Insertion 62bp upstream of the translational start site.
pirkEY00723/pirkEY00723 mutants do not exhibit a significant change in survival in response to P. rettgeri or L. monocytogenes infection, as compared to wild type.
pirkEY00723 flies infected with E.carotovora show reductions in mean lifespan compared to wild-type.
pirkEY00723 mutant flies display a higher than wild-type (2.5 fold) immune response to genital infection with E.carotovora.
pirkEY00723 mutant flies infected with the gram-negative pathogen Erwinia carotovora carotovora show significantly improved survival compared to wild-type flies.
pirk[EY00723] homozygous mutant animals are viable and fertile but display a marked reduction of their life span, as compared to controls.
Df(2R)PGRP-SCΔ, PGRP-LBΔ, pirkEY00723 has increased occurrence of cell division | adult stage phenotype
PGRP-LBΔ/Df(2R)PGRP-SCΔ, Dredd1, pirkEY00723 has long lived phenotype
PGRP-LBΔ/Df(2R)PGRP-SCΔ, RelE20, pirkEY00723 has long lived phenotype
pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ and pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ, Df(3L)PGRP-SBΔ5 flies are viable, although not fully fertile.
After oral infection with E. carotovora, the addition of pirkEY00723 to PGRP-LBΔ; Df(3L)PGRP-SC1Δ results in an enhancement of the immune response locally and systemically. As with septic injury, pirkEY00723, PGRP-LBΔ; Df(3L)PGRP-SC1Δ flies being to day within 4 days of oral infection with E. carotovora.
pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ flies begin to die within 4 days of oral infection with E. carotovora. Although pirkEY00723 Df(2R)PGRP-SCΔ flies show the same level of response as pirkEY00723 flies, it is important to note that the response of pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ flies is significantly higher than that of pirkEY00723 Df(2R)PGRP-SCΔ flies.
The stronger immune responses to E. carotovora oral infection of Df(2R)PGRP-SCΔ PGRP-LBΔ flies is correlated with a further decrease in lifespan compared to single mutant flies. pirkEY00723 Df(2R)PGRP-SCΔ; PGRP-LBΔ 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.
Dredd1; pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ and pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ, RelE20 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 pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ flies.
pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ and Df(2R)PGRP-SCΔ; PGRP-LBΔ 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 pirkEY00723, Df(2R)PGRP-SCΔ; PGRP-LBΔ 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.