Overexpression of p38bScer\UAS.cAa in clock neurons using either Scer\GAL4P0.5.Pdf or Scer\GAL4cry.PZ results in an increased tau as well as an increase in the number of arrhythmic animals.
Flies expressing p38bScer\UAS.cAa in muscles throughout their lifetimes under the control of either Scer\GAL4Mhc.PW, Scer\GAL4Mef2.PR, Scer\GAL4how-24B, Scer\GAL4EDTP-DJ694 or Scer\GAL4DJ757 live significantly longer than controls. Pan-neuronal expression under the control of Scer\GAL4elav-C155 has no effect on lifespan.
Expression of p38bScer\UAS.cAa in muscles under the control of Scer\GAL4Mhc.PW, and restricted to post-eclosion stages using Scer\GAL80ts.αTub84B, results in a modest increase in lifespan compared to controls. Restricting p38bScer\UAS.cAa expression to adult stage neurons under the control of Scer\GAL4elav-C155 has no effect on lifespan.
Expression of p38bScer\UAS.cAa in muscles under the control of Scer\GAL4Mhc.PW suppresses the lethality that is usually seen in response to heat and dry starvation. No suppression of the phenotype occurs when p38bScer\UAS.cAa is expressed in neurons under the control of Scer\GAL4elav-C155.
Expression of p38bScer\UAS.cAa in muscles under the control of Scer\GAL4Mef2.PR confers additional resistance to hydrogen peroxide-induced oxidative stress compared to wild type. A similar phenotype is seen when p38bScer\UAS.cAa is expressed in the p38Kb expression domain under the control of Scer\GAL4p38b-83.
Expression of p38bScer\UAS.cAa using Scer\GAL4da.G32 or Scer\GAL4Pxn.PS suppresses Salmonella-induced lethality without a subsequent reduction in bacterial load.
The tolerance of p38bScer\UAS.cAa Scer\GAL4da.G32 flies to Salmonella infection is abolished if the engulfing function of hemocytes is blocked through the introduction of non-digestible latex beads.
Following infection with Salmonella, Scer\GAL4Pxn.PS, p38bScer\UAS.cAa flies show an increase in intracellular persistence of Salmonella. This contrasts with controls, in which the intracellular Salmonella count clearly decreases during infection.
Suppression by Df(2L)b82a2 or p38bDN.Scer\UAS of the wing phenotype caused by tkvCA.Scer\UAS expressed under the control of Scer\GAL471B is reduced if the flies are also coexpressing p38bScer\UAS.cAa.
Scer\GAL4cry.PZ, p38bUAS.cAa has abnormal circadian rhythm phenotype, suppressible by per01/per[+]
Scer\GAL4cry.PZ, p38bUAS.cAa has abnormal neuroanatomy phenotype, suppressible by Mef2EnR.UAS, Scer\GAL4cry.PZ
Scer\GAL4Mef2.PR, p38bUAS.cAa has long lived phenotype, suppressible by Sod2RNAi.UAS.cKa/Scer\GAL4Mef2.PR
p38bUAS.cAa, Scer\GAL4cry.PZ is a suppressor of abnormal circadian rhythm phenotype of Mef2EnR.UAS, Scer\GAL4cry.PZ
p38bUAS.cAa/Scer\GAL4Mef2.PR is a suppressor of short lived phenotype of p38a1, p38bΔ25
p38bUAS.cAa/Scer\GAL4Mef2.PR is a suppressor of abnormal oxidative stress response phenotype of p38a1, p38bΔ25
p38bUAS.cAa/Scer\GAL4Mef2.PR is a suppressor of partially lethal - majority die phenotype of p38a1, p38bΔ25
p38bUAS.cAa/Scer\GAL4Mef2.PR is a suppressor of abnormal locomotor behavior | adult stage phenotype of p38a1, p38bΔ25
p38bUAS.cAa, Scer\GAL4sca-537.4 is a suppressor of visible phenotype of RalaS25N.cMa.UAS, Scer\GAL4sca-537.4
Scer\GAL4elav-C155/p38bUAS.cAa is a non-suppressor of abnormal locomotor behavior | adult stage phenotype of p38a1, p38bΔ25
Scer\GAL4elav-C155/p38bUAS.cAa is a non-suppressor of short lived phenotype of p38a1, p38bΔ25
p38bUAS.cAa, Scer\GAL4sca-537.4 is a suppressor of microchaeta phenotype of RalaS25N.cMa.UAS, Scer\GAL4sca-537.4
p38bUAS.cAa, Scer\GAL4sca-537.4 is a suppressor of macrochaeta phenotype of RalaS25N.cMa.UAS, Scer\GAL4sca-537.4
A per01 heterozygous background rescues the circardian arrhythmia phenotype found upon expression of p38bScer\UAS.cAa under the control of Scer\GAL4cry.PZ.
Overexpression of p38bScer\UAS.cAa background, rescues the arrhythmia phenotype in a Mef2Scer\UAS.T:Rep-en expressing flies, from 84% of flies to 53% displaying arrhythmia.
Expression of p38bScer\UAS.cAa under the control of Scer\GAL4cry.PZ results in an increased level of tau in cry-expressing neurons, which is further enhanced by inhibition of Mef2 through co-expression of Mef2Scer\UAS.T:Rep-en.
Expression of p38bScer\UAS.cAa in muscles under the control of Scer\GAL4Mef2.PR significantly rescues the reduction in lifespan seen in p38bΔ25 Mpk21 double mutants. No rescue is seen when p38bScer\UAS.cAa is expressed in neurons under the control of Scer\GAL4elav-C155.
Expression of p38bScer\UAS.cAa in muscles under the control of Scer\GAL4Mef2.PR suppresses the geotaxis and walking defects seen in p38bΔ25 Mpk21 double mutant females. No suppression is seen when p38bScer\UAS.cAa is expressed pan-neuronally under the control of Scer\GAL4elav-C155.
Expression of p38bScer\UAS.cAa in muscles under the control of Scer\GAL4Mef2.PR significantly rescues the increased sensitivity to hydrogen peroxide-induced oxidative stress seen in p38bΔ25 Mpk21 double mutants.
Expression of p38bScer\UAS.cAa in muscles under the control of Scer\GAL4Mef2.PR completely rescues the reduced viability seen in p38bΔ25 Mpk21 double mutants.
Expression of Sod2dsRNA.Scer\UAS.cKa suppresses the lifespan extension phenotype seen when p38bScer\UAS.cAa is expressed in muscles under the control of Scer\GAL4Mef2.PR.
Expression of p38bScer\UAS.cAa under the control of Scer\GAL4da.G32 rescues the survival rate of Mpk213 p38b156A adults infected with either Enterobacter cloacae, Listeria monocytogenes or Beauveria bassiana to a level close to wild type.
Scer\GAL4da.G32-mediated expression of p38bScer\UAS.cAa rescues the Salmonella-induced mortality of p38bex9 flies.