42 research outputs found
An Endophyte Constructs Fungicide-Containing Extracellular Barriers for Its Host Plant
No full textSummarySurface cracks create sites for pathogen invasion. Yew trees (Taxus) hyperbranch from long-lived buds that lie underneath the bark [1], resulting in persistent bark cracking and deep air pockets, potentially allowing pathogens to enter the nutrient-rich vascular system (vertical phloem and inter-connected radial medullary rays [MR]). Yew is famous as the source of the anti-cancer diterpenoid drug Taxol. A mystery has been why both the tree and its resident non-pathogenic fungi (endophytes) synthesize Taxol, apparently redundantly [2–7]. These endophytes, as well as pure Taxol, suppress fungal pathogens including wood-decaying fungi (WDF) [8–11]. Here we show that a Taxol-producing fungal endophyte, Paraconiothyrium SSM001 [12], migrates to pathogen entry points including branch cracks. The fungus sequesters Taxol in intracellular hydrophobic bodies that are induced by WDF for release by exocytosis, after which the bodies can coalesce to form remarkable extracellular barriers, laced with the fungicide. We propose that microbial construction of fungicide-releasing hydrophobic barriers might be a novel plant defense mechanism. We further propose that the endophyte might be evolutionarily analogous to animal immune cells, in that it might expand plant immunity by acting as an autonomous, anti-pathogen sentinel that monitors the vascular system
The effect of altered dosage of a mutant allele of Teosinte branched 1 (tb1-ref) on the root system of modern maize
No full textBackgroundThere was ancient human selection on the wild progenitor of modern maize, Balsas teosinte, for decreased shoot branching (tillering), in order to allow more nutrients to be diverted to grain. Mechanistically, the decline in shoot tillering has been associated with selection for increased expression of the major domestication gene Teosinte Branched 1 (Tb1) in shoot primordia. Therefore, TB1 has been defined as a repressor of shoot branching. It is known that plants respond to changes in shoot size by compensatory changes in root growth and architecture. However, it has not been reported whether altered TB1 expression affects any plant traits below ground. Previously, changes in dosage of a well-studied mutant allele of Tb1 in modern maize, called tb1-ref, from one to two copies, was shown to increase tillering. As a result, plants with two copies of the tb1-ref allele have a larger shoot biomass than heterozygotes. Here we used aeroponics to phenotype the effects of tb1-ref copy number on maize roots at macro-, meso- and micro scales of development.ResultsAn increase in the tb1-ref copy number from one to two copies resulted in: (1) an increase in crown root number due to the cumulative initiation of crown roots from successive tillers; (2) higher density of first and second order lateral roots; and (3) reduced average lateral root length. The resulting increase in root system biomass in homozygous tb1-ref mutants balanced the increase in shoot biomass caused by enhanced tillering. These changes caused homozygous tb1-ref mutants of modern maize to more closely resemble its ancestor Balsas teosinte below ground.ConclusionWe conclude that a decrease in TB1 function in maize results in a larger root system, due to an increase in the number of crown roots and lateral roots. Given that decreased TB1 expression results in a more highly branched and larger shoot, the impact of TB1 below ground may be direct or indirect. We discuss the potential implications of these findings for whole plant coordination of biomass accumulation and maize domestication
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Mucoricin is a ricin-like toxin that is critical for the pathogenesis of mucormycosis.
No full textFungi of the order Mucorales cause mucormycosis, a lethal infection with an incompletely understood pathogenesis. We demonstrate that Mucorales fungi produce a toxin, which plays a central role in virulence. Polyclonal antibodies against this toxin inhibit its ability to damage human cells in vitro and prevent hypovolemic shock, organ necrosis and death in mice with mucormycosis. Inhibition of the toxin in Rhizopus delemar through RNA interference compromises the ability of the fungus to damage host cells and attenuates virulence in mice. This 17 kDa toxin has structural and functional features of the plant toxin ricin, including the ability to inhibit protein synthesis through its N-glycosylase activity, the existence of a motif that mediates vascular leak and a lectin sequence. Antibodies against the toxin inhibit R. delemar- or toxin-mediated vascular permeability in vitro and cross react with ricin. A monoclonal anti-ricin B chain antibody binds to the toxin and also inhibits its ability to cause vascular permeability. Therefore, we propose the name 'mucoricin' for this toxin. Not only is mucoricin important in the pathogenesis of mucormycosis but our data suggest that a ricin-like toxin is produced by organisms beyond the plant and bacterial kingdoms. Importantly, mucoricin should be a promising therapeutic target
Metabolic Profiling of Candida auris, a Newly-Emerging Multi-Drug Resistant Candida Species, by GC-MS
No full textThe effect of altered dosage of a mutant allele of Teosinte branched 1 (tb1-ref) on the root system of modern maize
No full textAcute Myeloid Leukemia With Inv(16)(p13q22) Associated With Hidden Systemic Mastocytosis: Case Report and Review of Literature
No full textSystemic mastocytosis (SM) is a condition associated with clonal neoplastic proliferation of mast cells. In up to 40% of systemic mastocytosis cases, an associated clonal hematological disease of non–mast cell lineage, such as acute myeloid leukemia (AML), is diagnosed before, simultaneously with, or after the diagnosis of SM. Herein, we report a case of a 30-year-old man diagnosed with AML with inv(16)(p13;q22) CBFB:MYH11. Associated mastocytosis was not noted at diagnosis and was only detected in the bone marrow at time of remission after successful chemotherapy. The diagnosis of mastocytosis was based on the demonstration of a multifocal dense mast cell infiltrate in the marrow biopsy with aberrant immunophenotype, with coexpression of tryptase, CD117, and CD25. The mast cells showed atypical morphology mostly with irregular nuclear contour, bilobed or multilobed nuclei with cytoplasmic hypogranulation or irregular metachromatic granule distribution, and some cells with eccentric nucleus or spindle shape. Reexamination of the pretherapeutic bone marrow with immunostain for tryptase and CD25 revealed that mastocytosis was present from the start but masked by extensive blast proliferation. This case indicates that mast cell infiltrates are sometimes underappreciated at the original diagnosis of AML with inv(16) and that the concurrent diagnosis of SM with AML requires a high index of suspicion supported with comprehensive morphologic and immunohistochemical evaluation for a neoplastic mast cell proliferation
Dickkopf-3: An Update on a Potential Regulator of the Tumor Microenvironment
No full textDickkopf-3 (Dkk-3) is a member of the Dickkopf family protein of secreted Wingless-related integration site (Wnt) antagonists that appears to modulate regulators of the host microenvironment. In contrast to the clear anti-tumorigenic effects of Dkk-3-based gene therapies, the role of endogenous Dkk-3 in cancer is context-dependent, with elevated expression associated with tumor promotion and suppression in different settings. The receptors and effectors that mediate the diverse effects of Dkk-3 have not been characterized in detail, contributing to an ongoing mystery of its mechanism of action. This review compares the various functions of Dkk-3 in the tumor microenvironment, where Dkk-3 has been found to be expressed by subpopulations of fibroblasts, endothelial, and immune cells, in addition to epithelial cells. We also discuss how the activation or inhibition of Dkk-3, depending on tumor type and context, might be used to treat different types of cancers
Fig 1 -
No full textPie chart representing the abundance of sphingolipids in (A) Parental MCF-7 and (B) Dox-resistant MCF-7. Identified sphingolipids included sphingomyelin (SM), dihydrosphingomyelin (DHSM), ceramide (Cer), dihydroceramide (DHCer), hexosylceramide (HexCer). The data display the mean of four replica ± Std.</p
