene expression profile analyses from different sources of human clinical samples and cell line data to link specific hypermethylation events at the Septin9 intronic loci, which initiate alternative transcription of the Septin9 gene. Through our investigation of TCGA-COAD RNA-seq samples (n=287), we found that there was no significant difference in global Septin9 levels between normal and tumor samples. However, we did observe a significant alteration in the transcript variant ratio between v1 and v2, suggesting the use of an alternative promoter. Our findings were further supported by our analysis of ATAC-seq data, which revealed that the v2 promoter conferred higher chromatin accessibility, which correlated with the expression of the v2 isoform. However, this was not supported by promoter or enhancer activity as measured by H3K27ac signals. Hypermethylation at the v2 promoter was confirmed in tumor samples, providing a possible explanation for the switch in variants. Protein sequence analysis confirmed small differences between Septin9 variant A(v1) and B(v2). However, AlphaFold2 indicates a substantial difference at the N terminus, which could impact protein phosphorylation. We hypothesize, that variant A (v1) and variant B (v2) are required for normal cell functions but shifting the balance towards v1 is more favourable for the tumor. Although very little is known about Septin9 and its function in CRC biology, we are confident that our study will help to emphasize the importance of understanding regulatory mechanisms behind tumor-specific biomarkers and helps to improve the application.

cancer biology↗