Genetic Insights Research Articles

Monogenic Diabetes: Genetic Insight and Precision Therapeutics in the Management of MODY

A monogenic diabetes, specifically, the Maturity-onset diabetes of the young (MODY) is the consequence of the single-gene mutations that are responsible for transcription factors such as HNF1A and GCK taking effect on the insulin synthesis, glucose detection, and the formation of beta cells. This genetic basis necessitates a precise clinical approach for accurate diagnosis and personalized treatment, emphasizing precision medicine. Sulfonylureas are a cornerstone treatment for specific MODY subtypes, especially those with KATP channel mutations, as they enhance insulin secretion and alleviate hyperglycemia by targeting the genetic defect. Genetic testing is crucial in identifying the molecular causes of monogenic diabetes, guiding clinicians in tailoring treatment strategies to optimize therapeutic outcomes. This personalized approach integrates genetic insights with precision therapeutics, revolutionizing the management of monogenic diabetes by offering targeted treatments that improve glycemic control and long-term health outcomes. Healthcare professionals can treat patients more effectively and individually by knowing the genetic pathways behind monogenic diabetes. This advances diabetology toward more effective therapeutic strategies. Even the management of diseases can benefit from the invention of precision medicine as applied to the monogenic diabetes, which allows the personalized methods that lead to a positive effect on patients and provide better care to the patient.

Genetic and Immunological Insights into Tick-Bite Hypersensitivity and Alpha-Gal Syndrome: A Case Study Approach

Tick-bite hypersensitivity encompasses a range of clinical manifestations, from localized allergic reactions to systemic conditions like alpha-gal syndrome (AGS), an IgE-mediated allergy to galactose-α-1,3-galactose (α-Gal). This study investigated the clinical, molecular, immunological, and genetic features of two hypersensitivity cases. Two cases were analyzed: a 30-year-old woman with fixed drug reaction (FDR)-like hypersensitivity and a 10-year-old girl with AGS exhibiting borderline α-Gal-specific IgE. Diagnostic methods included allergen-specific IgE quantification, HLA genotyping, histopathological examination, and the molecular detection of tick-borne pathogens using microfluidic PCR. Case I demonstrated histopathological features of chronic lymphocytic inflammation and eosinophilic infiltrates, with HLA-B13 and DRB113 alleles indicating genetic susceptibility to hypersensitivity, while histological findings suggested a localized FDR-like reaction. Case II exhibited borderline α-Gal-specific IgE, resolving completely with a mammalian-free diet. The presence of HLA-DRB101 and DQB1*05 in the second patient indicated a genetic predisposition to AGS and other atopic conditions. No infectious etiology was identified in either case. These findings emphasize the heterogeneity of tick-related hypersensitivity and the importance of HLA genotypes in susceptibility. Comprehensive molecular, immunological, and genetic profiling offers valuable insights into the mechanisms of hypersensitivity, supporting personalized approaches for the diagnosis and management of tick-induced allergic conditions.

Genetic insight into dissecting the immunophenotypes and inflammatory profiles in the pathogenesis of Sjogren syndrome

BackgroundSjogren syndrome (SS) is a chronic systemic autoimmune disease and its pathogenesis often involves the participation of numerous immune cells and inflammatory factors. Despite increased researches and studies recently focusing on this area, it remains to be fully elucidated. We decide to incorporate genetic insight into investigation of the causal link between various immune cells, inflammatory factors and pathogenesis of Sjogren syndrome (SS).MethodsOur study leveraged the genetic variants of multi-omics statistics extracted from genome-wide association study (GWAS), the University of Bristol and the FinnGen study. We performed a bidirectional Mendelian randomization and mediation study based on randomly allocated instrumental variables to infer causality, followed by external validation with UK Biobank data and Bayesian colocalization.ResultsWe demonstrated that an elevated level of CD27 on IgD + CD24 + B cell, a subset of B cells expressing both IgD and CD24, was associated with a higher risk of SS (OR = 1.119, 95% CI: 1.061–1.179, P < 0.001), while CD3 on CD45RA + CD4 + Treg was a protective factor (OR = 0.917, 95%CI: 0.877–0.959, P < 0.001). Results of meta-analysis and colocalization further supported the significant results identified in the primary analysis. A total of 4 inflammatory cytokines and 7 circulating proteins exhibited potential causal relationships with SS despite no significant result achieved after FDR correction. Finally, results of mediation analysis indicated that CD40L receptor levels had significant mediating effects (β = 0.0314, 95% CI: 0.0004–0.0624, P = 0.0471) at a mediation proportion of 28% (95% CI: 0.364%-55.6%) in causal relationship between CD27 on IgD + CD24 + B cell and SS.ConclusionsBy providing a novel genetic insight into unveiling the roles of autoimmunity and inflammation in Sjogren syndrome, our findings may potentially lead to identifying new clinical biomarkers for disease monitoring and therapeutic targets that offer more effective alternatives for treating this condition. Therefore, our study may provide valuable evidence for future clinical intervention and targeted immunotherapy.

Genetic correlation, pleiotropic loci and shared risk genes between major depressive disorder and gastrointestinal tract disorders.

Major depressive disorder (MDD) is associated with gastrointestinal tract (GIT) disorders, while genetic correlation, pleiotropic loci and shared risk genes remain to be explored. Leveraging genome-wide association study statistics for MDD (n = 170,756), peptic ulcer disease (PUD; n = 16,666), gastroesophageal reflux disease (GORD; n = 54,854), PUD and/or GORD and/or medications (PGM; n = 90,175), irritable bowel syndrome (IBS; n = 28,518), and inflammatory bowel disease (IBD; n = 7045), we determined global and local genetic correlations, identified pleiotropic loci, performed gene-level evaluations, and inferred causal associations using bidirectional Mendelian randomization. We found global correlation of MDD with PUD (rg = 0.444, P = 3.135 × 10-24), GORD (rg = 0.459, P = 2.568 × 10-65), PGM (rg = 0.498, P = 6.094 × 10-114), IBS (rg = 0.621, P = 2.483 × 10-63), and IBD (rg = 0.171, P = 1.824 × 10-5). We identified 12 locally correlated regions between MDD and GIT disorders except for IBD, and one shared region (chr11:111985737-113,103,996) for PGM, GORD, and IBS. We found one pleiotropic locus for PUD, 12 for GORD, 30 for PGM, eight for IBS, and seven for IBD, and five shared loci (rs138786869, rs2284189, rs3130063, rs35789010, rs7568369) for GORD and PGM. We respectively observed 14 and 20 overlapping genes for MDD-GORD and MDD-PGM. We showed genetic liabilities to GORD, PGM, and IBS causally increase MDD risk, while all reverse causalities are significant. Our work identifies genetic architectures shared between MDD and GIT disorders, contributes genetic insights to understand depression in the context of gut-brain interactions, and provides potential targets to treat gastrointestinal symptoms in depressive patients.

Genetic parameters and genomic insights for meat colour traits of Canadian crossbred beef cattle

Genetic parameters and genomic insights for meat colour traits of Canadian crossbred beef cattle

Phylogeographic and genetic insights into Sinonychia martensi: an endemic cave-dwelling harvestman in Beijing

Caves are one of the most exciting environments on earth, often considered an evolutionary laboratory due to the suite of convergent adaptive traits (troglomorphisms) of organisms inhabiting them. Sinonychia martensi Zhang & Derkarabetian, 2021, is the first and only Travunioidea species recorded in China and is endemic to Beijing, being known from multiple caves. However, nothing is known regarding its phylogeographic or evolutionary history. In this study, we assessed the species boundaries of S. martensi from nine caves using morphological and molecular methods to elucidate its phylogenetic position and genealogical relationships. We also investigated the genetic diversity, population genetic structure and demographic history of S. martensi to clarify the population-level relationships and make inferences about historical phylogeography. The results indicate that the species from different caves all belonged to S. martensi but represent different populations. These populations exhibit strong population structure and low genetic diversity. Cave populations may share a common ancestor and multiple independent invasions to different caves. The diversification within S. martensi was likely driven by climate change and subtropical evergreen broadleaf forests associated with the middle Miocene. This study highlights the need for further conservation efforts and exploration in Beijing caves.

Genetic insights into MIS-C Post-COVID-19 in Kuwaiti children: investigating monogenic factors

Genetic insights into MIS-C Post-COVID-19 in Kuwaiti children: investigating monogenic factors

Genetic insights and therapeutic avenues: unraveling the role of polyunsaturated fatty acids as mediators between hypothyroidism and Von Willebrand disease through Mendelian randomization

Genetic insights and therapeutic avenues: unraveling the role of polyunsaturated fatty acids as mediators between hypothyroidism and Von Willebrand disease through Mendelian randomization

Uncovering selection pressures on the IRF gene family in bats' immune system.

Unlike other mammals, bats serve as natural reservoirs for several highly pathogenic viruses without exhibiting symptoms of infection. Recent research has explored the complex mechanisms underlying the balance between bats' antiviral defenses and their pathological responses. However, the evolution of the molecular drivers behind bats' antiviral strategies remains largely unknown. Interferon regulatory factors (IRFs) are essential transcription factors that bind to DNA and regulate the expression of numerous genes involved in antiviral defense, inflammation, immune cell differentiation, apoptosis, and oncogenesis. Our research focused on members of the IRF family, using 17 bat species and four terrestrial mammals available in GenBank. We employed CodeML to detect signs of positive selection through three different models. Statistically significant results were obtained for the IRF-1, IRF-4, IRF-5, IRF-6, and IRF-9 genes, which are known to play pivotal roles in various regulation mechanisms. Specifically, IRF-4 and IRF-5 are key in modulating the inflammatory response, while IRF-1 is essential for antiviral defense in bats, and IRF-9 regulates genes activated by type I interferon. Although the role of IRF-6 in these mechanisms requires further investigation in bats, all these genes show signs of positive selection, suggesting an optimization of the processes they regulate. These findings highlight the adaptive role of IRF elements in enhancing, among other things, the bat immune system, potentially improving their resilience and efficacy. Our study not only provides new genetic insights into bats but also underscores the remarkable molecular evolution within this unique group of mammals.

Causal effects of circulating inflammatory proteins on oral phenotypes: Deciphering immune-mediated profiles in the host-oral axis

BackgroundOral manifestations function as precursors to potential systemic pathologies, signaling early indicators of underlying health complications or immunological dysfunctions. Within these dynamics, circulating inflammatory proteins are recognized as critical mediators in immunopharmacology, bridging holistic health, immune response, and oral health. MethodsWe employed genetic data from genome-wide association studies to perform comprehensive Mendelian randomization (MR) analyses on 91 circulating inflammatory proteins and 17 oral phenotypes. Six MR algorithms and five auxiliary control measures were utilized to estimate the causal effects. Subsequently, the MR-Bayesian model averaging (MR-BMA) approach was conducted to elucidate the priorities in host-oral communication, followed by network analyses to explore the interactions among phenotypes. ResultsAfter multiple corrections, MR identified five genetically predicted proteins associated with oral phenotypes. Specifically, FGF21 was correlated with Nteeth and DMFS; hGDNF with gingival pain; CCL4 with stomatitis; and S100A12 with denture use. The causal associations remained robust in sensitivity analyses. Nine protein-phenotype clusters were prioritized using MR-BMA. Among these, S100A12, FGF19, FGF21, and CCL4 exhibited extensive correlations with various oral phenotypes. ConclusionsOur study offers novel genetic insights into the causal relationships, prioritizations, and connections between circulating inflammatory proteins and oral phenotypes. These findings comprehensively depict immune-mediated proteomic profiles underlying the host-oral axis, providing significant implications for clinical practice, public health, and immunopharmacology.

Genetic insights into the risk of hip osteoarthritis on stroke: A single-variable and multivariable Mendelian randomization.

Hip osteoarthritis has been identified as a potential risk factor for stroke, with previous studies have demonstrated an association between hip osteoarthritis and stroke. This study aims to further elucidate the causal relationship between the two, employing Two-Sample and Multivariable Mendelian randomization methods. SNPs, derived from two extensive GWAS, served as instruments in exploring the association between genetically predicted hip osteoarthritis and stroke risk, utilizing two-sample Mendelian randomization. In Multivariable Mendelian randomization, factors such as cigarettes per day, alcoholic drinks per week, hypertension, body mass index, type 2 diabetes, C-reactive protein, rheumatoid arthritis were incorporated to further account for the independent causal effects of multiple correlated exposures. Two-sample Mendelian randomization analysis revealed that hip osteoarthritis exerts a potential causal effect on any stroke, any ischemic stroke, and cardioembolic stroke, while it did not influence large artery stroke and small vessel stroke. Multivariable MR analysis indicated that the causal effect of hip osteoarthritis on any ischemic stroke and cardioembolic stroke was no longer evident after adjusting for C-reactive protein, and similarly, the effect on any ischemic stroke was not observed after adjusting for type 2 diabetes. However, the effects on any stroke, any ischemic stroke, and cardioembolic stroke remained significant after adjustments for hypertension, alcoholic drinks per week, cigarettes per day, body mass index, and rheumatoid arthritis. The study demonstrated that elevated hip osteoarthritis, as predicted by genetic factors, was potential associated with an increased risk of any stroke, any ischemic stroke, and cardioembolic stroke, but showed no correlation with hypertension, alcoholic drinks per week, cigarettes per day, type 2 diabetes, C-reactive protein, body mass index levels, and rheumatoid arthritis.

Prevalence, genetic variants, and clinical implications of hypocholesterolemia in children.

In contrast to extensively studied hypercholesterolemia, knowledge of hypocholesterolemia is limited. This study aims to assess the prevalence, clinical characteristics, and genetics of children and adolescents with hypocholesterolemia. This national prospective cross-sectional cohort study was part of Slovenia's universal opt-out cholesterol screening program. The first part assessed hypocholesterolemia prevalence among 3538 children aged 5 years, randomly selected at the mandatory check-up. The second part included analysis of demographic and clinical data and genetic testing of 71 individuals with suspected hypocholesterolemia (total cholesterol [TC]<3.0mmol/L [116.0mg/dL]) referred to the Lipid Clinic of University Children's Hospital Ljubljana. The prevalence of hypocholesterolemia among 3538 children was 2.66% (95% CI: 2.13-3.19%). Among the 71 genetically tested individuals with suspected hypocholesterolemia, those with pathogenic variants had lower TC (2.58±0.44mmol/L vs. 2.85±0.42mmol/L [99.77±17.02mg/dL vs. 110.20±16.24mg/dL]; p=0.037) and low-density lipoprotein cholesterol (1.00±0.40mmol/L vs. 1.33±0.40mmol/L [38.67±15.47mg/dL vs. 51.43±15.47mg/dL]; p=0.014) compared to those without such variants. Genetic testing identified pathogenic alterations in 15 subjects, including 4 novel loss-of-function variants in the APOB gene. All but one subject were asymptomatic. This study provides new clinical and genetic insights into hypocholesterolemia. Asymptomatic patients with hypocholesterolemia may not require further evaluation, but additional research is needed to understand hypocholesterolemia better.

Advancing de novo lipogenesis: Genetic and metabolic insights.

De novo lipogenesis (DNL) is the process whereby cells synthesize fatty acids from acetyl-CoA, contributing to steatosis in fatty liver disease. Two new studies, using genetic mouse models, metabolomics, and pharmacology, identified alternative pathways in DNL and unexpected physiological effects when targeting key enzymes in this pathway.

Comparative chloroplast genome analyses provide new insights into molecular markers for distinguishing Arnebiae Radix and its substitutes (tribe Lithospermeae, Boraginaceae).

Arnebiae Radix has long been used in traditional medicine for its pleiotropic properties. However, distinguishing Arnebiae Radix from its substitutes or closely related species has been challenging due to limited phenotypic characteristics. We aimed to identify the molecular markers for distinguishing Arnebiae Radix from its confusion species. Chloroplast genome sequences were used to identify the markers. Chloroplast genomes from 15 species across five genera, including all historically used source plants, were sequenced and assembled. The results revealed significant similarities across all chloroplast genomes in terms of structure, size, gene content, repeat sequences pattens, and codon usage patterns. Phylogenetic analysis showed that the genera Lithospermum, Buglossoides, and Aegonychon formed one clade, while Arnebia guttata, Ar. decumbens, and Ar. euchroma form another. Despite most regions of the chloroplast genomes are highly conserved, three regions-petA-psbJ, ndhF-rpl32, and ycf1-exhibited high variability among difference species, providing high-resolution markers for species identification. Specifically, 376 and 325 species-specific sites were identified in Ar. euchroma and Ar. guttata, respectively. Additionally, four species-specific sites were identified as novel molecular markers, potentially aiding in distinguishing Arnebiae Radix and its confusion or substitute species. This study provided new genetic insights for differentiating Arnebiae Radix and its confusion species, paving the way for further exploration of these medicinal plants.

Haemoglobin revisited: delineating population structure with the world’s first molecular genetic marker used in fisheries research

When haemoglobin genotyping was implemented in the early 1960s to investigate population genetic structure in Atlantic cod ( Gadus morhua ), it became one of the first molecular genetic markers deployed in fisheries research worldwide. However, its suitability was questioned due to its potential for selection. While the issue of neutrality concerned the first population geneticists, markers under selection are now routinely used to study population genetic structure. Here, we revisited haemoglobin genotyping half a decade later to analyse &gt;6000 mature Atlantic cod from 73 spawning locations throughout Norway’s approximately 2500 km coastline. A latitudinal gradient in allele frequencies, with a decrease in the HbI-2 allele towards the south, was observed. Our observed HbI-2 frequencies were consistently slightly lower than data from the 1960s, potentially reflecting adaptive changes to increasing sea temperatures. However, despite this difference, the observed north–south pattern in allele frequencies observed here and in the historical studies overlapped, aligning with current knowledge of population genetic structure in this species. We therefore conclude that this once questioned marker, which provided the first molecular genetic insights into genetic structure in Atlantic cod, provides knowledge consistent with the isolation by distance pattern revealed through decades of research in this species in this region.

The Polygenic Nature of Multiple Sclerosis: Genetic Variants, Immunological Modulation, and Environmental Connections.

Multiple Sclerosis (MS), a debilitating inflammatory disorder of the central nervous system characterized by demyelination, is significantly influenced by polygenic variations. Although the precise cause of MS remains unclear, it is believed to arise from a complex interplay of genetic and environmental factors. Recent investigations have focused on the polygenic nature of genetic alterations linked to MS risk. This review highlights the critical role of these genetic variants in shaping disease susceptibility and progression. Specific Human Leukocyte Antigen (HLA) alleles, such as HLA-DRB1*15:01, HLA-DRB50*101, HLA-DR2+, HLA-DQ6, DQA 0102, and DQB1 0602, are implicated in immune modulation, significantly increasing the risk of developing MS. Additionally, Genome-wide Association Studies (GWAS) have identified non-HLA genetic variants that contribute to MS susceptibility, including IL-2RA (rs2104286), IL-7R (rs6897932), CD40 (rs1883832 T), CD58 (rs2300747), and others, each playing a role in immune regulation and disease progression. Dysfunctions in genes regulating myelin integrity, such as MOG (Myelin Oligodendrocyte Glycoprotein), MAG (Myelin-associated Glycoprotein), and PLP1 (Proteolipid Protein 1), further drive MS pathogenesis. Moreover, viral infections, notably Epstein-Barr Virus (EBV), Human Herpesvirus 6 (HHV-6), and measles virus, may exacerbate the development of MS by triggering immune responses. Understanding the contribution of these genetic and viral factors may shed light on the complex etiology of MS. Polygenic Risk Scores (PRS) provide a valuable tool for estimating MS susceptibility based on the cumulative effect of genetic variants. However, translating these genetic insights into clinical practice requires further validation, including environmental considerations. Investigating MS polygenicity could lead to personalized therapies, enhancing diagnosis, prognosis, and treatment, ultimately improving outcomes for MS patients.

Genetic insights into therapeutic targets for gout: evidence from a multi-omics mendelian randomization study

BackgroundConsidering that the treatment of gout is poor, we performed a Mendelian randomization (MR) study to identify candidate biomarkers and therapeutic targets for gout.MethodsA drug-targeted MR study was performed for gout by integrating the gout genome-wide association studies (GWAS) summary data and cis expression quantitative trait loci of 2,633 druggable genes from multiple cohorts. Summary data-based Mendelian randomization (SMR) analyses based on transcript and protein levels were further implemented to validate the reliability of the identified potential therapeutic targets for gout. Phenome-wide MR (Phe-MR) analysis was conducted in 1403 diseases to investigate incidental side effects of potential therapeutic targets for gout.ResultsEight potential therapeutic targets (ALDH3B1, FCGR2B, IL2RB, NRBP1, RCE1, SLC7A7, SUMF1, THBS3) for gout were identified in the discovery cohort using MR analysis. Replication analysis and meta-analysis implemented in the replication cohort validated the robustness of the MR findings (P < 0.05). Evidence from the SMR analysis (P < 0.05) further strengthened the reliability of the 8 potential therapeutic targets for gout also revealed that high levels of ALDH3B1 reduced the gout risk possibly modified by the methylation site cg25402137. SMR analysis (P < 0.05) at the protein level added emphasis on the impact of the risk genes NRBP1 and SUMF1 on gout. Phe-MR analysis indicated significant causality between 7 gout causal genes and 45 diseases.ConclusionThis study identified several biomarkers associated with gout risk, providing new insights into the etiology of gout and promising targets for the development of therapeutic agents.

Leptin Signaling: Decoding of Genetic Pathways using Bioinformatics; Shaping Bariatric Surgery Outcomes

Background: Leptin, a hormone central to energy homeostasis and appetite regulation, plays a pivotal role in obesity and metabolic health. Single nucleotide polymorphisms (SNPs) in the leptin (LEP) and leptin receptor (LEPR) genes influence leptin signaling and may explain variability in outcomes following bariatric surgery. This bioinformatics-driven study examines the role of LEP and LEPR SNPs in modulating weight loss, metabolic changes, and hormonal responses post-surgery. Methods: A total of 55 leptin SNPs and 216 leptin receptor SNPs were assessed for functional impact using SIFT, PolyPhen-2, and Mutation Assessor. Pathway enrichment analyses using DAVID and g:Profiler identified biological processes and signaling pathways linked to leptin function. Protein-protein interaction (PPI) networks were constructed via STRING and visualized in Cytoscape to explore molecular interactions. Statistical models evaluated associations between SNPs and surgical outcomes, including weight loss and metabolic improvements. Key pathways with false discovery rates (FDR) &lt; 0.01 were highlighted to emphasize significance. Results: Bioinformatics analyses revealed LEP and LEPR as critical variants associated with bariatric surgery outcomes. Specifically, LEP rs7799039 G allele carriers exhibited diminished weight loss (p &lt; 0.05) and metabolic improvements. Functional prediction tools consistently indicated deleterious effects on leptin signaling. Pathway enrichment analyses identified leptin's involvement in critical pathways, including the adipocytokine signaling pathway (hsa04920, 2 of 68 genes, strength = 2.46, FDR = 0.0042)," "AMPK signaling pathway (hsa04152, 2 of 120 genes, strength = 2.22, FDR = 0.0064)," and "non-alcoholic fatty liver disease (NAFLD) pathway (hsa04932, 2 of 146 genes, strength = 2.13, FDR = 0.0064). PPI networks underscored leptin’s interactions with key metabolic and inflammatory regulators, such as TNF-α and IL-6, suggesting a broader impact on energy metabolism and inflammation. Conclusion: This study demonstrates the utility of bioinformatics in elucidating the genetic basis of variable bariatric surgery outcomes. LEP and LEPR SNPs modulate critical pathways influencing weight loss and metabolic responses. Integrating genetic insights with bariatric care could advance precision medicine approaches for obesity management. Future studies with larger cohorts are warranted to confirm these findings and strengthen predictive models.

Genetic Insights into Facial Variation and Craniofacial Development: Unraveling the Interplay of Genes, Expression Patterns, and Evolutionary Significance.

The development of genome technology has opened new possibilities for comparative primate genomics. Non-human primates share approximately 98% genome similarity and provides vital information into the genetic similarities and variances among species utilized as disease models. DNA study links unique genetic variations to common facial attributes such as nose and eyes. This is because of higher adaptation and improved cognitive skills over these sensual areas. Non-protein coding sequences represent approximately 85% of the human DNA under evolutionary restrictions, and the primary part of this is the cis regulatory regions. In this study, a total of 103 tissue specific human enhancers were finalized with help of VISTA Enhancer Browser that showed distinctive expression in the facial tissues and their orthologs were collected. A total of 43 out of 190 transcription factors from TRANSFAC were seen as binding in both Human and Non-Human primate enhancers. It was observed that factor binding sites of 7 of the 43 transcription factors were exclusively gained in the human eye and nose enhancers (Oct, Pax, Sox, MyoD, Foxd3, cRel and Gata). Furthermore, we performed molecular docking through PyMol; DNA & Protein (pdb) structures were modelled by SCFBio & SWISSMODEL respectively to observe interactions of the transcription factors, either by placing the contact surface of the protein exclusively to identify the DNA, to enable a representation to gain information about identification and genetic expression.

Genetic diversity and structure of 15 full-sib families of Litopenaeus vannamei based on SSR markers

To clarify the genetic diversity and structure of the nucleus population of F1-generation Litopenaeus vannamei, this study utilized 15 pairs of highly polymorphic microsatellite primers to analyze the simple sequence repeat (SSR) markers and genetic diversity in 15 full-sib families of L. vannamei. A total of 112 alleles (Na) and 60.453 effective alleles (Ne) were identified among the selected 15 SSR loci, with the average polymorphic information content (PIC) of 0.648. The average Ne, observed heterozygosity (Ho), and expected heterozygosity (He) in the 15 F1 families varied from 1.925 to 2.626, 0.425 to 0.783, and 0.403 to 0.572, respectively. The 15 full-sib families were primarily clustered into three categories in the phylogenetic analysis, with the genetic distance between families ranging from 0.252 to 0.574. Additionally, the genetic differentiation coefficient (Fst) among the families varied from 0.112 to 0.278, indicating substantial genetic differentiation. Overall, this study suggested that the genetic diversity of the 15 full-sib families was moderate, providing valuable genetic insights for the subsequent breeding initiatives aimed at enhancing the tolerance of L. vannamei to high levels of soybean meal.