Nucleotide substitution: G?A.
The G to A mutation is in the AG acceptor splice site of the first intron.
This mutation is predicted to result in a severely truncated protein.
G18865660A
G?A
G to A mutation in the AG splice acceptor site of the first intron.
Many antero-dorsal antennal lobe projection neurons (adPN) in tupisl-1 homozygous somatic clones fail to target the correct glomeruli although in some cases (antennal glomeruli D and VA1d) targeting occur correctly. Mis-targeted dendrites from these neurons frequently end up occupying glomeruli DA1. Many lateral antennal lobe projection neurons (lPN) in these clones are also mis-targeted with a fraction of the dendrites ending up in the subesophageal ganglion and others spread diffusely throughout the antennal lobe. However, Targeting of DA1 and DL3 by lPN occurs normally. Targeting of ventral antennal lobe projection neurons (vPN) in these clones occurs normally.
Homozygous clones can give rise to cuticle defects on the scutum and scutellum, such as small, tubercle-like disruptions with a corrugated appearance and roundish contour.
Homozygous clones induced in the first instar generally give result in large clones with a smooth border when examined in the notum region of third instar wing discs. These clones are sometimes associated with an ectopic fold of the notum epithelium.
In tupisl-1/+ embryos 2% of muscles 12 and 13 fail to be innervated and 3% of ISNb axons leave the ventral muscle field and target the transverse nerve (TN) fascicle. In stage 16 tupisl-1/Df(2L)OD15 embryos, 29% of hemisegments have no transverse nerve, while 27% of hemisegments have transverse nerve fasciculation defects.
Class I and II interneurons fail to form their distinct fascicles in the connective in homozygous and hemizygous embryos. Class III local interneurons often appear defasciculated and highly disorganised. SNb motor neurons show a range of defects in target selection, including failing to innervate the cleft between muscles 12 and 13, 6 and 7 or 6 and 13, and leaving the muscle field and joining the transverse nerve (TN). The TMN25 and TMNp neurons often fail to enter the TN, instead projecting axons either across the midline or into adjacent segments. The peripheral LBD neurons extend abnormal ventral processes into the ventral muscle area, often joining segmental nerve branch b. The serotonin-dopamine fascicle does not form in most segments, and the serotonin and dopamine neurons project abnormally within the commissures and connectives. tupisl-1 mutants expressing tupScer\UAS.cTa using Scer\GAL4elav.PLu do not hatch.
tupisl-1 has abnormal neuroanatomy | dominant phenotype, enhanceable by vvl[+]/vvldfr-B129
tupisl-1, vvl[+]/vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by Lim3[+]/Lim36
tupisl-1/tup[+], vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by Lim3[+]/Lim36
tupisl-1 has abnormal neuroanatomy | dominant phenotype, enhanceable by Df(2L)TE35D-19/+
tupisl-1 has abnormal neurophysiology | recessive | first instar larval stage phenotype, suppressible by Sh14/Sh14
tupisl-1/tup[+] is an enhancer of abnormal neuroanatomy | dominant phenotype of vvldfr-B129
tupisl-1/tup[+] is an enhancer of abnormal neuroanatomy | dominant phenotype of Lim3[+]/Lim36, vvldfr-B129
tupisl-1/tup[+] is an enhancer of abnormal neuroanatomy | dominant phenotype of Lim36, vvl[+]/vvldfr-B129
Sh14, tupisl-1 has lethal - all die during embryonic stage phenotype
tupisl-1 has larval transverse nerve | embryonic stage 16 phenotype, enhanceable by Df(2L)TE35D-19/+
tupisl-1 has larval intersegmental nerve | embryonic stage 16 phenotype, enhanceable by vvl[+]/vvldfr-B129
tupisl-1 has larval transverse nerve | embryonic stage 16 phenotype, enhanceable by vvl[+]/vvldfr-B129
tupisl-1, vvl[+]/vvldfr-B129 has larval intersegmental nerve | embryonic stage 16 phenotype, enhanceable by Lim3[+]/Lim36
tupisl-1/tup[+], vvldfr-B129 has larval intersegmental nerve | embryonic stage 16 phenotype, enhanceable by Lim3[+]/Lim36
tupisl-1 has embryonic/larval motor neuron | first instar larval stage phenotype, suppressible by Sh14/Sh14
tupisl-1/tup[+] is an enhancer of scutellar bristle | increased number phenotype of ChiE
tupisl-1/tup[+] is an enhancer of larval intersegmental nerve | embryonic stage 16 phenotype of vvldfr-B129
tupisl-1/tup[+] is an enhancer of larval transverse nerve | embryonic stage 16 phenotype of vvldfr-B129
tupisl-1/tup[+] is an enhancer of larval intersegmental nerve | embryonic stage 16 phenotype of Lim3[+]/Lim36, vvldfr-B129
tupisl-1/tup[+] is an enhancer of larval intersegmental nerve | embryonic stage 16 phenotype of Lim36, vvl[+]/vvldfr-B129
tupisl-1 is a suppressor of dorsocentral bristle | increased number phenotype of pnrD1
tupisl-1 is a suppressor of scutellar bristle | increased number phenotype of pnrD1
In tupisl-1/+ embryos 2% of muscles 12 and 13 fail to be innervated and 3% of ISNb axons leave the ventral muscle field and target the transverse nerve (TN) fascicle. The expressivity of these phenotypes is enhanced to 21% and 16% respectively by vvldfr-B129/+. In stage 16 tupisl-1/+ Df(2L)TE35D-19/+ embryos, 11.5% of hemisegments have no transverse nerve, while 42% of hemisegments have transverse nerve fasciculation defects. In stage 16 tupisl-1/+ Lim36/+ Df(2L)TE35D-19/+ embryos, 9.3% of hemisegments have no transverse nerve, while 36% of hemisegments have transverse nerve fasciculation defects. In stage 16 tupisl-1/+ Lim36/+ Df(2L)TE35D-19/+ embryos, 4% of hemisegments have no transverse nerve, while 46% of hemisegments have transverse nerve fasciculation defects. In tupisl-1/+, Lim36/+; vvldfr-B129/+ embryos, the ISNb motoneurons fail to project to and innervate their specific target muscles, including muscles 12 and 13.
