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Royal jelly is a gelatinous nutrient secretion produced by the mandibular glands of young worker honey bees and has a critical role in honey bee life. In the honey bee colonies, queen and worker honey bees have very different morphologies and behaviors due to their diet in the larval period, despite having the same genome. In comparison, queen bees formed from larvae that feed royal jelly exclusively, and worker bees formed from larvae that feed on much less royal jelly. DNA methylation has been shown to play a critical role in the development of queen and worker honeybees. Alterations in DNA methylation, one of the epigenetic mechanisms defined as hereditable nucleotide modifications that occur in gene expression without changes in the DNA sequence, are closely related to many diseases, especially cancer. Hypermethylation of CpG islands located in the promoter regions of genes causes gene silencing and tumor suppressor genes epigenetically have silenced in cancer. The inactivation of tumor suppressor genes disrupts nearly all cellular pathways in cancer. In contrast to genetic alterations, gene silencing by epigenetic modifications may potentially be reversed and used in cancer treatment. Royal jelly, which causes epigenetic changes in bee colonies, has the potential to cause a change in cancer cells. In our study, royal jelly's effects on DNA methyltransferase enzyme and gene methylation of RASSF1A tumor suppressor were investigated in human cancer cell lines (HeLa, HT29, and A549), and modifications in the gene expression profile of royal jelly were determined by next generation sequencing.

Non-coding, single-stranded RNA molecules known as microRNAs (miRNAs) regulate gene expression via mRNA degradation after transcription. As a result, they affect a number of pathways in organisms that are important for both health and disease. miRNAs can be utilized as potential diagnostic, prognostic, and therapeutic biomarkers for neurodegenerative diseases such as Amyotrophic Lateral Sclerosis (ALS). Neuronal cells are highly dependent on mitochondria, and mitochondrial dysfunction has been linked to neurodegenerative diseases. Pathological changes in ALS are associated with disruptions in mitochondrial structure, bioenergetics, and calcium homeostasis. In this study, we used an in silico approach to identify miRNAs associated with mitochondrial dysfunction in ALS based on target genes that are implied in both ALS and mitochondrial dysfunction. A literature search revealed the genes SOD1, FUS, TARDBP, C9orf72, CHCHD10, OPTN, VCP, TBK1 and BCL2 that cause mitochondrial dysfunction and are involved in the pathogenesis of ALS. Pathway enrichment analyses using Enrichr, g:Profiler, and CROssBAR tools confirmed that the identified genes have significant associations with ALS, mitochondrial dysfunction, and neuron differentiation. In silico miRNA predictions have been made using the databases miRWalk, miRTargetLink, TargetScan, and miRNet. A Venn diagram tool was used to select common miRNAs, and finally 28 miRNAs were discovered. One set of 28 miRNAs were subjected to set analysis using the miRNet and TAM tools for functional and enrichment analyses, respectively. In both databases, three common miRNAs, hsa-miR-9-5p, hsa-miR-141-3p and hsa-miR-125b, were found to be linked to ALS.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible coronavirus and has caused a pandemic of acute respiratory disease, named ‘coronavirus disease 2019’ (COVID-19). COVID-19 has a deep impact on public health as one of the most serious pandemics in the last century. Tracking SARS-CoV-2 is important for monitoring and assessing its evolution. This is only possible by detecting all mutations in the viral genome through genomic sequencing. Moreover, accurate detection of SARS-CoV-2 and tracking its mutations is also required for its correct diagnosis. Potential effects of mutations on the prognosis of the disease can be observed. Assignment of epidemiological lineages in an emerging pandemic requires efforts. To address this, we collected 1000 SARS-CoV-2 samples from different geographical regions in Turkey and analyze their genome comprehensively. To track the virus across Turkey we focus on 10 distinct cities in different geographic regions. Each SARS-CoV-2 genome was analyzed and named according to the nomenclature system of Nextclade and Pangolin Lineage. Furthermore, the frequency of the variations observed in 10 months was also determined by region. In this way, we have observed how the virus mutations and what kind of transmission mechanism it has. The effects of age and disease severity on lineage distribution were other considered parameters. The temporal rates of SARS-CoV-2 variants by time in Turkey were close to the global trend. This study is one of the most comprehensive whole genome analyses of SARS-CoV-2 that represents a general picture of the distribution of SARS-CoV-2 variations in Turkey in 2021.Author SummarySince the outbreak of the COVID-19 pandemic in 2019, the viral genome of SARS-CoV-2 was analysed intensively all over the world both to detect its zoonotic origin and the emerging variants worldwide together with the variants’ effect on the prognosis and treatment, respectively, of the infection. Remarkable COVID-19 studies were also made in Turkey as it was in the rest of the world. To date, indeed, almost all studies on COVID-19 in Turkey either sequenced only a small number of the viral genome or analysed the viral genome which was obtained from online databases. In respect thereof, our study constitutes a milestone regarding both the huge sample size consisting of 1000 viral genomes and the widespread geographic origin of the viral genome samples. Our study provides new insights both into the SARS-CoV-2 landscape of Turkey and the transmission of the emerging viral pathogen and its interaction with its vertebrate host.

Multiple Sclerosis (MS) is an autoimmune and central nervous system disease characterized by an inflammatory demyelinating process in the brain. Although the exact cause of MS is still unclear, environmental, and genetic factors are known to play a role in the development of disease. New molecular markers must be identified to understand the mechanism of disease formation and progression. We investigated the effects of MS-related non-synonymous single-nucleotide polymorphisms (nsSNPs) on the structure and function of identified proteins in this study.Missense variations associated with MS were extracted from the NHGRI-EBI GWAS database. Functional and structural analysis of nsSNPs on mapped genes was performed using g:Profiler, Wikipathway, KEGG, Reactome and Gene ontology programs (p 0.05 was accepted statistically significant). Amino acid sequence-based analysis was performed to identify deleterious variants by using PROVEAN and PredictSNP tools. Finally, protein structure analyzes were performed on deleterious protein variants by DynaMut, Mutabind2 and Missense3D servers to identify changes in protein stability and flexibility.10 target nsSNPs were identified. Among these rs34536443, rs10936599, rs2293152, rs11808092, rs1129183 were found deleterious according to amino acid sequence-based analysis. Furthermore, structure-based analyses show that TYK2 (P1104A), MYNN (H6Q), EVI5 (Q612H), and LZTFL1 (D246N) substitutions increase protein stability and decrease structure flexibility, whereas STAT3 (R426G) substitution decreases protein stability and increases structure flexibility.We revealed that identified nsSNPs have potential effects on stability and flexibility of the target proteins. The prominent target genes are thought to have significant impacts on the pathogenesis of MS. Further in vitro and in vivo studies are required to validate our in silico results.

MicroRNAs (miRNAs) regulate gene expression post-transcriptionally via mRNA degradation. As a result, they have an impact on a variety of pathways in organisms that are important for both health and disease. miRNAs can be used as potential diagnostic, prognostic and therapeutic biomarkers for immune and nervous system-related diseases such as MS.Differentially expressed miRNAs from peripheral blood samples of patient and control groups were selected from NCBI GEO Datasets using GEO2R. Common miRNAs and their related pathways were analyzed using miRNet, miRWalk, DIANA mirpath, KEGG pathway. Target genes and their protein-protein interactions were also evaluated using STRING and GeneMANIA.We found 12 common miRNAs, four of which were determined to be more important in MS-related pathways such as the immune and neural signaling networks. These include pathways neurotrophin, JAK-STAT, B cell receptor, ErbB, MAPK, Fc gamma R-mediated phagocytosis, Chemokine and T cell receptor signaling pathways. Moreover, target gene analyses were performed and MAPK1, PIK3CD, PIK3R1, PIK3R2, PIK3R3, PIK3R5, AKT2, SOS2, RAF1 genes were found. Further analysis showed that the identified genes and related pathways have interactions at multiple points, and that the overlapping points are commonly found in the PI3K-Akt signaling pathway.In this paper, MS-related miRNAs and their potential effects on related pathways were evaluated. This study can be used for understanding MS pathogenesis and provides new tools for the discovery of new therapies.