Puccinia striiformis f.sp. tritici (Pst) is the causal agent of stripe (yellow) rust on wheat. It seriously threatens wheat production worldwide. The obligate biotrophic fungus is highly capable of producing new virulent races that can overcome resistance. Studying the inheritance of Pst virulence using the classical genetic approach was not possible until the recent discovery of its sexual stage on barberry plants. In the present study, 127 progeny isolates were obtained by selfing a representative Chinese Yellow Rust (CYR) race, CYR32, on Berberis aggregate. The parental isolate and progeny isolates were characterized by testing them on 25 wheat lines with different Yr genes for resistance and 10 simple sequence repeat (SSR) markers. The 127 progeny isolates were classified into 27 virulence phenotypes (VPs), and 65 multi-locus genotypes (MLGs). All progeny isolates and the parental isolate were avirulent to Yr5, Yr8, Yr10, Yr15, Yr24, Yr26, Yr32, and YrTr1; but virulent to Yr1, Yr2, Yr3, Yr4, Yr25, Yr44, and Yr76. The VPs of the parental isolate to nine Yr genes (Yr6, Yr7, Yr9, Yr17, Yr27, Yr28, Yr43, YrA, and YrExp2) and the avirulence phenotype to YrSP were found to be heterozygous. Based on the segregation of the virulence/avirulence phenotypes, we found that the VPs to Yr7, Yr28, Yr43, and YrExp2 were controlled by a dominant gene; those to Yr6, Yr9, and YrA (Yr73, Yr74) by two dominant genes; those to Yr17 and Yr27 by one dominant and one recessive gene; and the avirulence phenotype to YrSP by two complementary dominant genes. Molecular mapping revealed the linkage of 10 virulence/avirulence genes. Comparison of the inheritance modes of the virulence/avirulence genes in this study with previous studies indicated complex interactions between virulence genes in the pathogen and resistance genes in wheat lines. The results are useful for understanding the plant-pathogen interactions and developing wheat cultivars with effective and durable resistance.
Seven new 3,4,6-trisubstituted α-pyrone derivatives, violapyrones A-G (1-7), were isolated from Streptomyces violascens obtained from Hylobates hoolock feces. Their structures were elucidated on the basis of detailed spectroscopic analysis. The antimicrobial activities of 1-7 were evaluated against Gram-positive and Gram-negative bacteria and against fungi. Compounds 1-3 showed moderate antibacterial activities against Bacillus subtilis and Staphylococcus aureus with MIC values of 4-32 μg/mL.
Ubiquitin and ubiquitin-like proteins are known to be covalently conjugated to a variety of cellular substrates via a three-step enzymatic pathway. These modifications lead to the degradation of substrates or change its functional status. The ubiquitin-activating enzyme (E1) plays a key role in the first step of ubiquitination pathway to activate ubiquitin or ubiquitin-like proteins. Ubiquitin-activating enzyme E1-domain containing 1 (UBE1DC1) had been proved to activate an ubiquitin-like protein, ubiquitin-fold modifier 1 (Ufm1), by forming a high-energy thioester bond. In this report, UBE1DC1 is proved to activate another ubiquitin-like protein, SUMO2, besides Ufm1, both in vitro and in vivo by immunological analysis. It indicated that UBE1DC1 could activate two different ubiquitin-like proteins, SUMO2 and Ufm1, which have no significant similarity with each other. Subcellular localization in AD293 cells revealed that UBE1DC1 was especially distributed in the cytoplasm; whereas UBE1DC1 was mainly distributed in the nucleus when was cotransfected with SUMO2. It presumed that UBE1DC1 greatly activated SUMO2 in the nucleus or transferred activated-SUMO2 to nucleus after it conjugated SUMO2 in the cytoplasm.
Various mycoviruses have been isolated from Sclerotinia sclerotiorum. Here, we identified a viral RNA sequence contig, representing a novel virus, Sclerotinia sclerotiorum deltaflexivirus 2 (SsDFV2), from an RNA_Seq database. We found that SsDFV2 was harbored in the hypovirulent strain, 228, which grew slowly on potato dextrose agar, produced a few sclerotia, and could not induce typical lesions on detached rapeseed (Brassica napus) leaves. Strain 228 was also infected by Botrytis porri RNA Virus 1 (BpRV1), a virus originally isolated from Botrytis porri. The genome of SsDFV2 comprised 6711 nucleotides, excluding the poly (A) tail, and contained a single large predicted open reading frame encoding a putative viral RNA replicase. Phylogenetic analysis demonstrated that SsDFV2 is closely related to viruses in the family Deltaflexiviridae; however, it also differs significantly from members of this family, suggesting that it may represent a new species. Further we determined that SsDFV2 could be efficiently transmitted to host vegetative incompatible individuals by dual culture. To our best knowledge, this is the first report that a (+) ssRNA mycovirus can overcome the transmission limitations of the vegetative incompatibility system, a phenomenon that may facilitate the potential use of mycoviruses for the control of crop fungal diseases.
Metastasis causes the main lethality in esophageal cancer patient. Garcinol, a natural compound extracted from Gambogic genera , is a histone acetyltransferase (HAT) inhibitor that has shown anticancer activities such as cell cycle arrest and apoptosis induction. In this study, we investigated the effects of garcinol on the metastasis of esophageal cancer in vitro and in vivo. We found that garcinol (5–15 μM) dose-dependently inhibited the migration and invasion of human esophageal cancer cell lines KYSE150 and KYSE450 in wound healing, transwell migration, and Matrigel invasion assays. Furthermore, garcinol treatment dose-dependently decreased the protein levels of p300/CBP (transcriptional cofactors and HATs) and p-Smad2/3 expression in the nucleus, thus impeding tumor cell proliferation and metastasis. Knockdown of p300 could inhibit cell metastasis, but CBP knockdown did not affect the cell mobility. It has been reported that TGF-β1 stimulated the phosphorylation of Smad2/3, which directly interact with p300/CBP in the nucleus, and upregulating HAT activity of p300. We showed that garcinol treatment dose-dependently suppressed TGF-β1-activated Smad and non-Smad pathway, inhibiting esophageal cancer cell metastasis. In a tail vein injection pulmonary metastasis mouse model, intraperitoneal administration of garcinol (20 mg/kg) or 5-FU (20 mg/kg) significantly decreased the number of lung tumor nodules and the expression levels of Ki-67, p300, and p-Smad2/3 in lung tissues. In conclusion, our study demonstrates that garcinol inhibits esophageal cancer metastasis in vitro and in vivo, which might be related to the suppression of p300 and TGF-β1 signaling pathways, suggesting the therapeutic potential of Garcinol for metastatic tumors.
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