Amino acid replacement: Q643term.
C27388592T
Q643term | side-PA; Q643term | side-PB; Q643term | side-PC; Q643term | side-PD
Q643term
Site and nature of nucleotide substitution in mutant inferred by FlyBase curator based on reported amino acid change.
sideD609/Df(3R)Tl-P embryos show defects in all of the motor axon projection branches; 88% of hemisegments lack the ISNd branch, 67% lack the SNc branch, 93% lack the ISNb branch at the M6/7 muscle cleft, 80% lack the ISNb branch at the M13 muscle cleft, 85% lack the ISNb branch at the M12 muscle cleft, 12% lack the dorsal SNa branch, 6% lack the lateral SNa branch, 6% lack the first branch of the ISN, 7% lack the second branch of the ISN, 39% lack the third branch of the ISN and 4% of hemisegments show crossing of the segment boundary by the ISN. RP3 motor axons extend along the ISN beyond the ventral muscle region in stage 17 mutant embryos (instead of innervating the cleft between muscle 6 and 7 as in wild type). Many of the mutant axons extend well beyond their normal target region, exploring the area near dorsal muscle 4. Similarly, the RP1 and RP4 neurons, which normally innervate muscle 13, extend axons along the ISN to locations ranging from beneath muscle 12 to further dorsally, near muscle 4. Ventral muscles such as muscles 6 and 7 are devoid of innervation in third instar mutant larvae. In hemisegments in which innervation is absent in the ventral muscle domain, hyperinnervation of muscle 4 is seen. Expression of sideScer\UAS.cSa under the control of Scer\GAL4elav.PLu in sideD609 embryos exacerbates the sideD609 mutant phenotype, particularly in those branches of the motor projection that are less disrupted in sideD609 embryos; failure to innervate the lateral musculature is increased for both the dorsal and lateral SNa branches and the ISN stalls earlier and more frequently. The ISNb, ISNd and SNc branches are largely absent. These gain of function phenotypes are more severe than those seen when sideScer\UAS.cSa is expressed under the control of Scer\GAL4elav.PLu in a wild-type background.
Defasciculation defect, motor axons have two instead of five characteristic branches of motor projection. Motor axons remain fasciculated with pioneer axons and consequently extend further into the periphery beyond the muscle target.
sideD609 has larval abdominal intersegmental nerve phenotype, non-suppressible by Fas2e76
sideD609 is partially rescued by Scer\GAL4C142/sideUAS.cSa
sideD609 is not rescued by sideUAS.cSa/Scer\GAL4elav.PLu
Expression of sideScer\UAS.cSa under the control of Scer\GAL4C142 in sideD609 embryos results in reversion of most branches of the motor projection towards wild type.