Imprecise excision of the progenitor insertion resulting in a 1.53kb deletion extending from 802bp upstream to 732bp downstream of the Oli translation start site.
Reported as a 1.53 kb deletion resulting from the imprecise excision of P{GSV2}OliGS5080, which extends from 802 bp upstream to 732 bp downstream of the Oli translation start.
Approximately 80.4% of homozygous embryos survive to the larval stage. Under non-crowded conditions, only 42% of adults emerge from the pupal case. Under normal population conditions, only 3.4% of homozygotes emerge as adults.
Homozygous wandering stage third instar larvae remain largely on the surface on agar plates, in contrast to wild-type larvae which burrow into the agar at this stage. The mutant larvae show irregular, slower crawling behaviour compared to wild type and frequently appear to drag their abdominal segments. Homozygous adult escapers are unable to fly and have slow, uncoordinated leg movements, circling and wobbling.
The distribution and number of ventral nerve cord glia and the organisation of the ventral nerve cord scaffold appear normal in mutant embryos. The number and positions of eve-positive neurons also appear normal.
Btau\MAPTisl.H.T:Hsap\MYC-positive motorneuron axons show abnormal trajectories at the ventral nerve cord exit in mutant embryos; they fail to exit via the transverse nerve (TN) in 54.6% of hemisegments and ectopically extend axons through the SN branch in 58.8% of hemisegments. ISNb and TN motorneurons show muscle targeting defects in 51.7% of hemisegments. In 19.3% of hemisegments, ISNb motorneuron axons do not correctly defasciculate from each other, resulting in the stalling of thicker axon bundles between muscles 6 and 13 and a failure to innervate the muscle 12/13 cleft. In 27.8% of hemisegments, ISNb or TN axons extend processes that form abnormal contacts between them and in 14.2% of hemisegments, lateral bipolar dendrite /TN neurons have ectopic processes onto ventral muscles.
OliΔ9 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by exexGal4/exexKK30
OliΔ9 has lethal phenotype, suppressible | partially by Scer\GAL4elav-C155/Ggal\Olig2UAS.cOa
OliΔ9 has abnormal locomotor behavior | adult stage phenotype, suppressible | partially by Scer\GAL4elav-C155/Ggal\Olig2UAS.cOa
OliΔ9/OliΔ9 is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of exexGal4/exexKK30
OliΔ9 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, enhanceable by exexGal4/exexKK30
OliΔ9/OliΔ9 is an enhancer of larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype of exexGal4/exexKK30
Expression of Ggal\Olig2Scer\UAS.cOa under the control of Scer\GAL4elav-C155 partially rescues eclosion rates and walking defects in OliΔ9 adults.
OliΔ9 is partially rescued by Scer\GAL4elav-C155/OliUAS.cOa
OliΔ9 is partially rescued by Scer\GAL4sca.PU/OliUAS.cOa
OliΔ9 is partially rescued by Scer\GAL4VGlut1-OK371/OliUAS.cOa
OliΔ9 is not rescued by OliUAS.cOa/Scer\GAL4repo
Expression of OliScer\UAS.cOa under the control of Scer\GAL4elav-C155 fails to rescue the motorneuron axon targeting defects seen in OliΔ9 embryos. Survival to adulthood and adult locomotor defects are significantly rescued.
Expression of OliScer\UAS.cOa under the control of Scer\GAL4sca.PU partially rescues the motorneuron axon targeting defects seen in OliΔ9 embryos. Survival to adulthood and adult locomotor defects are significantly rescued.
Expression of OliScer\UAS.cOa under the control of Scer\GAL4repo fails to rescue eclosion rates or walking defects in OliΔ9 adults.
Expression of OliScer\UAS.cOa under the control of Scer\GAL4VGlut-OK371 partially rescues eclosion rates and walking defects in OliΔ9 adults.