Discerning the molecular mechanisms of erythrophagocytosis

The procedure involves the following steps: Each step was controlled by fluorescence microscopy.

Discerning the molecular mechanisms of erythrophagocytosis

Discerning the molecular mechanisms of erythrophagocytosis

Find articles by Ada V. Welter Find articles by Brenda H. Koushik Find articles by Amrita B. Gordon Find articles by Lindsay N. Temesvari Find articles by Lesly A. The authors have declared that no competing interests exist. Conceived and designed the experiments: This article has been cited by other articles in PMC.

Abstract Functional genomics and forward genetics seek to assign function to all known genes in a genome. Entamoeba histolytica is a protozoan parasite for which forward genetics approaches have not been extensively applied. It is the causative agent of amoebic dysentery and liver abscess, and infection is prevalent in developing countries that cannot prevent its fecal-oral spread.

It is responsible for considerable global morbidity and mortality. Given that the E. We used a genome-wide over-expression screen to uncover genes regulating an important virulence function of E. We developed an episomal E. The screen was based on the phagocytic uptake of human red blood cells loaded with the metabolic toxin, tubercidin.

Expression plasmids were isolated from trophozoites that survived exposure to tubercidin-charged erythrocytes phagocytosis mutantsand the cDNAs were sequenced. We isolated the gene encoding profilin, a well-characterized cytoskeleton-regulating protein with a known role in phagocytosis.

This supports the validity of our approach. Furthermore, we assigned a phagocytic role to several genes not previously known to function in this manner. To our knowledge, this is the first genome-wide forward genetics screen to be applied to this pathogen.

The study demonstrates the power of forward genetics in revealing genes regulating virulence in E. In addition, the study validates an E. Introduction Functional genomics is a branch of molecular biology that seeks to assign roles to all known genes in a genome.

[BINGSNIPMIX-3

It encompasses a wide variety of techniques which may be classified as reverse or forward genetics. Reverse genetics begins by mutating a gene of interest.Molecular mechanisms of erythrophagocytosis.

Characterization of the senescent erythrocytes that are phagocytized by macrophages. 6 Pages. Molecular mechanisms of erythrophagocytosis. Characterization of the senescent erythrocytes that are phagocytized by macrophages.

Virulence Potential of Ehrlichia chaffeensis Strains of Distinct Genome Sequences

Author. Daniela Bratosin. Molecular Mechanisms of Erythrophagocytosis. Erythrophagocytosis is a well-described feature of macrophages, and Prussian blue stains of hemosiderin iron show punctuate staining similar to what is observed in current study (19, Fig 1).

Prior work has shown macrophage involvement in cerebral microbleeds (4, 6). Molecular Mechanisms of Erythrophagocytosis: Flow Cytometric Quantitation of In Vitro Erythrocyte Phagocytosis by Macrophages Daniela Bratosin,1 Joe¨l Mazurier,2 Christian Slomianny,3 David.

Mechanism for phosphatidylserine-dependent erythrophagocytosis in mouse liver. Sung-Jin Lee, Seung-Yoon Park, much remains to be determined regarding the molecular mechanism, including specific receptors and ligands.

Mechanism for phosphatidylserine-dependent erythrophagocytosis in mouse liver. Sung-Jin Lee, Seung-Yoon Park. Further scrutiny of this fraction indicates that a) it shows the greatest reactivity with annexin V, which is specific for the detection of phosphatidylserine (PS) exposed on the outer leaflet of the erythrocyte membrane, b) it is the most susceptible to erythrophagocytosis by resident murine peritoneal macrophages, and c) this erythrophagocytosis of PKH labeled erythrocytes can be inhibited by .

Discerning the molecular mechanisms of erythrophagocytosis

HME is caused by infection with Ehrlichia chaffeensis, apoptosis, poorly formed granulomas, erythrophagocytosis, microvesicular fatty metamorphosis, and confluent severe necrosis (29, 43). The pathogenetic mechanisms of hepatic inflammation in HME are arteensevilla.com by: