Explore the vast range of titles available.

A plant cell wall is a highly complex structure consisting of networks of polysaccharides, proteins, and polyphenols that dynamically change during growth and development in various tissues. The cell wall not only acts as a physical barrier but also dynamically responds to disturbances caused by biotic and abiotic stresses. Plants have well-established surveillance mechanisms to detect any cell wall perturbations. Specific immune signaling pathways are triggered to contrast biotic or abiotic forces, including cascades dedicated to reinforcing the cell wall structure. This review summarizes the recent developments in molecular mechanisms underlying maintenance of cell wall integrity in plant–pathogen and parasitic interactions. Subjects such as the effect of altered expression of endogenous plant cell-wall-related genes or apoplastic expression of microbial cell-wall-modifying enzymes on cell wall integrity are covered. Targeted genetic modifications as a tool to study the potential of cell wall elicitors, priming of signaling pathways, and the outcome of disease resistance phenotypes are also discussed. The prime importance of understanding the intricate details and complete picture of plant immunity emerges, ultimately to engineer new strategies to improve crop productivity and sustainability.

Background Cotton fiber development relies on complex and intricate biological processes to transform newly differentiated fiber initials into the mature, extravagantly elongated cellulosic cells that are the foundation of this economically important cash crop. Here we extend previous research into cotton fiber development by employing controlled conditions to minimize variability and utilizing time-series sampling and analyses to capture daily transcriptomic changes from early elongation through the early stages of secondary wall synthesis (6 to 24 days post anthesis; DPA). Results A majority of genes are expressed in fiber, largely partitioned into two major coexpression modules that represent genes whose expression generally increases or decreases during development. Differential gene expression reveals a massive transcriptomic shift between 16 and 17 DPA, corresponding to the onset of the transition phase that leads to secondary wall synthesis. Subtle gene expression changes are captured by the daily sampling, which are discussed in the context of fiber development. Coexpression and gene regulatory networks are constructed and associated with phenotypic aspects of fiber development, including turgor and cellulose production. Key genes are considered in the broader context of plant secondary wall synthesis, noting their known and putative roles in cotton fiber development. Conclusions The analyses presented here highlight the importance of fine-scale temporal sampling on understanding developmental processes and offer insight into genes and regulatory networks that may be important in conferring the unique fiber phenotype.

The plant cell wall (CW) is an outer cell skeleton that plays an important role in plant growth and protection against both biotic and abiotic stresses. Signals and molecules produced during host–pathogen interactions have been proven to be involved in plant stress responses initiating signal pathways. Based on our previous research findings, the present study explored the possibility of additively or synergistically increasing plant stress resistance by stacking beneficial genes. In order to prove our hypothesis, we generated transgenic Arabidopsis plants constitutively overexpressing three different Aspergillus nidulans CW-modifying enzymes: a xylan acetylesterase, a rhamnogalacturonan acetylesterase and a feruloylesterase. The two acetylesterases were expressed either together or in combination with the feruloylesterase to study the effect of CW polysaccharide deacetylation and deferuloylation on Arabidopsis defense reactions against a fungal pathogen, Botrytis cinerea. The transgenic Arabidopsis plants expressing two acetylesterases together showed higher CW deacetylation and increased resistance to B. cinerea in comparison to wild-type (WT) Col-0 and plants expressing single acetylesterases. While the expression of feruloylesterase alone compromised plant resistance, coexpression of feruloylesterase together with either one of the two acetylesterases restored plant resistance to the pathogen. These CW modifications induced several defense-related genes in uninfected healthy plants, confirming their impact on plant resistance. These results demonstrated that coexpression of complementary CW-modifying enzymes in different combinations have an additive effect on plant stress response by constitutively priming the plant defense pathways. These findings might be useful for generating valuable crops with higher protections against biotic stresses.

Soybean is one of the most important crops grown across the globe. In the United States, approximately 15% of the soybean yield is suppressed due to various pathogen and pests attack. Sudden death syndrome (SDS) is an emerging fungal disease caused by Fusarium virguliforme. Although growing SDS resistant soybean cultivars has been the main method of controlling this disease, SDS resistance is partial and controlled by a large number of quantitative trait loci (QTL). A proteinacious toxin, FvTox1, produced by the pathogen, causes foliar SDS. Earlier, we demonstrated that expression of an anti-FvTox1 single chain variable fragment antibody resulted in reduced foliar SDS development in transgenic soybean plants. Here, we investigated if synthetic FvTox1-interacting peptides, displayed on M13 phage particles, can be identified for enhancing foliar SDS resistance in soybean. We screened three phage-display peptide libraries and discovered four classes of M13 phage clones displaying FvTox1-interacting peptides. In vitro pull-down assays and in vivo interaction assays in yeast were conducted to confirm the interaction of FvTox1 with these four synthetic peptides and their fusion-combinations. One of these peptides was able to partially neutralize the toxic effect of FvTox1 in vitro. Possible application of the synthetic peptides in engineering SDS resistance soybean cultivars is discussed.

Fusarium virguliforme causes the serious disease sudden death syndrome (SDS) in soybean. Host resistance to this pathogen is partial and is encoded by a large number of quantitative trait loci, each conditioning small effects. Breeding SDS resistance is therefore challenging and identification of single-gene encoded novel resistance mechanisms is becoming a priority to fight this devastating this fungal pathogen. In this transcriptomic study we identified a few putative soybean defense genes, expression of which is suppressed during F. virguliforme infection. The F. virguliforme infection-suppressed genes were broadly classified into four major classes. The steady state transcript levels of many of these genes were suppressed to undetectable levels immediately following F. virguliforme infection. One of these classes contains two novel genes encoding ankyrin repeat-containing proteins. Expression of one of these genes, GmARP1, during F. virguliforme infection enhances SDS resistance among the transgenic soybean plants. Our data suggest that GmARP1 is a novel defense gene and the pathogen presumably suppress its expression to establish compatible interaction.

Fusarium virguliforme is a soil borne root pathogen that causes sudden death syndrome (SDS) in soybean [Glycine max (L.) Merrill]. Once the fungus invades the root xylem tissues, the pathogen secretes toxins that cause chlorosis and necrosis in foliar tissues leading to defoliation, flower and pod drop and eventually death of plants. Resistance to F. virguliforme in soybean is partial and governed by over 80 quantitative trait loci (QTL). We have conducted genome-wide association study (GWAS) for a group of 254 plant introductions lines using a panel of approximately 30,000 SNPs and identified 19 single nucleotide polymorphic loci (SNPL) that are associated with 14 genomic regions encoding foliar SDS and eight SNPL associated with seven genomic regions for root rot resistance. Of the identified 27 SNPL, six SNPL for foliar SDS resistance and two SNPL for root rot resistance co-mapped to previously identified QTL for SDS resistance. This study identified 13 SNPL associated with eight novel genomic regions containing foliar SDS resistance genes and six SNPL with five novel regions for root-rot resistance. This study identified five genes carrying nonsynonymous mutations: (i) three of which mapped to previously identified QTL for foliar SDS resistance and (ii) two mapped to two novel regions containing root rot resistance genes. Of the three genes mapped to QTL for foliar SDS resistance genes, two encode LRR-receptors and third one encodes a novel protein with unknown function. Of the two genes governing root rot resistance, Glyma.01g222900.1 encodes a soybean-specific LEA protein and Glyma.10g058700.1 encodes a heparan-alpha-glucosaminide N-acetyltransferase. In the LEA protein, a conserved serine residue was substituted with asparagine; and in the heparan-alpha-glucosaminide N-acetyltransferase, a conserved histidine residue was substituted with an arginine residue. Such changes are expected to alter functions of these two proteins regulated through phosphorylation. The five genes with nonsynonymous mutations could be considered candidate SDS resistance genes and should be suitable molecular markers for breeding SDS resistance in soybean. The study also reports desirable plant introduction lines and novel genomic regions for enhancing SDS resistance in soybean.

Biosynthetic gene clusters are common in microbial organisms, but rare in plants, raising questions regarding the evolutionary forces that drive their assembly in multicellular eukaryotes. Here, we characterize the biochemical function of a rice (Oryza sativa) cytochrome P450 monooxygenase, CYP76M7, which seems to act in the production of antifungal phytocassanes and defines a second diterpenoid biosynthetic gene cluster in rice. This cluster is uniquely multifunctional, containing enzymatic genes involved in the production of two distinct sets of phytoalexins, the antifungal phytocassanes and antibacterial oryzalides/oryzadiones, with the corresponding genes being subject to distinct transcriptional regulation. The lack of uniform coregulation of the genes within this multifunctional cluster suggests that this was not a primary driving force in its assembly. However, the cluster is dedicated to specialized metabolism, as all genes in the cluster are involved in phytoalexin metabolism. We hypothesize that this dedication to specialized metabolism led to the assembly of the corresponding biosynthetic gene cluster. Consistent with this hypothesis, molecular phylogenetic comparison demonstrates that the two rice diterpenoid biosynthetic gene clusters have undergone independent elaboration to their present-day forms, indicating continued evolutionary pressure for coclustering of enzymatic genes encoding components of related biosynthetic pathways.

Nonhost resistance is defined as the immunity of a plant species to all nonadapted pathogen species. Arabidopsis (Arabidopsis thaliana) ecotype Columbia-0 is nonhost to the oomycete plant pathogen Phytophthora sojae and the fungal plant pathogen Fusarium virguliforme that are pathogenic to soybean (Glycine max). Previously, we reported generating the pss1 mutation in the pen1-1 genetic background as well as genetic mapping and characterization of the Arabidopsis nonhost resistance Phytophthora sojae-susceptible gene locus, PSS1. In this study, we identified six candidate PSS1 genes by comparing single-nucleotide polymorphisms of (1) the bulked DNA sample of seven F2:3 families homozygous for the pss1 allele and (2) the pen1-1 mutant with Columbia-0. Analyses of T-DNA insertion mutants for each of these candidate PSS1 genes identified the At3g59640 gene encoding a glycine-rich protein as the putative PSS1 gene. Later, complementation analysis confirmed the identity of At3g59640 as the PSS1 gene. PSS1 is induced following P. sojae infection as well as expressed in an organ-specific manner. Coexpression analysis of the available transcriptomic data followed by reverse transcriptase-polymerase chain reaction suggested that PSS1 is coregulated with ATG8a (At4g21980), a core gene in autophagy. PSS1 contains a predicted single membrane-spanning domain. Subcellular localization study indicated that it is an integral plasma membrane protein. Sequence analysis suggested that soybean is unlikely to contain a PSS1-like defense function. Following the introduction of PSS1 into the soybean cultivar Williams 82, the transgenic plants exhibited enhanced resistance to F. virguliforme, the pathogen that causes sudden death syndrome.

KEY MESSAGE : Soybean deploys multiple genetic mechanisms to confer tolerance to Fusarium virguliforme toxins. This study revealed that F. virguliforme culture filtrates could be used in mapping QTL underlying foliar SDS resistance. Sudden death syndrome (SDS) is a major soybean disease throughout most of the soybean growing regions in the world including the United States. The disease is caused by the fungal pathogen, Fusarium virguliforme (Fv). The fungus produces several toxins that are responsible for development of interveinal leaf chlorosis and necrosis, which are typical foliar SDS symptoms. Growing of resistant cultivars has been the most effective method in controlling the disease. The objective of the present study was to identify quantitative trait loci (QTL) underlying host responses of soybean to Fv toxins present in culture filtrates. To accomplish this objective, two recombinant inbred line (RIL) populations, AX19286 (A95-684043 × LS94-3207) and AX19287 (A95-684043 × LS98-0582), segregating for SDS resistance were evaluated for foliar symptom development by applying two screening protocols, the stem cutting and the root feeding assays. The AX19286 population revealed two major and seven minor QTL for SDS resistance. In the AX19287 population, we identified five major QTL and three minor QTL. The two QTL mapped to Chromosome 7 [molecular linkage group (MLG) M] and Chromosome 20 (MLG I) are most likely novel, and were detected through screening of the AX19287 population with stem cutting and root feeding assays, respectively. This study established that Fv culture filtrates could be employed in mapping QTL underlying foliar SDS resistance. The outcomes of the research also suggest that multiple genetic mechanisms might be used by soybean to overcome the toxic effects of the toxins secreted by the pathogen into culture filtrates.

The soil borne fungus, Fusarium virguliforme, causes sudden death syndrome (SDS) in soybean, which is a serious foliar and root rot disease. The pathogen has never been isolated from the diseased foliar tissues; phytotoxins produced by the pathogen are believed to cause foliar SDS symptoms. One of these toxins, a 13.5-kDa acidic protein named FvTox1, has been hypothesized to interfere with photosynthesis in infected soybean plants and cause foliar SDS. The objective of this study is to determine if FvTox1 is involved in foliar SDS development. We created and studied five independent knockout fvtox1 mutants to study the function of FvTox1. We conducted Agrobacterium tumefaciens-mediated transformation to accomplish homologous recombination of FvTox1 with a hygromycin B resistance gene, hph, to generate the fvtox1 mutants. Approximately 40 hygromycin-resistant transformants were obtained from 10⁶ conidial spores of the F. virguliforme Mont-1 isolate when the spores were co-cultivated with the A. tumefaciens EHA105 but not with LBA4044 strain carrying a recombinant binary plasmid, in which the hph gene encoding hygromycin resistance was flanked by 5′- and 3′-end FvTox1 sequences. We observed homologous recombination-mediated integration of hph into the FvTox1 locus among five independent fvtox1 mutants. In stem-cutting assays using cut soybean seedlings fed with cell-free F. virguliforme culture filtrates, the knockout fvtox1 mutants caused chlorophyll losses and foliar SDS symptoms, which were over twofold less than those caused by the virulent F. virguliforme Mont-1 isolate. Similarly, in root inoculation assays, more than a twofold reduction in foliar SDS development and chlorophyll losses was observed among the seedlings infected with the fvtox1 mutants as compared to the seedlings infected with the wild-type Mont-1 isolate. These results suggest that FvTox1 is a major virulence factor involved in foliar SDS development in soybean. It is expected that interference of the function of this toxin in transgenic soybean plants will lead to generation of SDS-resistant soybean cultivars.