The expression of witScer\UAS.cMa under the control of Scer\GAL4elav.PU does not lead to significant changes in the number of synaptic boutons at the third instar larval neuromuscular junction, as compared to controls.
Expression of witScer\UAS.cMa under the control of Scer\GAL4elav.PLu has no obvious effect on bouton number per muscle are at the third instar larval neuromuscular junction.
witUAS.cMa/Scer\GAL4elav.PLu is a suppressor of abnormal neuroanatomy phenotype of ImpĪ²1170, wit[+]/witHA1
witUAS.cMa/Scer\GAL4elav.PLu is a suppressor of bouton phenotype of ImpĪ²1170, wit[+]/witHA1
Scer\GAL4elav.PU/witUAS.cMa is a non-suppressor of neuromuscular junction | third instar larval stage phenotype of Nrx-1273
Scer\GAL4elav.PU/witUAS.cMa is a non-suppressor of terminal bouton | third instar larval stage phenotype of Nrx-1273
Scer\GAL4elav.PLu, Smn73Ao, witUAS.cMa has NMJ bouton phenotype
Scer\GAL4elav.PLu, Smnf01109, witUAS.cMa has NMJ bouton phenotype
The expression of witScer\UAS.cMa under the control of Scer\GAL4elav.PU does not suppress the decreased number of synaptic boutons at the third instar larval neuromuscular of Nrx-1273 homozygotes.
Neuronal expression of witScer\UAS.cMa (under the control of Scer\GAL4elav.PLu reverses the reduction in bouton number in Ranbp1170/+ ; witHA1/+ larvae.
Expression of witScer\UAS.cMa under the control of Scer\GAL4elav.PLu in a Smnf01109/+ or Smn73Ao/+ background results in a reduction in bouton number per muscle area at the third larval instar neuromuscular junction compared to wild type.
Scer\GAL4CCAP.PP/witUAS.cMa partially rescues witB11/witA12
Scer\GAL4elav-C155/witUAS.cMa partially rescues witA12/witC175
Scer\GAL4Mhc.PW/witUAS.cMa fails to rescue witunspecified
Scer\GAL4twi.2PE/witUAS.cMa fails to rescue witunspecified
The addition of witScer\UAS.cMa driven by Scer\GAL4elav-C155 rescues the lethality and muscular growth defects seen in witHA2 homozygotes or witHA2/witHA4 mutants. The addition of witScer\UAS.cMa driven by Scer\GAL4OK6 rescues the lethality and synaptic defects seen in witHA2 homozygotes.
The addition of witScer\UAS.cMa driven by Scer\GAL4elav-C155 to witA12/witC175 animals partially rescues the EJC amplitude reduction phenotype seen in mutants.