Excision of P{SUPor-P}p38bKG01337 results in the removal of 1065bp which includes most of the p38b coding region.
Estimated boundaries of a 1065bp deletion resulting from the excision of P{SUPor-P}p38bKG01337 that removes most of the p38b coding region.
Mutant larvae show an increase in maximum bouton diameter at the neuromuscular junction compared to controls. Mutant larvae show a mild defect in axonal transport.
The ability of injured axons to sprout after injury is normal in mutant larvae.
Homozygous p38bΔ45 mutants have significantly reduced lifespans compared to controls, although no change in lifespan is seen in heterozygotes. 3 day old p38bΔ45 females occasionally exhibit aberrant walking behaviour and 1-2 day old flies are significantly more sensitive to heat shock and hydrogen peroxide-induced oxidative stress compared to controls.
p38bΔ45 has short lived phenotype, suppressible by Sod2UAS.cMa/Scer\GAL4Mef2.PR
Df(3L)ED229/+, p38bΔ45 has abnormal neuroanatomy | dominant | larval stage phenotype
Sod2n283/Sod2[+], p38bΔ45 has short lived | dominant phenotype
Df(3L)ED229/+, p38bΔ45 has NMJ bouton | larval stage phenotype
p38bΔ45/+ ; Df(3L)ED229/+ double heterozygous larvae show an increase in maximum bouton diameter at the larval neuromuscular junction compared to controls.
Expression of Sod2Scer\UAS.cMa under the control of Scer\GAL4Mef2.PR significantly rescues the abbreviated lifespan seen in p38bΔ45 mutants.
Transheterozygous Sod2n283 p38bΔ45 mutants have significantly reduced lifespans compared to controls.