scholarly journals Hitting the Sweet Spot: Glycans as Targets of Fungal Defense Effector Proteins

Molecules ◽  
2015 ◽  
Vol 20 (5) ◽  
pp. 8144-8167 ◽  
Author(s):  
Markus Künzler
Keyword(s):  
Effector Proteins ◽  
Sweet Spot ◽  
Fungal Defense

POPDC proteins and cardiac function

2019 ◽  
Vol 47 (5) ◽  
pp. 1393-1404 ◽  
Author(s):  
Thomas Brand
Keyword(s):  
Potential Role ◽  
Striated Muscle ◽  
Short Review ◽  
Effector Proteins ◽  
Muscle Disease ◽  
Disease Genes ◽  
Protein Protein Interaction ◽  
Interaction Partners ◽  
And Function

Abstract The Popeye domain-containing gene family encodes a novel class of cAMP effector proteins in striated muscle tissue. In this short review, we first introduce the protein family and discuss their structure and function with an emphasis on their role in cyclic AMP signalling. Another focus of this review is the recently discovered role of POPDC genes as striated muscle disease genes, which have been associated with cardiac arrhythmia and muscular dystrophy. The pathological phenotypes observed in patients will be compared with phenotypes present in null and knockin mutations in zebrafish and mouse. A number of protein–protein interaction partners have been discovered and the potential role of POPDC proteins to control the subcellular localization and function of these interacting proteins will be discussed. Finally, we outline several areas, where research is urgently needed.

Effect of Escherichia Coli Infection on Metabolism of Dietary Protein in Intestine

2020 ◽  
Vol 21 (8) ◽  
pp. 772-776
Author(s):  
Xiao-Pei Peng ◽  
Wei Ding ◽  
Jian-Min Ma ◽  
Jie Zhang ◽  
Jian Sun ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Intestinal Tract ◽  
Effector Proteins ◽  
Physical Injury ◽  
Dietary Proteins ◽  
Pathogenic Role ◽  
E Coli ◽  
Low Protein ◽  
Pathogenic Escherichia Coli ◽  
Escherichia Coli Infection

Dietary proteins are linked to the pathogenic Escherichia coli (E. coli) through the intestinal tract, which is the site where both dietary proteins are metabolized and pathogenic E. coli strains play a pathogenic role. Dietary proteins are degraded by enzymes in the intestine lumen and their metabolites are transferred into enterocytes to be further metabolized. Seven diarrheagenic E. coli pathotypes have been identified, and they damage the intestinal epithelium through physical injury and effector proteins, which lead to inhibit the digestibility and absorption of dietary proteins in the intestine tract. But the increased tryptophan (Trp) content in the feed, low-protein diet or milk fractions supplementation is effective in preventing and controlling infections by pathogenic E. coli in the intestine.

scholarly journals The Epichloë festucae Antifungal Protein Efe-AfpA Is Also a Possible Effector Protein Required for the Interaction of the Fungus with its Host Grass Festuca rubra subsp. rubra

2021 ◽  
Vol 9 (1) ◽  
pp. 140
Author(s):  
Ruying Wang ◽  
Simin Luo ◽  
Bruce B. Clarke ◽  
Faith C. Belanger
Keyword(s):  
Disease Resistance ◽  
Insect Resistance ◽  
Effector Proteins ◽  
Antifungal Protein ◽  
Grass Species ◽  
Effector Protein ◽  
Festuca Rubra ◽  
Symbiotic Interaction ◽  
Red Fescue ◽  
Epichloë Festucae

Strong creeping red fescue (Festuca rubra subsp. rubra) is a commercially important low-maintenance turfgrass and is often naturally infected with the fungal endophyte Epichloë festucae. Epichloë spp. are endophytes of several cool-season grass species, often conferring insect resistance to the grass hosts due to the production of toxic alkaloids. In addition to insect resistance, a unique feature of the strong creeping red fescue/E. festucae symbiosis is the endophyte-mediated disease resistance to the fungal pathogen Clarireedia jacksonii, the causal agent of dollar spot disease. Such disease resistance is not a general feature of other grass/ Epichloë interactions. E. festucae isolates infecting red fescue have an antifungal protein gene Efe-afpA, whereas most other Epichloë spp. do not have a similar gene. The uniqueness of this gene suggests it may, therefore, be a component of the unique disease resistance seen in endophyte-infected red fescue. Here, we report the generation of CRISPR-Cas9 Efe-afpA gene knockouts with the goal of determining if absence of the protein in endophyte-infected Festuca rubra leads to disease susceptibility. However, it was not possible to infect plants with the knockout isolates, although infection was possible with the wild type E. festucae and with complemented isolates. This raises the interesting possibility that, in addition to having antifungal activity, the protein is required for the symbiotic interaction. The antifungal protein is a small secreted protein with high expression in planta relative to its expression in culture, all characteristics consistent with effector proteins. If Efe-AfpA is an effector protein it must be specific to certain interactions, since most Epichloë spp. do not have such a gene in their genomes.

scholarly journals Effectors Targeting the Unfolded Protein Response during Intracellular Bacterial Infection

2021 ◽  
Vol 9 (4) ◽  
pp. 705
Author(s):  
Manal H. Alshareef ◽  
Elizabeth L. Hartland ◽  
Kathleen McCaffrey
Keyword(s):  
Bacterial Infection ◽  
Er Stress ◽  
Unfolded Protein Response ◽  
Host Defense ◽  
Effector Proteins ◽  
Dual Nature ◽  
Unfolded Protein ◽  
Bacterial Replication ◽  
The Unfolded Protein Response ◽  
Protein Response

The unfolded protein response (UPR) is a homeostatic response to endoplasmic reticulum (ER) stress within eukaryotic cells. The UPR initiates transcriptional and post-transcriptional programs to resolve ER stress; or, if ER stress is severe or prolonged, initiates apoptosis. ER stress is a common feature of bacterial infection although the role of the UPR in host defense is only beginning to be understood. While the UPR is important for host defense against pore-forming toxins produced by some bacteria, other bacterial effector proteins hijack the UPR through the activity of translocated effector proteins that facilitate intracellular survival and proliferation. UPR-mediated apoptosis can limit bacterial replication but also often contributes to tissue damage and disease. Here, we discuss the dual nature of the UPR during infection and the implications of UPR activation or inhibition for inflammation and immunity as illustrated by different bacterial pathogens.

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