G to A mutation at the splice acceptor site at the end of the third intron. This results in the production of two mutant mRNAs; in one case, an alternative splice site is used, resulting in a deletion of part of the fourth exon and a frameshift that results in mistranslation of most of the synaptobrevin domain. In the other case, the transcript contains an unspliced intron that results in a premature stop codon in the synaptobrevin domain.
G807353A
Nucleotide substitution: AG changed to AA in the third intron splice acceptor.
lethal (with Df(1)ED6443)
lethal (with Dp(1;3)DC012)
lethal (with Dp(1;3)DC013)
viable (with Df(1)BSC534)
Sec22ERM1 homozygous clones within mosaic fat bodies exhibit an accumulation and enlargement of ER and late endosomes (marked by KDEL-GFP and Rab7-GFP) and exhibit a more diffuse Golgi (marked by ManII-GFP), but do not show any obvious defects in mitochondria or in starvation-induced autophagy (monitored by Atg8-GFPRFP and p62), as compared to controls.
Sec22ERM1 homozygous clones within mosaic eyes exhibit small and irregularly shaped rhabdomeres which sometimes are fused with each other, as compared to controls; inside photoreceptor cells, the ER is highly expanded with numerous stacks and gradually loses its normal morphology with aging, and lipid droplets can be detected in the cytoplasm, as compared to controls.
Scer\GAL4GMR.PU, Sec22ERM1, Syx5JF03330 has decreased cell size phenotype
CG42383UAS.Tag:MYC, Scer\GAL4GMR.PU, Sec22ERM1 has decreased cell size phenotype
Scer\GAL4GMR.PU, Sec22ERM1, Syx5JF03330 has fat body phenotype
CG42383UAS.Tag:MYC, Scer\GAL4GMR.PU, Sec22ERM1 has fat body phenotype
Fat body clones that are both mutants for Sec22ERM1 and express either Syx5JF03330 or CG42383UAS.Tag:MYC under the control of Scer\GAL4GMR.PU show small cells, as compared to controls.
Sec22ERM1 is rescued by Sec22+t3.3