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

Posted on by

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.

Whole‐genome versus per‐chromosome targeted recombination: Simulations and predicted gains in maize with an integer programming model

Posted on by

Abstract

Per-chromosome targeted recombination, with one to two recombinations at specific marker intervals on each chromosome, doubles the predicted genetic gains in biparental populations. We developed an integer programing model to identify where a fixed number of targeted recombinations should occur across the whole genome, without restrictions on the number of targeted recombinations on each chromosome. We compared whole-genome and per-chromosome targeted recombination in 392 biparental maize (Zea mays L.) populations and in simulation experiments. For yield, moisture, test weight, and a simulated trait controlled by 2000 quantitative trait loci (QTL), predicted gains were 8%–9% larger with 10 targeted recombinations across the entire genome than with one targeted recombination on each of the 10 chromosomes. With whole-genome targeted recombination, the number of recombinations on a given chromosome was correlated (r = 0.76–0.91) with the chromosome size (in cM). Simulation results suggested that previous results on gains from targeted recombination relative to nontargeted recombination were too optimistic by around 20%. Because the underlying QTL are unknown, studies on targeted recombination have relied on genomewide marker effects as proxies for QTL information. The simulation results indicated a 25% (for 10 recombinations) to 33% (for 20 recombinations) reduction in response due to the use of genomewide marker effects as proxies for QTL information. Overall, the results indicated that the integer programming model we developed is useful for increasing both the predicted and true gains from targeted recombination, but the predicted gains are likely to overestimate the true gains.

Evaluation of Ascochyta resistance in chickpea genotypes with quantitative polymerase chain reaction assay

Posted on by

Abstract

Ascochyta blight caused by Ascochyta rabiei is a globally important chickpea disease. Host resistance to Ascochyta blight is considered the most practical and effective means of control, but breeding has been hindered by a lack of effective resistance sources, and time-consuming, labour-intensive traditional methods to screen the resistance level of chickpea genotypes. This paper evaluated the progression of pathogen infection and the disease reaction of chickpea genotypes to Ascochyta blight by traditional and molecular methods. The resistance level of 84 chickpea genotypes was assessed by a quantitative polymerase chain reaction assay (qPCR) using a standard curve produced by various known amounts of pathogen DNA and compared with disease scores based on visual assessments 8 days after inoculation. Disease assessments revealed statistically significant differences between the resistance levels of chickpea genotypes, while the quantity of target DNA in the samples inoculated with the pathogen ranged from 0.004 to 83.37 ng. Our results showed a close relationship between the visual assessment of disease severity and the quantification of the target DNA in chickpea genotypes. The genotypes Tüb-35, Tüb-47, Tüb-26, Tüb-82, Tüb-65 and Tüb-69 were classified as highly resistant to Ascochyta blight based on the results of both assays used for screening chickpea genotypes. This qPCR analysis could be used to quantify disease progression in plant tissues and screen chickpea genotypes as a potential alternative to visual assessment of resistance levels in breeding programmes.

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

Posted on by
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.

A streak through history: Solving the riddle of chlorotic streak disease of sugarcane

Posted on by
A streak through history: Solving the riddle of chlorotic streak disease of sugarcane

This review spans the 90 years that passed between the emergence of chlorotic streak disease of sugarcane and the discovery of its pathogen in 2018, and provides epidemiological information on the disease and its management.


Abstract

Until recently, the identity of the pathogen of chlorotic streak disease (CSD) was one of the most enduring mysteries of sugarcane pathology. The mystery continued when the causal agent was revealed as a member of a large group of free-living eukaryotic microbes that had not previously been associated with any plant diseases. CSD has impacted worldwide sugarcane production since at least the 1920s when it was first noticed simultaneously in Java, Australia and Hawaii. Readily identified by irregular, yellow to creamy-white chlorotic streaks on the leaves, the identity of the pathogen remained unknown for 90 years. CSD negatively affects germination speed, ratooning, stalk numbers and stalk weight, and later causes stunting of crop growth, leading to major losses in sugar production. Prior to the discovery of the pathogen, CSD was found to be waterborne and spread by infected vegetative propagation material. As such it is particularly damaging in poorly drained soils and areas subject to high rainfall. In severe cases it can lead to crop death. The implementation of successful CSD management strategies has been limited by the lack of knowledge surrounding the nature of this disease. However, these strategies are likely to be augmented with the recent identification of the causal agent, a novel cercozoan described as Phytocercomonas venanatans. This review provides insight into the history, causal agent and potential future developments of CSD management strategies.

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

Posted on by
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

Posted on by
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

Posted on by
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.