Molecular Biology Reports最新文献

Background: Plant lipoxygenase (Lox) genes, catalyze polyunsaturated fatty acids and play essential roles in plant growth, development, and stress responses. It is extensively studied under various stresses, their role in abiotic stress responses remains unexplored in sesame.

Methods and results: This study identified seven Lox genes in sesame divided into two subfamilies: 9-Lox (Silox1, Silox2 and Silox3) are likely involved in pathogen defence and signalling and 13-Lox (Type-I: Silox4 and Type-II: Silox5, Silox6 and Silox7) play crucial roles in jasmonic acid biosynthesis and abiotic stress responses. Silox genes have undergone purifying selection, promoting the stability of gene function and prefer codons with A or T in the third position. The chromosomal distribution, sequence similarity, and subcellular localization, with conserved lipoxygenase domains and motifs were analysed. Promoter regions contained 34 cis-acting regulatory elements (e.g. WRKY, ERF, and bHLH) and 35 transcription factors binding sites (TFBS) linked to light, stress (e.g. MYC, W-box, ERE and STRE), phytohormones, and growth. Differential Gene Expression (DGE) analysis showed Lox1 was upregulated in Drought sensitive (DS) and in Drought tolerant (DT) the Lox1 & Lox3 were upregulated when compared to control. In addition, weighted gene co-expression network analysis (WGCNA) of Lox, showed that blue module is positively correlated with drought tolerance. Fourteen hub genes related to stress were identified, which closely associated with Lox1. Gene ontology and KEGG pathway analyses showed that these genes were linked to linoleic acid metabolism, lipid metabolism, and stress response. Quantitative Real-Time PCR (qRT-PCR) analysis confirmed that Silox genes showed time-varying differential expression under drought, salt and a combined drought-salt stress treatments.

Conclusion: This research lays the groundwork for future studies on the role of Lox genes in sesame's growth and stress adaptation.

Background: Microbes within the rumen play a pivotal role in the digestion of feed ingested by the ruminants. Researchers have been investigating microbes within rumen to assess its genetic capabilities, which hold immense potential across various fields including agro-industrial advantages. Since rumen is preliminary an anaerobic sac, numerous anaerobic bacteria and fungi have been isolated and characterized, however facultative anaerobic bacteria yet not fully investigated.

Methods and results: In present study, we isolated, characterized and performed whole genome analysis of 101 facultative anaerobic bacteria from rumen, offering a unique perspective compared to metagenomic approaches. All assembled genomes were of high quality, i.e. completeness 100% (only seven were between 92 and 99.5%) and only two had contamination > 5%. We identified 9,542 sequences of Carbohydrate-Active Enzymes (CAZymes). Over 8,136 of these CAZymes were full-length sequences, with 2,048 harbouring signal peptides also. Xylan (n = 634), pectin (n = 604), and starch (n = 312) degrading enzyme sequences were dominant. Several isolates also harbour secondary metabolite biosynthesis gene clusters for various metabolites, including fengycin, lichenysin, bacillibactins, bacilysin etc. All the isolates have metabolic versatility, encompassing pathways such as carbohydrate, amino acid, lipid, and vitamin and cofactor metabolism. Intriguingly, lipoic acid metabolism was absent in most of these facultative bacterial isolates.

Conclusion: This comprehensive study sheds light on the genetic potential of culturable facultative rumen bacteria, emphasizing their pivotal roles in carbohydrate degradation, secondary metabolite production, and metabolic diversity. These findings hold promise for enhancing ruminant nutrition, advancing eco-friendly biomass conversion, and bolstering bioprospecting of industrially important biocules and enzymes biofuel production.

The Hippo signaling pathway is a pivotal regulator of tissue homeostasis, organ size, and cell proliferation. Its dysregulation is profoundly implicated in various forms of cancer, making it a highly promising target for therapeutic intervention. This review extensively evaluates the mechanisms underlying the dysregulation of the Hippo pathway in cancer cells and the molecular processes linking these alterations to tumorigenesis. Under normal physiological conditions, the Hippo pathway is a guardian, ensuring controlled cellular proliferation and programmed cell death. However, numerous mutations and epigenetic modifications can disrupt this equilibrium in cancer cells, leading to unchecked cell proliferation, enhanced survival, and metastatic capabilities. The pathway's interaction with other critical signaling networks, including Wnt/β-catenin, PI3K/Akt, TGF-β/SMAD, and EGFR pathways, further amplifies its oncogenic potential. Central to these disruptions is the activation of YAP and TAZ transcriptional coactivators, which drive the expression of genes that promote oncogenesis. This review delves into the molecular mechanisms responsible for the dysregulation of the Hippo pathway in cancer, elucidating how these disruptions contribute to tumorigenesis. We also explore potential therapeutic strategies, including inhibitors targeting YAP/TAZ activity and modulators of upstream signaling components. Despite significant advancements in understanding the Hippo pathway's role in cancer, numerous questions remain unresolved. Continued research is imperative to unravel the complex interactions within this pathway and to develop innovative and effective therapies for clinical application. In conclusion, the comprehensive understanding of the Hippo pathway's regulatory mechanisms offers significant potential for advancing cancer therapies, regenerative medicine, and treatments for chronic diseases. The translation of these insights into clinical practice will necessitate collaborative efforts from researchers, clinicians, and pharmaceutical developers to bring novel and effective therapies to patients, ultimately improving clinical outcomes and advancing the field of oncology.

Background: The tiger population in Southwest Primorye is small and predominantly isolated from the main Sikhote-Alin population, which constitutes approximately 90% of the wild Amur tiger population. By 1996, this population declined to fewer than 10 individuals, but it has since grown and expanded into nearby habitats, now numbering over 50 individuals. Therefore, the regular genetic monitoring of this population is essential, as it has grown from a few founding members and remained geographically isolated.

Methods and results: Genetic diversity was assessed using nine heterologous microsatellite markers amplified from non-invasively collected samples of 20 individual tigers. The Southwest Primorye tiger population exhibited moderate genetic diversity, with allelic richness (Na) at 3.67 and observed heterozygosity (Ho) at 0.63. Additionally, we detected a slight tendency toward heterozygosity excess at several loci, with an overall negative FIS, which may be influenced by recent genetic admixture or subtle population structuring. comparative assessment between our study and Sugimoto et al. (2012) revealed a marginal increase in genetic diversity over time, suggesting improved genetic health of the population, potentially due to genetic exchange with other populations.

Conclusions: The significant growth and expansion of the Southwest Primorye tiger population into adjacent areas of Northeast China over the past two decades suggest a positive population trajectory. This modest increase in genetic diversity indicates a potentially favorable population condition. However, continuous genetic monitoring remains essential to track genetic trends, detect potential risks, and inform conservation strategies. This study highlights the need for ongoing evaluations to ensure the long-term survival of the Amur tiger population in Southwest Primorye.

Background: The oxylipins 10-HpOME and 7,10-DiHoME derive from oleic acid and have been extensively studied for their ability to regulate contractions, microcolony formation and biofilm formation in the model organism Pseudomonas aeruginosa.

Methods and results: Xylella fastidiosa subsp. pauca strain de Donno has been reported to produce 10-HpOME and 7,10-DiHOME in vivo when inoculated in the model plant Nicotiana tabacum or in naturally occurring infected olive trees. In this study, we deciphered the relationship among cell adhesion and oxylipins in Xylella fastidiosa subsp. fastidiosa (Temecula1 strain) and subsp. multiplex (AlmaEM3 strain). The role of the PD0744 gene, encoding for XadA2, a non-fimbrial adhesin belonging to the trimeric autotransporter family, probably involved in the surface attachment required in the initial phase of biofilm formation was investigated. PD0744 deletion mutants in two X. fastidiosa strains were generated, through homologous recombination, and the impact of its deletion on bacterial lifestyle was assessed. In vitro assays were performed to characterize the mutant phenotype, particularly in twitching motility and its capability to grow and form biofilm. Mutants showed a reduced twitching motility and biofilm formation compared to wild type strains. HPLC-MS/MS analysis revealed a decrease in 7,10-DiHOME production together with an increase of its precursor 10-HpOME in the mutants.

Conclusions: 7,10-DiHOME could be a crucial signaling molecule to promote biofilm formation and twitching motility, whose synthesis likely depends on a signal transduction requiring the presence of the adhesin XadA2 and thus not working if this protein is depleted. These results help understanding the complex regulation of biofilm formation in this devastating pathogen.

The ATP-binding cassette (ABC) transporter family is among the largest protein superfamilies, consisting of seven subfamilies, and plays an important role in various physiological processes and in the clinical manifestations of many diseases. The early clinical signs of head and neck cancer (HNC) are often subtle, resulting in most patients being diagnosed at more advanced stages. This late diagnosis adversely affects tumor treatment, and the resistance of certain tumors to chemotherapy further poses significant challenges for clinical management. Several previous studies have indicated a correlation between the ABC protein family and multidrug resistance (MDR) in tumors. This article offers a thorough review of the subfamilies, structures, functions, and roles of ABC transporters in MDR related to head and neck tumors, with the aim of providing insights and recommendations for overcoming MDR in this context.

Neglected tropical diseases (NTDs) include more than a dozen of diseases which despite their fatality receive less attention from the research community worldwide. High cost diagnosis of these diseases and lack of trained community which can accurately interpret them is the major drawback in the healthcare system. Nowadays, in the genetic engineering era more emphasis is given to the modern gene editing tools such as Transcription Activator-Like Effector Nucleases (TALENS), Zinc Finger Nucleases (ZFNs) and Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) due to their unique tailoring molecular machinery. This review article details the applicability of CRISPR/Cas9 as a modern gene editing tool in case of NTD parasites such as trypanosomatids with an aim to target their virulent genes. It has been observed through a number of studies that knocking in/out virulent genes of these parasites have led to a significant decrease in infectivity, growth rates along with morphological defects. The article also mentions various advanced CRISPR/Cas based diagnostics such as Specific High-Sensitivity Enzymatic Reporter unLOCKing (SHERLOCK) and SHERLOCK4HAT which can detect parasite concentration as low as 2 attomolar/L (aM: 10^- 18) and 1 parasite/µL respectively. This review also enlists various regulatory and biosafety issues, for example ecological imbalance which can arise as a consequence of CRISPR/Cas based gene drives employed to target parasitic vectors. Despite its wide applications, CRISPR/Cas is associated with several limitations like off-target effects and ecological imbalance to name a few.

Background: Host DNA depletion is a critical tool for accessing the microbiomes of samples that have a small amount of microbial DNA contained in a high host background. Of critical practical importance is the ability to identify microbial DNA sequences in frozen tissue specimens. Here, we compare four existing commercial methods and two newly introduced methods involving chromatin immunoprecipitation (ChIP) on frozen human and pig intestinal biopsies.

Results: We find that all methods that rely on differential lysis of host and microbial cells introduce substantial biases as assessed by 16 S rRNA gene amplicon profiling. However, ChIP enables 10-fold enrichment of microbial DNA while introducing less bias, sufficient to make assessment possible against background, in both pigs and humans.

Conclusions: We recommend ChIP in situations where host depletion is important but where minimizing taxonomic bias is essential, and the MolYsis or Zymo kit for situations where host depletion level is more important than taxonomic bias.

Conclusions: We recommend ChIP in situations where host depletion is important but where minimizing taxonomic bias is essential, and the MolYsis or Zymo kit for situations where host depletion level is more important than taxonomic bias.

Due to the significant energy requirements of nerve cells, glucose is rapidly oxidized to generate ATP and works in conjunction with mitochondria in metabolic pathways, resulting in a combinatorial impact. The purpose of this review is to show how glucose metabolism disorder invariably disrupts the normal functioning of neurons, a phenomenon commonly observed in neurodegenerative diseases. Interventions in these systems may alleviate the degenerative load on neurons. Research on the concepts of metabolic adaptability during disease progression has become a key focus. The majority of the existing treatments are effective in mitigating some clinical symptoms, but they are unsuccessful in preventing neurodegeneration. Hence, there is an urgent need for breakthrough and highly effective therapies for neurodegenerative diseases. Here, we summarise the interactions that various neurodegenerative diseases have with abnormalities in insulin signalling, lipid metabolism, glucose control, and mitochondrial bioenergetics. These factors have a crucial role in brain activity and cognition, and also significantly contribute to neuronal degeneration in pathological conditions. In this article, we have discussed the latest and most promising treatment methods, ranging from molecular advancements to clinical trials, that aim at improving the stability of neurons.