The P{PZ}Syx1A06737 insertion maps within both Syx1A and 4EHP (nested genes).
P-element insertion 880bp upstream of the translation start site.
Homozygous embryos do not exhibit cuticle defects. Germline clones produce eggs with poorly differentiated cuticle.
Mutation compromises neurotransmission at the embryonic neuromuscular junction. Mature embryos fail to exhibit contraction waves but do emerge from the egg case. Cuticular structures are normal. Syx1A06737/Syx1A15ts transheterozygotes give progeny that exhibit reduced viability, rough eyes (disrupted ommatidial array, ommatidia may be missing, fused, improperly rotated or misaligned) and notching along the posterior margin of the wing. Clones cannot be recovered in the eye as lack of Syx1A activity in cells of the developing eye causes lethality.
Embryos do not exhibit typical peristaltic construction waves and reduced movements of the mouth hooks and muscles in the head region. Embryos were also unable to clear their tracheal system of fluid. Endogenous transmission is blocked but spontaneous vesicle release continues. The ability of vesicles to fuse and release neurotransmitter in response to calcium ion stimulus is impaired, reflected by the severely reduced excitatory junction current.
Syx1A06737 is a suppressor of visible phenotype of Hsap\HTT128Q.1-336.UAS, Scer\GAL4GMR.PU
Syx1A06737 is a suppressor of eye phenotype of Hsap\HTT128Q.1-336.UAS, Scer\GAL4GMR.PU
Syx1A06737 is rescued by Syx1AI212A
Syx1A06737 is rescued by Syx1A+t13.5
Syx1A06737 is rescued by Syx1AI236A
Syx1A06737 is rescued by Syx1A+t11
Syx1A06737 is rescued by Syx1A+t6
Syx1A06737 is partially rescued by Syx1AH3-C
Syx1A06737 is not rescued by Syx1AH3-N
Lethality is rescued by one copy of the Syx1A+t11 or Syx1A+t6 constructs, rescued adults are viable, fertile and morphologically normal. Less than 10% Syx1A287/Syx1A06737 and Syx1A204/Syx1A06737 transheterozygous adults are viable.
A. Spradling.
Lethality can be reverted by precise excision of the P-element.