A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\PGRP-LE112

General Information
SymbolDmel\PGRP-LE112SpeciesD. melanogaster
NameFlyBase IDFBal0182386
Feature typealleleAssociated geneDmel\PGRP-LE
Allele class
MutagenP-element activity
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
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Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Imprecise excision of the P{GS}PGRP-LEGS1068 insertion has created a 2542bp deletion which includes the PGRP-LE start codon.
Cytology
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Statement
Reference
Mutant flies show reduced survival after infection with Erwinia carotovora carotovora by septic injury compared to controls.
PGRP-LE[112] flies show lower survival rates after L. monocytogenes infection compared to controls.
Hemolymph clots from PGRP-LE[112] third instar larvae show normal melanization.
The survival rate of mutant animals after bacterial infections is similar to that of wild-type except for infection by P.carotovorum.carotovorum, and Gram-positive bacterial infections, B.megaterium, B.subtilis, E.faecalis and M.luteus. After infection with E.coli weak melanisation is induced at the injury site in mutant animals.
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Reference
PGRP-LE112 is a non-suppressor of visible | adult stage phenotype of PGRP-LF200
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Reference
PGRP-LE112 is a non-suppressor of wing phenotype of PGRP-LF200
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Statement
Reference
The reduced survival of PGRP-LB[Δ] flies after infection with Erwinia carotovora carotovora is suppressed if they are also mutant for PGRP-LE[112].
Expression of Listericin[Scer\UAS.cGa] using Scer\GAL4[Cg.PA] restores the survival phenotype against L. monocytogenes infection in a PGRP-LE[112] background.
PGRP-LE[112];PGRP-LC[ΔE] double mutant flies are rapidly killed by infection with the gram-negative pathogen Erwinia carotovora carotovora.
PGRP-LE[112] does not suppress the notching phenotypes and low adult viability seen in homozygous PGRP-LF[200] mutants.
Unlike single mutants, PGRP-LC7454/PGRP-LE112 double mutant animals exhibit a reduced resistance to E.coli and B.megaterium infection, but not E.faecalis and M.luteus infection.
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Bloomington
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hide References ( 9 )
Research paper
Bosco-Drayon et al., 2012, Cell Host Microbe 12(2): 153--165
Peptidoglycan Sensing by the Receptor PGRP-LE in the Drosophila Gut Induces Immune Responses to Infectious Bacteria and Tolerance to Microbiota. [FBrf0219236]
Neyen et al., 2012, J. Immunol. 189(4): 1886--1897
Tissue- and Ligand-Specific Sensing of Gram-Negative Infection in Drosophila by PGRP-LC Isoforms and PGRP-LE. [FBrf0219094]
Tsuzuki et al., 2012, Sci. Rep. 2: 210
Drosophila growth-blocking peptide-like factor mediates acute immune reactions during infectious and non-infectious stress. [FBrf0217467]
Goto et al., 2010, J. Biol. Chem. 285(21): 15731--15738
Cooperative regulation of the induction of the novel antibacterial Listericin by peptidoglycan recognition protein LE and the JAK-STAT pathway. [FBrf0210770]
Aggarwal et al., 2008, PLoS Pathog. 4(8): e1000120
Rudra interrupts receptor signaling complexes to negatively regulate the IMD pathway. [FBrf0205806]
Davis et al., 2008, Mol. Cell. Biol. 28(15): 4883--4895
A member of the p38 mitogen-activated protein kinase family is responsible for transcriptional induction of Dopa decarboxylase in the epidermis of Drosophila melanogaster during the innate immune response. [FBrf0215839]
Maillet et al., 2008, Cell Host Microbe 3(5): 293--303
The Drosophila peptidoglycan recognition protein PGRP-LF blocks PGRP-LC and IMD/JNK pathway activation. [FBrf0204914]
Bidla et al., 2007, J. Cell Sci. 120(7): 1209--1215
Crystal cell rupture after injury in Drosophila requires the JNK pathway, small GTPases and the TNF homolog Eiger. [FBrf0192653]
Takehana et al., 2004, EMBO J. 23(23): 4690--4700
Peptidoglycan recognition protein (PGRP)-LE and PGRP-LC act synergistically in Drosophila immunity. [FBrf0180202]