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Salinity stress tolerance prediction for biomass‐related traits in maize (Zea mays L.) using genome‐wide markers

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Abstract

Maize (Zea mays L.) is the third most important cereal crop after rice (Oryza sativa) and wheat (Triticum aestivum). Salinity stress significantly affects vegetative biomass and grain yield and, therefore, reduces the food and silage productivity of maize. Selecting salt-tolerant genotypes is a cumbersome and time-consuming process that requires meticulous phenotyping. To predict salt tolerance in maize, we estimated breeding values for four biomass-related traits, including shoot length, shoot weight, root length, and root weight under salt-stressed and controlled conditions. A five-fold cross-validation method was used to select the best model among genomic best linear unbiased prediction (GBLUP), ridge-regression BLUP (rrBLUP), extended GBLUP, Bayesian Lasso, Bayesian ridge regression, BayesA, BayesB, and BayesC. Examination of the effect of different marker densities on prediction accuracy revealed that a set of low-density single nucleotide polymorphisms obtained through filtering based on a combination of analysis of variance and linkage disequilibrium provided the best prediction accuracy for all the traits. The average prediction accuracy in cross-validations ranged from 0.46 to 0.77 across the four derived traits. The GBLUP, rrBLUP, and all Bayesian models except BayesB demonstrated comparable levels of prediction accuracy that were superior to the other modeling approaches. These findings provide a roadmap for the deployment and optimization of genomic selection in breeding for salt tolerance in maize.

Genetic diversity of an effector gene, AvrPi9, of rice blast pathogen in Thailand and characterization of its promoter

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Genetic diversity of an effector gene, AvrPi9, of rice blast pathogen in Thailand and characterization of its promoter

MoHox6, a transcription factor, binds to the AvrPi9 promoter and helps the expression of the AvrPi9 gene in the rice blast fungus during infection and in rice protoplasts.


Abstract

Rice blast is one of the most destructive diseases of rice and is caused by the fungus Magnaporthe oryzae. The disease causes enormous yield losses in rice production worldwide. The rice blast fungus delivers effector proteins into rice cells. The effector proteins play an essential role in fungal virulence by manipulating and controlling host cellular pathways and inhibiting host immune responses to enhance pathogenicity. An effector gene, AvrPi9, which corresponds to the resistance gene Pi9, was cloned and characterized. However, a regulatory molecular mechanism for AvrPi9 gene expression has not been determined. In this study, the genetic variation of the AvrPi9 and its promoter function were characterized. The results showed that 98% (116/118) of the samples carried the AvrPi9 gene without any sequence variation, whilst two isolates, 10576 from Kalasin and NYK56003 from Nakhon Nayok, lacked the AvrPi9 gene. A homeobox domain-containing protein (MoHOX6) was identified as a candidate transcription factor. The AvrPi9 gene expression was delayed in the MoHOX6 knockout mutant. Moreover, the AvrPi9 promoter was able to drive the expression of a luciferase gene in rice protoplasts. This study provides the first insight into the function and regulation of the AvrPi9 promoter of rice blast fungus.

Modulatory effects of point‐mutated IL‐32θ (A94V) on tumor progression in triple‐negative breast cancer cells

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Modulatory effects of point-mutated IL-32θ (A94V) on tumor progression in triple-negative breast cancer cells

IL-32θ (A94V) inhibits phosphorylation of FAK and IκBα. IL-32θ (A94V) inhibits the expression and translocation of β-catenin by inhibiting phosphorylated FAK. Additionally, NF-κB is inhibited by IL-32θ (A94V) via the suppression of phosphorylated IκBα. Thus, IL-32θ (A94V) reduces migration, proliferation, and inflammation in breast cancer via the FAK-PI3K-GSK3 and NF-κB pathways.


Abstract

Breast cancer is a frequently diagnosed cancer and the leading cause of death among women worldwide. Tumor-associated macrophages stimulate cytokines and chemokines, which induce angiogenesis, metastasis, proliferation, and tumor-infiltrating immune cells. Although interleukin-32 (IL-32) has been implicated in the development and modulation of several cancers, its function in breast cancer remains elusive. Mutation of interleukin-32θ (IL-32θ) in the tissues of patients with breast cancer was detected by Sanger sequencing. RT-qPCR was used to detect the mRNA levels of inflammatory cytokines, chemokines, and mediators. The secreted proteins were detected using respective enzyme-linked immunosorbent assays. Evaluation of the inhibitory effect of mutant IL-32θ on proliferation, migration, epithelial–mesenchymal transition (EMT), and cell cycle arrest in breast cancer cells was conducted using MTS assays, migration assays, and Western blotting. A point mutation (281C>T, Ala94Val) was detected in IL-32θ in both breast tumors and adjacent normal tissues, which suppressed the expression of pro-inflammatory factors, EMT factors, and cell cycle related factors. Mutated IL-32θ inhibited the expression of inflammatory factors by regulating the NF-κB pathway. Furthermore, mutated IL-32θ suppressed EMT markers and cell cycle related factors through the FAK/PI3K/AKT pathway. It was inferred that mutated IL-32θ modulates breast cancer progression. Mutated IL-32θ (A94V) inhibited inflammation, EMT, and proliferation in breast cancer by regulating the NF-κB (p65/p50) and FAK-PI3K-GSK3 pathways.

Biochemical and cellular studies of three human 3‐phosphoglycerate dehydrogenase variants responsible for pathological reduced L‐serine levels

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Biochemical and cellular studies of three human 3-phosphoglycerate dehydrogenase variants responsible for pathological reduced L-serine levels

In the brain, L-serine is produced through the phosphorylated pathway (PP). hPHGDH catalyzes the first and rate-limiting step in the PP. Three variants related to hPHGDH deficiency and Neu-Laxova syndrome have been studied. V261M, V425M, and V490M substitutions alter the kinetic and structural properties of hPHGDH. Variants ectopic expression results in protein aggregation and reduced L-serine level.


Abstract

In the brain, the non-essential amino acid L-serine is produced through the phosphorylated pathway (PP) starting from the glycolytic intermediate 3-phosphoglycerate: among the different roles played by this amino acid, it can be converted into D-serine and glycine, the two main co-agonists of NMDA receptors. In humans, the enzymes of the PP, namely phosphoglycerate dehydrogenase (hPHGDH, which catalyzes the first and rate-limiting step of this pathway), 3-phosphoserine aminotransferase, and 3-phosphoserine phosphatase are likely organized in the cytosol as a metabolic assembly (a “serinosome”). The hPHGDH deficiency is a pathological condition biochemically characterized by reduced levels of L-serine in plasma and cerebrospinal fluid and clinically identified by severe neurological impairment. Here, three single-point variants responsible for hPHGDH deficiency and Neu-Laxova syndrome have been studied. Their biochemical characterization shows that V261M, V425M, and V490M substitutions alter either the kinetic (both maximal activity and K m for 3-phosphoglycerate in the physiological direction) and the structural properties (secondary, tertiary, and quaternary structure, favoring aggregation) of hPHGDH. All the three variants have been successfully ectopically expressed in U251 cells, thus the pathological effect is not due to hindered expression level. At the cellular level, mistargeting and aggregation phenomena have been observed in cells transiently expressing the pathological protein variants, as well as a reduced L-serine cellular level. Previous studies demonstrated that the pharmacological supplementation of L-serine in hPHGDH deficiencies could ameliorate some of the related symptoms: our results now suggest the use of additional and alternative therapeutic approaches.

Diversity of plant‐parasitic nematodes (PPNs) associated with medicinal plants in Vietnam, Vietnamese PPN checklist and a pictorial key for their identification

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Diversity of plant-parasitic nematodes (PPNs) associated with medicinal plants in Vietnam, Vietnamese PPN checklist and a pictorial key for their identification

This study reveals the diverse and damaging nature of plant-parasitic nematodes in Vietnamese medicinal plants, providing a Vietnamese nematofauna list of 217 species and offering an online key for global identification.


Abstract

Plant-parasitic nematodes (PPNs) are one of the most damaging pests to plants and are able to cause significant damage to all parts of plants, including stems, leaves, flowers, fruits and roots. Studies on the diversity, host range, distribution and identification methods of PPNs are therefore vital in order to create a basis for management. This current study represents the first dedicated investigation of PPNs from medicinal plants in Vietnam, focusing on the diversity of nematodes associated with 23 different plant species. In combination with a literature review of PPNs in Vietnam, this work has resulted in an updated list of 217 PPN species belonging to 40 genera, 15 families and three orders and also provides a pictorial online key for the identification of 52 most common and important PPN genera of the world. This key is based on the most crucial diagnostic features of PPN females, including female body shape, cuticle, labial shape, cephalic framework, stylet, stylet base, pharynx, median bulb, pharyngeal gland, vulva, tail shape and phasmid. Pictorial representations of these genera and their diagnostic characters are included in the browser-based key to benefit users from all levels in nematology, be they beginners or experts.

Downregulation of microRNA‐326 enhances ZNF322A expression, transcriptional activity and tumorigenic effects in lung cancer

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Downregulation of microRNA-326 enhances ZNF322A expression, transcriptional activity and tumorigenic effects in lung cancer

Oncogenic ZNF322A transcription factor is overexpressed in lung cancer. Downregulated miR-326 promotes ZNF322A-induced tumor growth and metastasis. This study reveals that miR-326-low/ZN322A-high profile is a biomarker to predict poor prognosis in lung cancer.


Abstract

Zinc finger protein ZNF322A is an oncogenic transcription factor. Overexpression of ZNF322A activates pro-metastasis, cancer stemness, and neo-angiogenesis-related genes to enhance lung cancer progression. However, the upstream regulator of ZNF322A is not well defined. Dysregulation of microRNAs (miRNAs) can mediate cancer cell growth, migration, and invasion to promote tumorigenesis. Here, we uncover the mechanism of miRNA-mediated transcriptional regulation in ZNF322A-driven oncogenic events. ZNF322A harbors several putative miRNA-binding sites in the 3′-untranslated region (UTR). We validated that miR-326 downregulated ZNF322A-3′-UTR luciferase activity and mRNA expression. Furthermore, miR-326 suppressed the expression of ZNF322A-driven cancer-associated genes such as cyclin D1 and alpha-adducin. Reconstitution experiments by ectopic overexpression of ZNF322A abolished miR-326-suppressed cancer cell proliferation and cell migration capacity. Moreover, miR-326 attenuated ZNF322A-induced tumor growth and lung tumor metastasis in vivo. Clinically, the expression of miR-326 negatively correlated with ZNF322A mRNA expression in surgically resected tissues from 120 non-small cell lung cancer (NSCLC) patients. Multivariate Cox regression analysis demonstrated that NSCLC patients with low miR-326/high ZNF322A profile showed poor overall survival. Our results reveal that the deregulated expression of miR-326 leads to hyperactivation of ZNF322A-driven oncogenic signaling. Targeting the miR-326/ZNF322A axis would provide new therapeutic strategies for lung cancer patients.

Advances in screening, synthesis, modification, and biomedical applications of peptides and peptide aptamers

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Advances in screening, synthesis, modification, and biomedical applications of peptides and peptide aptamers

This comprehensive review explores the latest advancements in the screening, synthesis, modification, and biomedical applications of peptides and peptide aptamers. It discusses screening techniques, diverse synthesis strategies, and various modification approaches employed to enhance their properties. The review also highlights the broad range of biomedical applications where peptides and peptide aptamers have shown promise, including drug delivery, therapeutics, diagnostics, and biomaterials.


Abstract

Peptides and peptide aptamers have emerged as promising molecules for a wide range of biomedical applications due to their unique properties and versatile functionalities. The screening strategies for identifying peptides and peptide aptamers with desired properties are discussed, including high-throughput screening, display screening technology, and in silico design approaches. The synthesis methods for the efficient production of peptides and peptide aptamers, such as solid-phase peptide synthesis and biosynthesis technology, are described, along with their advantages and limitations. Moreover, various modification techniques are explored to enhance the stability, specificity, and pharmacokinetic properties of peptides and peptide aptamers. This includes chemical modifications, enzymatic modifications, biomodifications, genetic engineering modifications, and physical modifications. Furthermore, the review highlights the diverse biomedical applications of peptides and peptide aptamers, including targeted drug delivery, diagnostics, and therapeutic. This review provides valuable insights into the advancements in screening, synthesis, modification, and biomedical applications of peptides and peptide aptamers. A comprehensive understanding of these aspects will aid researchers in the development of novel peptide-based therapeutics and diagnostic tools for various biomedical challenges.

Intracellular and mitochondrial proteomic analysis reveals antifungal mechanisms of borate on mango black spot pathogen Alternaria alternata

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Intracellular and mitochondrial proteomic analysis reveals antifungal mechanisms of borate on mango black spot pathogen Alternaria alternata

The antifungal effect of potassium tetraborate on the proteomics of Alternaria alternata involves multiple metabolic pathways and could be used as a potential substitute for fungicides to control postharvest diseases of mango.


Abstract

Boron, in the form of potassium tetraborate, has previously been found to be effective at inhibiting mango black spot disease, caused by Alternaria alternata. However, the mechanisms involved in this inhibition are largely unknown. In this study, A. alternata was treated in vitro with potassium tetraborate at a concentration of 5–10 mM for 48 or 72 h. The intracellular and mitochondrial proteins were extracted from mycelium and separated using two-dimensional electrophoresis (2-DE). Differentially expressed proteins (DEPs) were identified using bioinformatics tools and differences between protein spots were derived from mass spectrometry (MS). Using matrix-assisted laser desorption ionization time-of-flight tandem mass spectrometry (MALDI-ToF-MS/MS), 96 intracellular and 56 mitochondrial DEPs were identified. The intracellular proteins identified were found to be involved in posttranslational modifications, protein turnover and chaperones, while the mitochondrial proteins were involved in electron transport chains. Our results demonstrate that various metabolic pathways are involved in the antifungal activity of boron. The differential expression of 20 genes was also verified at the mRNA level by reverse transcription-quantitative PCR. Our study suggests that borate could be used as a potential substitute for synthetic fungicides to control this postharvest disease of mango fruits.