Insertion of a P{PZ} element in the open reading frame, C-terminal to the PACAP and GHRH homology regions.
amnchpd mutants do not exhibit any behavioral memory at 24 hours and only a small amount is present at 9 hours after conditioning. Unlike wild-type, there is no significant increase in odor-evoked calcium influx into the α branch of the mushroom body neurons in amnchpd mutants at either 9 or 24 hours after conditioning.
amnchpd flies have a defective olfactory memory. These flies fail to produce the increased calcium influx seen in the dorsal paired medial neurons of wild-type flies at 30 minutes after a conditioning of 3s exposure to odour, followed by a 60s odour stimulus applied simultaneously with 12 electric-shock pulses.
amnchpd mutant flies show similar response profiles to wild-type flies in response to ethanol: flies have an initial startle response, a brief moment of quiescence followed by a sustained period of hyperactivity and a reduction in locomotor speed leading to eventual immobility. However, the amnchpd mutants have a more intense hyperactive phase and reach maximal hyperactivity more quickly, leading to a faster onset of immobility. During the hyperactive phase, amnchpd mutants initiate activity bouts less often than wild-type flies, but stay active for longer and spend more time moving fast. As these mutants begin to sedate, their bout frequency actually increases but their bout length is shorter.
Hemizygous males and homozygous females show increased sensitivity to ethanol; they elute from an inebriometer with a mean elution time (MET) of approximately 15 minutes compared with an MET of 20 minutes for wild-type controls. amnchpd flies show normal geotaxis and locomotor activity. Ethanol absorption and metabolism is normal in these flies. The ethanol-sensitive phenotype is reversed by treatment of the flies with forskolin (an adenylate cyclase activator) for 2 hours. A 4 hour treatment with forskolin further reduces ethanol sensitivity of amnchpd flies compared with control flies. Treatment of amnchpd flies with a cAMP analog that activates PKA also reverses the ethanol-sensitive phenotype. Treatment of amnchpd flies with an antagonist of cAMP that inhibits PKA partially reverses the ethanol-sensitive phenotype.
amnchpd has chemical sensitive | recessive phenotype, suppressible by Adcy1rut-2080
amnchpd is an enhancer of chemical sensitive phenotype of Arf6NP5226/Arf6EP2612
amnchpd is a suppressor of chemical sensitive phenotype of Adcy1rut-2080
rut[+]/Adcy1rut-1, amnchpd has abnormal thermotaxis | dominant phenotype
Pka-C1[+]/Pka-C1B10, amnchpd has abnormal thermotaxis | dominant phenotype
The sensitivity to ethanol-induced sedation seen in Arf51FNP5226/Arf51FEP2612 flies is enhanced if they also carry amnchpd.
Double heterozygotes for amnchpd and rut1 show an inability to find a preferred temperature, with temperature preference spread across a wide gradient.
Double heterozygotes for amnchpd and Pka-C1B10 show an inability to find a preferred temperature, with temperature preference spread across a wide gradient.
amnchpd is rescued by amnUAS.cWa/Scer\GAL4c316
The ethanol sensitive phenotype is rescued by amnhs.PM expressed using heat shock. Full rescue of the ethanol-sensitive phenotype is seen in animals given a daily heat shock throughout development, and is still seen 48 hours after the last heat shock, but the phenotype has reverted to ethanol-sensitivity 72 hours after the last heat shock. Three heat shocks at 24 hour intervals in adult flies is also sufficient to fully rescue the ethanol-sensitive phenotype.
Selected as: Altered ethanol sensitivity in an inebriometer assay.
Precise excision of the P{PZ} element restores the wild-type phenotype.