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General Information
Symbol
Dmel\PGRP-LCΔE
Species
D. melanogaster
Name
FlyBase ID
FBal0212184
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
PGRP-LCE12, PGRP-LCΔE12, PGRP-LCDE12
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology
Nature of the lesion
Statement
Reference

Recombination between P{XP}PGRP-LC0693 and P{XP}4396, resulting in an 8.7kb deletion which removes the entire PGRP-LC coding region.

Insertion components
P{XP-U}PGRP-LCΔE
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

PGRP-LE112, PGRP-LCΔE double homozygotes show a significant increase in viral load in the head upon infection with ZIKV, as compared to infected double heterozygotes.

PGRP-LCΔE mutant flies display increased sensitivity to systemic Escherichia coli infection.

PGRP-LCΔE homozygous adults exhibit an impaired capacity to eliminate bacteria and a significantly increased mortality after abdominal infection with Erwinia carotovora carotovora, as compared to controls.

The neuromuscular junctions of PGRP-LCΔE homozygous mutant third instar larvae present small but significant decreases in spontaneous miniature excitatory postsynaptic potential and in excitatory postsynaptic potential, but not in quantal content, as compared to controls.

The neuromuscular junctions of PGRP-LCΔE/PGRP-LC2 transheterozygous mutant third instar larvae present small but significant decrease in spontaneous miniature excitatory postsynaptic potential and increase in quantal content, but no significant effect in the excitatory postsynaptic potential, as compared to controls.

The neuromuscular junctions of PGRP-LCΔE homozygous mutant third instar larvae shows similar overall structure to controls, with similar number of synaptic boutons, similar number and length of active zones, similar average vesicle number, similar vesicle diameter, similar average vesicle distance from the T-bar centroid.

Mutant flies show reduced compared to wild type after injection with Ecc15 (Gram-negative bacterium).

PGRP-LCΔE mutants show no effect on mortality within 24 hours of mild wounding in 7-8 days old adults. The mortality rate is increased to ~50% in response to more severe wounding.

Mutant flies infected with Erwinia carotovora carotovora by septic injury rapidly succumb to the infection.

PGRP-LCΔE mutant flies do not show a systemic response to genital infection with E.carotovora.

PGRP-LCΔE mutants are susceptible to infection by Gram-negative bacteria.

Hemolymph clots from PGRP-LCΔE third instar larvae show normal melanization.

Mutant flies show reduced survival compared to wild-type controls after infection with E. coli.

PGRP-LCΔE flies show a marked susceptibility to infection by Agrobacterium tumefaciens.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

The reduced survival rate upon systemic infection with Escherichia coli observed in PGRP-LCΔE mutants is substantially decreased further in CG80461;PGRP-LCΔE as well as PGRP-LE112;PGRP-LCΔE double mutants.

PGRP-LCΔE, PGRP-LE112 double mutants do not exhibit any difference in survival rate of flies either untreated or treated with Leishmania amastigotes, as compared to wild type.

PGRP-LCΔE homozygosity reverses the decrease in spontaneous miniature excitatory postsynaptic potential and increase in quantal content observed in the neuromuscular junction of GluRIIASP16 homozygous mutant third instar larvae.

PGRP-LE112;PGRP-LCΔE double mutant flies are rapidly killed by infection with the gram-negative pathogen Erwinia carotovora carotovora.

A PGRP-LCΔE background suppresses the wing notches seen when PGRP-LFdsRNA.1.Scer\UAS is expressed under the control of Scer\GAL4ptc-559.1.

The increase in lethality seen in larvae expressing PGRP-SC1adsRNA.Scer\UAS (under the control of Scer\GAL4da.G32) is completely suppressed in a PGRP-LCΔE background.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

PGRP-LCΔE homozygous adults exhibit an impaired capacity to eliminate bacteria and a significantly increased mortality upon abdominal infection with Erwinia carotovora carotovora, which are fully rescued by PGRP-LCT:Avic\GFP-EGFP or fully and partially rescued, respectively, by PGRP-LCΔex5.T:Avic\GFP-EGFP; The progeny of PGRP-LCΔE homozygous female adults harboring either PGRP-LCT:Avic\GFP-EGFP or PGRP-LCΔex5.T:Avic\GFP-EGFP do not exhibit significant lethality as compared to the progeny of control females.

Expression of PGRP-LCScer\UAS.LCx.T:Avic\GFP-YFP.Venus under the control of either Scer\GAL4elav-C155 or Scer\GAL4VGlut-OK371, but not of Scer\GAL4Mhc.PW, rescues the decreased spontaneous miniature excitatory postsynaptic potential observed in neuromuscular junctions of PGRP-LCΔE homozygous mutant third instar larvae; expression of PGRP-LCScer\UAS.LCx.T:Avic\GFP-YFP.Venus under the control of Scer\GAL4elav-C155, but not of Scer\GAL4VGlut-OK371 or Scer\GAL4Mhc.PW, also rescues the decreased excitatory postsynaptic potential observed in neuromuscular junctions of PGRP-LCΔE homozygous mutant third instar larvae.

Expression of PGRP-LCΔC.Scer\UAS.LCx.T:Avic\GFP-YFP.Venus under the control of Scer\GAL4VGlut-OK371 rescues the decreased spontaneous miniature excitatory postsynaptic potential and decreased excitatory postsynaptic potential observed in neuromuscular junctions of PGRP-LCΔE homozygous mutant third instar larvae.

PGRP-LC+tNa (carried either in M{PGRP-LC.PGRP-LF} or in M{PGRP-LC}) rescues the susceptibility of PGRP-LCΔE flies to infection with Erwinia carotovora carotovora by septic injury.

PGRP-LCT:Avic\GFP-EGFP (carried in M{GFP-PGRP-LC.PGRP-LF}) rescues the susceptibility of PGRP-LCΔE flies to infection with Erwinia carotovora carotovora by septic injury.

PGRP-LCLCa and PGRP-LCLCy (either alone or in combination) fail to rescue the susceptibility of PGRP-LCΔE flies to infection with Erwinia carotovora carotovora by septic injury.

Expression of PGRP-LCA.TM+IC.Scer\UAS under the control of Scer\GAL4yolk rescues the susceptibility of PGRP-LCΔE mutants to infection by Gram-negative bacteria.

Expression of PGRP-LCA.EC.Scer\UAS under the control of Scer\GAL4yolk does not rescue the susceptibility of PGRP-LCΔE mutants to infection by Gram-negative bacteria.

Expression of PGRP-LCA.TM+EC.Scer\UAS under the control of Scer\GAL4yolk does not rescue the susceptibility of PGRP-LCΔE mutants to infection by Gram-negative bacteria.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (11)
References (45)