Genetic Variation Research Articles

Life history strategies complement niche partitioning to support the coexistence of closely related Gilliamella species in the bee gut.

The maintenance of bacterial diversity at both species- and strain-levels is crucial for the sustainability of honey bee gut microbiota and host health. Periodic or random fluctuation in diet typically alters the metabolic niches available to gut microbes, thereby continuously reshaping bacterial diversity and interspecific interactions. It remains unclear how closely related bacteria adapt to these fluctuations and maintain coexistence within the bee gut. Here, we demonstrate that the five predominant Gilliamella species associated with Apis cerana, a widely distributed Asiatic honey bee, have diverged in carbohydrate metabolism to adapt to distinct nutrient niches driven by dietary fluctuation. Specifically, the glycan-specialists gain improved growth on a pollen-rich diet, but are overall inferior in competition to non-glycan-specialist on either a simple sugar or sugar-pollen diet, when co-inoculated in the bee host and transmitted across generations. Strikingly, despite of their disadvantage in a high-sugar condition, the glycan-specialists are found prevalent in natural A. cerana guts. We further reveal that these bacteria have adopted a life history strategy characterized by high biomass yield on a low-concentration sugar diet, allowing them to thrive under poor nutritional conditions, such as when the bee hosts undergo periodical starvation. Transcriptome analyses indicate that the divergence in life history strategies is attributed to gene expression programming rather than genetic variation. This study highlights the importance of integrative metabolic strategies in carbohydrate utilization, which facilitate the coexistence of closely related Gilliamella species in a changing bee gut environment.

Abstract TMP51: Association between genetic variation and acute stroke characteristics

Introduction: Strokes lead to acute deficits with wide-ranging severity. Genetic variation may explain some of these inter-subject differences. The current report examined the relationship that candidate genetic variants have with acute injury and acute behavioral deficits. We hypothesized that variants known to be associated with poorer stroke recovery would also be associated with more a severe acute presentation. Methods: Infarcts were outlined on clinical scans acquired during acute stroke admission as part of the STRONG (“Stroke, sTress, RehabilitatiON, and Genetics”) study and resampled to MNI152 brain standard space. Multivariable linear regression modeling was used to examine association with genetic measures known to be related to stroke outcome: 3 single nucleotide polymorphisms (SNPs): BDNF (rs6265), ACE (rs4291), and FAAH (rs324420), plus ApoE e4 and ApoE e2; a dopamine polygene score was also explored. Acute injury (infarct volume) and acute deficits (NIHSS score, grip strength, and acute stress disorder inventory (ASDI)) were each examined as the dependent measure in separate models that used age, gender, and ancestry as covariates. To understand where in the brain these relationships occurred, voxel lesion symptom mapping (VLSM) was used to test for associations between acute injury and each genetic measure. Results: In 448 subjects (age 63.4±14.4 yr (mean±SD), 43.1% females), lesion volume ranged from 0.46 to 535.13 cc and involved cortical grey matter in 63% of patients. Larger lesion volume was associated with presence of the ACE SNP (β=8.77, p=0.03); lower NIHSS score, with ApoE e4 (β=-1.69, p=0.04); greater grip strength, with ApoE e2 SNPs (β=6.78, p=0.03); and higher ASDI, with the ACE SNP (β=0.56, p=0.05). VLSM revealed that acute injury to the postcentral gyrus was significantly more likely in the presence of the ACE SNP (z=-3.5), and that acute injury to the calcarine fissure was significantly more likely in the presence of the BDNF SNP (z=-2.53). Conclusions: Genetic variants known to be associated with differences in stroke recovery are also related to acute stroke deficits and injury. In particular, a common variant in the gene for ACE was associated with differences in lesion volume and location, findings that may suggest a personalized medicine approach to acute therapy. Measures of genetic variability may be useful to understand inter-subject differences in acute injury and symptom severity, and may have therapeutic implications.

Functional analysis of key members affecting egg production in the transglutaminase gene family in chickens.

The transglutaminase (TGMs) family plays a crucial role in regulating mammalian reproduction, yet its impact on poultry reproductive traits has not been extensively studied. In this study, we identified eight members of the TGMs family in chickens and examined the contributions of genetic variations of coagulation factor XIII A chain (F13A1), transglutaminase 4 (TGM4), and LOC101749664 to selective breeding in commercial layers through genetic variation response pattern analysis. Transcriptome data from various tissues of high- and low-egg-yielding Gushi chickens revealed significant positive correlations between the mRNA expression levels of TGM4 and F13A1 genes and egg production (P < 0.05). Genotype-phenotype correlation analysis showed that 26 single nucleotide polymorphisms (SNPs) within genomic sequences of TGM4 and F13A1 genes exhibited significant associations with egg production traits across different laying periods. Additionally, spatiotemporal expression patterns of TGM4 in ovarian follicles between high- and low-laying chicken breeds determined by RT-qPCR highlighted the pivotal role of TGM4 in follicle development. Functionally, the gain-of-function assay demonstrated that TGM4 promoted granulosa cell proliferation, inhibited apoptosis, and enhanced progesterone synthesis. In conclusion, this is the first study to elucidate the role of the TGMs gene family in regulating egg production in chickens, offering new insights for the selective breeding of layers with improved egg-laying traits.

Stages and causes of the evolution of language and consciousness: A theoretical reconstruction.

This article presents a refinement of theoretical explanations of the main stages of linguistic and cognitive evolution in anthropogenesis. The concepts of language, consciousness, self-consciousness, the self, the unconscious, the subconscious, and the relation between free will and determinism remain at the center of active and complex debates in philosophy and neuroscience. A basic theoretical apparatus comprising the central concepts of "concern" and "providing structure" (an extension of the biological concept of "adaptation") develops the paradigm of the extended evolutionary synthesis. Challenge-threats and challenge-opportunities are invariably associated with concerns pertaining to sustenance, safety, sexuality, parenthood, status, and emotional support. The consolidation of successful behavioral tries (tries), in response to these challenges occurs through the formation of a variety of providing structures including practices, abilities, and attitudes. These structures are formed through mechanisms of interactive rituals and internalization. These novel practices facilitate the transformation of both techno-natural environmental niches and group niches. The emergence of new structures gives rise to new challenges and concerns, which in turn necessitate undertaking of new tries. In the context of African multiregionalism, hominin groups and populations that experienced favorable periods of demographic growth, active migration, genetic, technological, and skill exchange also underwent significant demographic disasters. During the most unfavorable bottleneck periods only the most advanced groups, populations and species survived. The achieved potential for these abilities was consolidated as complexes of innate assignments in gene pools through the Baldwin effect and the multilevel selection. This logic provides an explanation for the main stages of language and speech complication (from holophrases and articulation to complex syntax), as well as the emergence of new abilities of consciousness (from the expansion of attention field to self-consciousness and the "I"-structure).

The potential of MAO inhibitors as chemotherapeutics in cancer: A literature survey.

Drug resistance in cancer is determined by genetic mutations and adaptations of tumor cells to drug treatments, raising a challenge in the treatment of cancer. Factors such as prolonged drug exposure, genetic variability among patients, and tumor heterogeneity have been established as contributors to rising incidence of drug resistance, prompting ongoing research into alternative therapies and combination treatments to overcome this challenge. Monoamine oxidases (MAOs), including both isoforms MAO-A and MAO-B, are mitochondrial enzymes responsible for the catabolism of monoamine neurotransmitters such as dopamine, norepinephrine, and serotonin. While these enzymes play a pivotal role in the nervous system, their role in tumorigenesis has garnered increasing attention in the last years. Recent studies, in fact, have highlighted the potential of MAO inhibitors (MAOIs) as antitumor agents, emphasizing their use as standalone treatments or in synergy with traditional anticancer therapies, focusing on pathways involved in tumorigenesis. This review aims to provide a comprehensive overview of MAOIs currently under study for their potential antitumor activity, focusing on their structural characteristics, mechanisms of action, and efficacy in preclinical and clinical settings, referencing key articles in the field.

Optimization of Clozapine Treatment: Study of Variables Affecting Response in Uruguayan Patients With Schizophrenia.

Clozapine is the recommended drug for treatment-resistant schizophrenia. Drug response could be affected by numerous factors such as age, sex, body mass index, co-medication, consumption of xanthine-containing beverages, smoking, and genetic variants of the enzymes involved in clozapine metabolism (CYP1A2, CYP3A4, and, to a lesser extent, CYP2C19 and CYP2D6). This study evaluated genetic and nongenetic variables that may affect clozapine plasma concentrations in Uruguayan patients with schizophrenia. Demographic data including sex, age, ethnicity, body weight, smoking habit, concomitant medication, and xanthine consumption were collected through a data collection form. Clozapine and norclozapine concentrations were determined using an HPLC system equipped with a UV detector. Genetic variants were determined through next-generation sequencing using Illumina sequencing technology and a panel of DNA probes. Fifty patients were included in the study. After evaluation, only tobacco use and obesity had a significant impact on clozapine exposure (P < 0.05). The high prevalence of the genetic variant CYP1A2*1F may account for the significant impact that tobacco smoking has on clozapine concentrations. Some common adverse effects observed in this study depend on clozapine plasma concentrations, such as constipation and sialorrhea. These types of studies provide the clinician with tools to optimize clozapine therapy, attempting to use the minimum effective dose and attenuating the burden of concentration-dependent adverse reactions.

Genetic variants and clinical factors affecting the response to 5-fluorouracil–based treatment in Chilean patients with advanced colorectal cancer.

114 Background: Colorectal cancer (CRC) ranks as the second most common cancer in Chile, affecting both men and women. Late diagnosis results in approximately 25% of patients presenting with metastatic disease, with a five-year survival rate of about 14%. Standard treatment includes tumor resection followed by adjuvant chemotherapy, commonly involving 5-fluorouracil (5-FU) combined with drugs like oxaliplatin or irinotecan. However, patient responses to 5-FU vary greatly due to genetic polymorphisms in enzymes like thymidylate synthase (TYMS) and dihydropyrimidine dehydrogenase (DPD), which affect the drug's pharmacokinetics and pharmacodynamics. Polymorphisms in genes related to oxaliplatin elimination and efficacy, such as glutathione-S-transferases (GSTs) and DNA repair enzymes, also play a role. However, the relationship between genetic variants and treatment outcomes remains unclear, often varying by population and cancer stage. Although predictive models for treatment response and risk exist for various diseases, no comprehensive model combining genetic and clinical variables to predict chemotherapy safety in Chilean CRC patients has been developed. Objective: This study aimed to identify relevant genetic variants in the genes TYMS , TYMP , DPYD , GSTP1 , MTHFR , ERCC2 , ABCB1 , ABCC2 , ABCC4 , and ABCG2 , which, along with clinical variables, could help create a predictive model for the safety of 5-FU-based chemotherapy in advanced CRC patients. Methods: A retrospective nested case-control study was conducted on 82 advanced CRC patients. Sixteen genetic variants were analyzed to assess their influence on adverse reactions (ADRs) and their severity, using logistic regression to identify potential associations. Multivariate models were developed to predict chemotherapy safety. Results: Among the 16 variants analyzed in 82 patients, several key findings emerged: The G allele of GSTP1 (rs1695) was found to be protective against neuropathy (OR = 0.147; p = 0.012) but increased the risk of mucositis (OR = 2.27; p = 0.036). The C allele of DPYD (rs1801265) was associated with an elevated risk of neuropathy (OR = 4.50; p = 0.05). The TYMS deletion (rs151264360) provided protection against cutaneous (OR = 0.029; p &lt; 0.0001) and hematological ADRs (OR = 0.098; p = 0.005). Additionally, TYMS deletion was protective against severe toxic ADRs (OR = 0.098; p = 0.005). Two multivariate models were created to predict anemia (p = 0.027) and pain (p = 0.01) development. Conclusions: This study represents an initial step toward developing predictive models for ADRs related to 5-FU, such as neuropathy, mucositis, and hematological and skin toxicities. In the future, these findings may contribute to pharmacogenetic-based dose adjustment models aimed at reducing ADRs in Chilean CRC patients undergoing 5-FU-based treatment.

Genetic and Phenotypic Variability in Siblings With Friedreich Ataxia

Genetic and Phenotypic Variability in Siblings With Friedreich Ataxia

Copper and iron as unique trace elements linked to fibromyalgia risk.

Fibromyalgia (FM) is a prevalent chronic pain condition with a complex and not fully understood etiology. Abnormal metabolism of trace elements is suspected to play a role in the pathogenesis of FM, though the exact relationships have yet to be clarified. This study employed Mendelian randomization (MR) to assess potential causal relationships between 15 major trace elements and the risk of FM, focusing on the specific roles of elements that show significant associations. Genetic instrumental variables (single nucleotide polymorphisms, SNPs), related to these trace elements and FM were extracted from genome-wide association studies (GWAS). Analyses were performed using various methods including inverse-variance weighting (IVW), MR Egger, weighted median, weighted mode, and simple mode. Furthermore, multivariable analysis controlled for selenium as a potential confounder to evaluate the independent associations of copper (Cu) and iron (Fe) with FM risk. Two-sample MR analysis indicated a positive association between Cu and increased risk of FM (IVW: OR = 1.095, 95% CI: 1.015 to 1.181, P = 0.018), and a negative association between Fe and FM risk (IVW: OR = 0.440, 95% CI: 0.233 to 0.834, P = 0.011). These associations remained significant in the multivariable analysis, highlighting the independent effects of Cu and Fe. No significant correlations were observed with other trace elements such as selenium and zinc. This study provides new evidence of the roles of Cu and Fe in the pathophysiology of FM and underscores the importance of considering trace elements in the prevention and treatment strategies for FM. Future research should further validate these findings and explore the specific biological mechanisms through which Cu and Fe influence FM risk.

Characteristics of patients with autosomal polycystic kidney disease reaching kidney failure by age 40.

Autosomal dominant polycystic kidney disease (ADPKD) demonstrates broad genetic and phenotypic variability, with kidney failure (KF) occurring across a wide age spectrum. Despite several predictor tools, there remains a need to identify factors associated with rapid disease progression. This study describes the phenotypic characteristics of a multicentric cohort experiencing early-onset KF by age 40. This retrospective, multicenter cohort study analyzed longitudinal data of rapidly progressive ADPKD patients (n = 199). The prevalence of established risk factors was compared to nine existing ADPKD cohorts (ntotal = 6782) with KF after 40years of age. We examined the longitudinal impact of early hypertension and urological events on the risk of developing KF. The median age at ADPKD diagnosis was 22.3years (IQR, 16.5-28.6) and median age of KF was 35.6years (31.7-38.0). Hypertension was observed in 68.1% of cases, with early-onset hypertension being more common among those with accelerated progression towards KF. Urological events were present in 60.1% of cases, with a high burden of gross hematuria (30.4%). Existing ADPKD cohorts had a mean age of 45.5years, with weighted prevalences of hypertension (71.1%), kidney stones (22.4%), hematuria (22.9%), and urinary tract infections (22.8%). Extrarenal manifestations were less prevalent compared to other ADPKD cohorts. This study outlines a cohort of ADPKD patients with accelerated disease progression, reaching KF before age 40. Hypertension and urological events were highly prevalent at a young age, emphasizing the importance of early and regular blood pressure monitoring.

Association between genetic variation rs57095329 of microRNA-146a and development of cognitive impairment after anesthesia: a case-control study in a Chinese Han population.

The latest studies have demonstrated that aberrant expression of microRNA-146a is related to cognitive decline. The rs57095329 polymorphism occurring in the miR-146a promoter modulates its expression and causes downstream pathogenicity. A case-control study in a Chinese Han population was established to investigate the genetic association between the miR-146a rs57095329 polymorphism and postoperative cognitive dysfunction (POCD). 242 patients with POCD and another 238 non-POCD cases were enrolled in the case-control study. Serum miR-146a levels were detected by qRT-PCR. miR-146a rs57095329 polymorphism was genotyped using the ABI PRISM SNaPshot method. The genetic association between the rs57095329 polymorphism and POCD was assessed by regression analysis. No significant difference was detected for age, gender and BMI between POCD and non-POCD groups. MiR-146a rs57095329 polymorphism revealed significant generic associations with POCD in both dominant and recessive models, and the AA genotype may increase the risk of developing POCD. qRT-PCR indicated the upregulation of miR-146a level in POCD group. Serum levels of miR-146a and inflammatory factors were higher in rs57095329 AA genotype carriers than in AG/GG genotype carriers. Rs57095329 polymorphism was independently associated with the development of POCD. In conclusion, miR-146a rs57095329 polymorphism was associated with POCD in the Chinese Han population. The rs57095329 AA genotype was the causative genotype for POCD and was related to the upregulation of miR-146a and inflammatory factor levels.

Linking plant genes to arthropod community dynamics: Current progress and future challenges.

Plant genetic variation can play a key role in shaping ecological communities. Prior work investigated the effects of coarse-grain variation among plant genotypes on their diverse arthropod communities. Several recent studies, however, have leveraged the boom of genomic resources to study how genome-wide plant variation influences associated communities. These studies have demonstrated that the effects of plant genomic variation are not just detectable but can be important drivers of arthropod communities in natural ecosystems. Field common gardens and lab-based mesocosm experiments are also revealing candidate genes that have large effects on arthropod communities. While we highlight these exciting results, we also discuss key challenges to address in future research. We argue that a major hurdle lies in the integration of genomic tools with hierarchical models of species communities (HMSC). HMSC are generative models that provide the opportunity to not only better understand the processes underlying community change, but to also predict community dynamics. We also advocate for future research to apply models of genomic prediction to explore the genetic architecture of arthropod community phenotypes. We hypothesize that this genetic architecture will follow an exponential distribution, where a few genes of large effect, but also many genes of small effect, contribute to variation in arthropod communities. The next generation of studies linking plant genes to community dynamics will require interdisciplinary collaborations to build truly predictive models of plant genetic and arthropod community change.

Genetic Diversity and Population Structure of Phyllosphere-Associated Xanthomonas euvesicatoria Bacteria in Physalis pubescens Based on BOX-PCR and ERIC-PCR in China

&lt;i&gt;Xanthomonas euvesicatoria&lt;/i&gt; has become a serious problem in &lt;i&gt;Physalis pubescens&lt;/i&gt;, leading to substantial crop losses. In our previous investigation, we used rapid molecular detection techniques to identify &lt;i&gt;X. euvesicatoria&lt;/i&gt;; however, this pathogen’s diversity and population structure remain poorly understood, despite their importance in disease management. To address this knowledge gap, we analyzed the diversity of &lt;i&gt;X. euvesicatoria&lt;/i&gt; using BOX-PCR and ERIC-PCR fingerprinting techniques. A total of 103 isolates were collected from 13 counties across Heilongjiang province during the 2018 and 2019 growing seasons. Our findings revealed 635 unique genetic patterns from ERIC-PCR fingerprinting, compared to 360 patterns from BOX-PCR. BOX-PCR analysis identified 12 distinct genotypic clusters, whereas ERIC-PCR identified 14 clusters through unweighted pair group approach with arithmetic average analysis, demonstrating substantial genetic variability. STRUCTURE analysis further identified five distinct genetic clusters in the BOX-PCR data and two in the ERIC-PCR data. The Hailin isolates showed the highest level of diversification compared to other regional isolates. AMOVA results indicated that 85% of the genetic variation in BOX-PCR was attributable to within-population differences, while 78% of ERIC-PCR variation was due to differences across populations. In addition, a Mantel test demonstrated a tenuous correlation between BOX-PCR and ERIC-PCR genetic markers, indicating distinct genetic profiles. This extensive genetic information enhances our understanding of the epidemiology of bacterial leaf spot and its potential therapeutic prospects. These data can provide insights into &lt;i&gt;Xanthomonas&lt;/i&gt; strains’ diversity and geographical dissemination.

LncRNA RNF144A-AS1 gene polymorphisms and their influence on lung cancer patients in the Chinese Han Population

Lung cancer is primarily classified as NSCLC, which is distinguished by a wide range of genetic variations. This study focused on RNF144A-AS1, a relatively unexplored lncRNA, to explore the impact of its genetic polymorphisms on the susceptibility to NSCLC. We detected RNF144A-AS1 expression and its correlation with prognosis and clinical pathological features using bioinformatics analysis. The association between RNF144A-AS1 polymorphism and NSCLC susceptibility was evaluated using case-control methods. This investigation featured a cohort of 700 NSCLC individuals and 700 healthy controls. The genotype of genetic variation was detected by PCR-RFLP and iMLDR, followed by subsequent calculation of OR and 95 % CI. Our data show that RNF144A-AS1 exhibits high expression levels in LUAD tissues and its expression is closely linked to LUAD progression and prognosis. Carrier of RNF144A-AS1 rs3806609 TT genotype increased NSCLC susceptibility compared to carrier of rs3806609 CC genotype (OR=2.21, 95%CI=1.57-3.13). Our study identifies RNF144A-AS1 genetic variants as potential susceptibility markers in NSCLC. RNF144A-AS1 promotes cell proliferation and migration in LUAD through the IFN-γ/JAK2/STAT1 signalling pathway. Collectively, these findings pave the way for developing targeted therapies and diagnostic tools based on RNF144A-AS1 and its variants.

Novel insights into sheep domestication in Southwest Asia based on genome-wide sequencing.

The origin of domestic sheep (Ovis aries) can be traced back to the Asian mouflon (Ovis gmelini), in the Near East around 10 000 years ago. Genetic divergence within mouflon populations can occur due to factors such as geographical isolation, social structures, and environmental pressures, leading to different affinities with domestic sheep. However, few studies have reported the extent to which mouflon sheep contribute to domestic sheep in different regions. Here, we implemented the demographic analyses of sheep populations across the globe based on the whole genome resequencing data of 410 samples, Y chromosome genetic variation of 417 rams, and 396 complete mitogenomes of O. aries. This revealed genetic differentiation within Iranian mouflons and a close genetic affinity between northern Iranian mouflons and worldwide domestic populations. The result illustrates that domestic sheep in our study may have derived from the same mouflon populations. Furthermore, analyses of paternal and maternal genetic diversity showed that five Y chromosome haplogroups and seven mitochondrial haplogroups were identified, of which the lineages mtF and mtG were newly found and defined. A phylogeographic interpretation of our data reveals a cline of north to south Iranian mouflons, which may be largely explained by increasing urial introgression.

Mycoplasma ovipneumoniae identified as the main aetiological agent of respiratory disease in goats from a case-control study in Savannakhet province of Lao PDR.

Clinical signs of respiratory disease are common in Lao goats. To identify the causative agents involved in this clinical syndrome, a matched case-control study was conducted across 70 smallholder goat holdings in Savannakhet province. Fifty paired nasal swab samples were collected from goats with respiratory signs (cases) and unaffected (control) goats from 27 goat holdings. The majority of cases (84 %) were from goats < 12 months of age. Samples were tested using quantitative PCR assays targeting possible pathogens causing respiratory disease. Mycoplasma ovipneumoniae, the cause of atypical pneumonia, was prevalent in both case (94 %) and control (76 %) groups and was identified as the principal causative agent based on odds ratio of presence (4.9) and a significantly higher pathogen load in case goats. Prolonged close contact between goats during confinement in often poorly constructed goat houses, likely facilitates transmission and progression from carrier to clinical status under the Lao goat production system. Mannheimia haemolytica was detected in 60 % of case and 52 % of control samples with no significant difference in pathogen load, while Pasteurella multocida was detected in only 2 % of control samples indicating no major role in causation for these pathogens. Mycoplasma capricolum subsp. capripneumoniae, respiratory syncytial virus and bovine parainfluenza 3 virus were not detected in any samples. Phylogenetic analysis showed no genetic variation of M. ovipneumoniae in the study samples and close similarity to recent isolates from China, US and Turkey. Improved housing conditions may be helpful in controlling atypical pneumonia in Lao goats and antibiotic treatment of goats with severe signs of respiratory disease was found to be effective.

Maize ZmWRKY71 gene positively regulates drought tolerance through reactive oxygen species homeostasis.

Drought stress severely affects plant growth and yield. The plant-specific WRKY transcription factors play an important role in regulating the plant response to abiotic stresses. In this study, we identified a group I WRKY gene from maize, designated ZmWRKY71. Real-time quantitative reverse transcription-PCR analysis revealed that ZmWRKY71 was predominantly expressed in the roots and was induced by drought. ZmWRKY71 was localized in the nucleus and showed transcriptional activity in yeast. Heterologous overexpression of ZmWRKY71 improved drought tolerance in yeast and Arabidopsis. Compared with the wild type, the overexpression lines showed a higher survival rate under drought stress with reduced malondialdehyde content and elevated antioxidant enzyme activities. In contrast, mutation of ZmWRKY71 in maize leads to increased sensitivity to drought stress, reduced survival, elevated concentrations of reactive oxygen species, and increased malondialdehyde content. RNA-sequencing analysis revealed that the expression patterns of genes associated with translation, membrane, and oxidoreductase activity pathways were altered under drought stress. Yeast one-hybrid, dual-luciferase, and electrophoretic mobility shift assays confirmed that ZmWRKY71 was capable of directly binding to the W-box element in the promoter region of ZmPOD42 (Zm00001eb330550). Taken together, the results show that ZmWRKY71 positively regulates maize drought tolerance. This research enriches the drought tolerance gene pool for maize and provides a theoretical basis for maize drought tolerance breeding.

Blastocystis and Giardia duodenalis infection in a male prison in Spain.

General conditions in a prison may facilitate water- or food-borne infections. Detection of intestinal parasites was achieved in 471 male prison inmates by standard microscopic procedures on their stool samples. Positive samples were processed by PCR amplification of a 600-bp fragment of the Blastocystis SSU rRNA gene and partial sequences of the Giardia duodenalis bg genes. Identification of subtypes/genotypes was based on Sanger sequencing methods. Blastocystis was found in 7.9% (37/471) and G. duodenalis was found in 2.1% (10/471). Out of the 37 Blastocystis positive samples, 54% (20/37) were successfully subtyped, allowing the identification of the subtypes ST3 (50%), ST1 (25%), ST2 (15%), ST4 (5%) and ST6 (5%). Out of 10G. duodenalis positive samples, 50% (5/10) were successfully genotyped, allowing the identification of genotypes A (80%) and B (20%). The predominance of ST3 within the prison inmates, together with its low intra-ST genetic variability, reflected inter-human transmission with spatial stability. The G. duodenalis distribution is not wide enough to consider the possibility of a generalized transmission via contaminated water or food. Personal hygiene practices among male prison inmates may be an important measure to prevent the transmission.

Do Different Wheat Ploidy Levels Respond Differently Against Stripe Rust Infection: Interplay between Reactive Oxygen Species (ROS) and the Antioxidant Defense System?

Wheat stripe rust (Puccinia striiformis f. sp. tritici, Pst) is the most damaging wheat disease, causing substantial losses in global wheat production and productivity. Our study aimed to unravel the complex reciprocity between reactive oxygen species and the antioxidant defense system as a source of resistance against stripe rust in diploid, tetraploid and hexaploid wheat genotypes. The significant genetic variability for stripe rust in the materials under study was evident as the genotypes showed contrasting responses during both the adult and seedling stages. Our thorough perspective on the biochemical responses of wheat genotypes to stripe rust infection revealed distinct patterns in oxidative damage, antioxidant enzymes and photosynthetic pigments. Principal component analysis revealed inverse correlations between antioxidants and ROS, underscoring their key function in maintaining the cellular redox balance and protecting plants against oxidative damage. Diploid (Ae. tauschii) wild wheat exhibited a better biochemical defense system and greater resistance to stripe rust than the tetraploid (T. durum) and hexaploid (Triticum aestivum) wheat genotypes. The antioxidant enzyme activity of durum wheat was moderate compared to diploid and hexaploid wheat genotypes. The hexaploid wheat genotypes exhibited increased ROS production, reduced antioxidant enzyme activity and decreased photosynthetic pigment levels. This study enhances understanding of the antioxidant defense system across different wheat ploidies facing stripe rust, serving as a valuable strategy for improving crop disease resistance. This study validated the biochemical response of stripe rust-resistant and susceptible candidate genotypes, which will be used to develop genetic resources for discovering stripe rust resistance genes in wheat.

Molecular epidemiology and antimicrobial resistance of Vibrio parahaemolyticus isolates from the Pearl River Delta region, China.

The Pearl River Delta (PRD) region in southern China is a densely populated area and a hotspot for Vibrio parahaemolyticus infections. However, systematic research on this pathogen, particularly comparing clinical and environmental strains, remains limited. This study analyzed the molecular epidemiology and antimicrobial resistance of 200 V. parahaemolyticus isolates from 12 cities in the PRD region from 2022 to 2023. The results indicated that the most prevalent serotypes were O3:K6 (39.5%) and O10:K4 (27.5%), predominantly found in clinical isolates. Most clinical isolates exhibited the characteristics of toxRS/new+, tdh+, and trh-, along with the sequence type 3 (ST3), while environmental isolates did not possess these genetic markers. Antimicrobial susceptibility testing showed that although clinically recommended antibiotics remain effective, some isolates have exhibited resistance, with environmental isolates displaying higher rates of antimicrobial resistance than clinical isolates. Moreover, a total of 26 antibiotic resistance genes (ARGs) associated with 10 antibiotic categories were identified, showing variations in distribution patterns among isolates from different sources. Phylogenetic analysis indicated that clinical isolates formed a distinct lineage, contrasting with the greater diversity observed in environmental isolates. Whole-genome analysis further revealed significant differences in pathogenicity-related genes between the two groups, with genes associated with biofilm formation and antimicrobial resistance being more commonly found in environmental isolates. These findings underscore the genetic variability and distinct patterns of antimicrobial resistance between clinical and environmental V. parahaemolyticus strains, highlighting the need for ongoing surveillance and targeted interventions to effectively address foodborne illnesses.