Amino acid replacement: E551K.
G5357604A
G?A
E551K | Klp64D-PA
E551K
The average peak electroantennogram response is reduced in homozygous, Klp64Dk5/Klp64Dl4 and Klp64Dk5/Klp64Dk1 adults compared to controls (in response to ethyl acetate, n-butanol, benzaldehyde or propionic acid).
The electron-dense basal bodies and the connecting cilium are often present in the sensilla basiconica of the antenna in mutant adults, but the outer segments of the basiconic cilia are less branched than in wild type.
The electron-dense basal bodies and the connecting cilium are often present in the sensilla basiconica of the antenna in Klp64Dk5/Klp64Dl4 adults, but the outer segments of the basiconic cilia usually contain a slender extension with several singlet microtubules.
The outer segments of the basiconic cilia of the sensilla basiconica of the antenna are less branched than normal in Klp64Dk5/Klp64Dk1 adults.
Klp64Dk5 homozygotes, Klp64Dk1/Klp64Dk5, and Klp64Dl4/Klp64Dk5 animals have a reduced auditory response, producing a severely reduced sound evoked potentials from the Johnston's organ neurons. The Johnston organ scolopidia contains complete sets of cilia. The basal body structures, ciliary roots and desmosomal junctions between inner dendritic segments appear normal. However, the ciliary dilations are deformed and disorganised and are often located in the same plane as the dendritic caps.
Homozygotes die at or before the early third larval instar stage in a typical crowded culture. If the homozygotes are raised in low density conditions without competition from wild-type larvae, a few mutant animals survive to be pharate pupae and occasionally eclose as fully formed adults. The adults show an acutely uncoordinated walk, are unable to stand and die in a few hours. Mutant third instar larvae show slight to severe sluggishness and roll abnormally from side to side during crawling.
Klp64Dk5/Klp64Dl4 has abnormal auditory perception phenotype, enhanceable by Kap3V6
Klp64Dk5/Klp64Dl4 has abnormal neurophysiology phenotype, enhanceable by Kap3V6
Klp64Dk5 is a suppressor of paralytic | posterior | larval stage phenotype of Aplip1EK4
Kap3V6, Klp64Dk5/Klp64Dl4 has partially lethal phenotype
Klp64Dk5/Klp64Dl4 has Johnston organ phenotype, enhanceable by Kap3V6
The addition of Kap3V6/+ significantly enhances the recessive lethality of Klp64Dl4/Klp64Dk5 animals. The addition of Kap3V6/Y causes complete lethality. The addition of Kap3V6/+ to Klp64Dl4/Klp64Dk5 also completely abolishes the sound evoked potentials usually obtained from the Johnston's organ neurons, and enhances the ciliary defects seen in these animals.
Klp64Dk5/Klp64Dk1 is rescued by Scer\GAL4da.PU/Klp64DUAS.cRa
Klp64Dk5 is rescued by Scer\GAL4JO15/Klp64DUAS.cRa
Klp64Dk5 is rescued by Scer\GAL4Tm1-C817/Klp64DUAS.cRa
Klp64Dk5 is rescued by Scer\GAL4MJ94/Klp64DUAS.cRa
Klp64Dk5/Klp64Dn123 is rescued by Klp64DUAS.cRa
Klp64Dk5 is rescued by Klp64DUAS.cRa
Expression of Klp64DScer\UAS.cRa under the control of Scer\GAL4da.G32 rescues the reduced electroantennogram response of Klp64Dk5/Klp64Dk1 adults in response to ethyl acetate, n-butanol, benzaldehyde or propionic acid.
Klp64DScer\UAS.cRa rescues the lethality and uncoordinated behaviour of Klp64Dk5, either in homozygous condition or in transheterozygous combination with Klp64Dn123, in the absence of a Scer\GAL4 driver.