|Feature type||allele||Associated gene||Dmel\PGRP-LB|
|Mutagen||gene targeting by homologous recombination|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
Mutant flies infected with Erwinia carotovora carotovora die after 2 weeks, in contrast to wild type.
After septic injury with the gram-negative E. carotovora bacterium, PGRP-LB[Δ] mutant flies exhibit a stronger and more sustained immune response than wild-type flies. PGRP-LB[Δ] mutant flies show a strong response to oral E. carotovora, similar to that observed after infection by septic injury with the same bacteria, in contrast to wild-type flies. PGRP-LB[Δ] flies infected with E. carotovora show reductions in mean lifespan compared to wild-type.
|Phenotype Manifest In|
The reduced survival of PGRP-LB[Δ] flies after infection with Erwinia carotovora carotovora is suppressed if they are also mutant for PGRP-LE.
After oral infection with E. carotovora, the addition of pirk[EY00723] to PGRP-LB[Δ]; Df(3L)PGRP-SC1[Δ] results in an enhancement of the immune response locally and systemically. As with septic injury, pirk[EY00723], PGRP-LB[Δ]; Df(3L)PGRP-SC1[Δ] flies beginning to die within 4 days of oral infection with E. carotovora. pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ] flies begin to die within 4 days of oral infection with E. carotovora. Although pirk[EY00723] Df(2R)PGRP-SC[Δ] flies show the same level of response as pirk[EY00723] flies, it is important to note that the response of pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ] flies is significantly higher than that of pirk[EY00723] Df(2R)PGRP-SC[Δ] flies. The stronger immune responses to E. carotovora oral infection of Df(2R)PGRP-SC[Δ] PGRP-LB[Δ] flies is correlated with a further decrease in lifespan compared to single mutant flies. pirk[EY00723] Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ] mutant flies do not simply show an incremental reduction in their lifespan, but rather die rapidly with oral E. carotovora infection, decreasing 50% after only 5 days. These flies are also susceptible to oral infection with dead sonicated E. carotovora, demonstrating that is it not bacteria that are killing the fly but rather its own excessive immune response. Dredd; pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ] and pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ], Rel[E20] flies, with impaired imd pathway activity due to the presence of Dredd or Rel mutations, exhibit an increased lifespan upon oral infection with E. carotovora bacteria, compared to pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ] flies. pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ] and Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ] flies in unchallenged conditions exhibit a marked reduction in lifespan. The level of epithelium renewal, as evidenced by the number of mitotic cells along the midgut, is very high in pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ] flies in the absence of bacterial infection, approaching the level seen in infected wild-type guts. The mitotic index of these flies doubles between unchallenged to E. carotovora oral infection conditions, suggesting that the level of epithelium renewal in the triple mutant is approaching the limit of cells available to undergo mitosis. pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ] and pirk[EY00723], Df(2R)PGRP-SC[Δ]; PGRP-LB[Δ], Df(3L)PGRP-SB[Δ5] flies are viable, although not fully fertile.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 1 )|
|Secondary FlyBase IDs|
|References ( 3 )|