Deletion that removes most of the Nprl3 coding region. Sequence encoding amino acids 61-559 is deleted, and a frameshift is generated, resulting in a new stop codon after 5 amino acid residues.
Approximate boundaries of a deletion that extends from amino acid 61-559 of Nprl3. The deletion causes a frameshift which leads to translation termination after 5 amino acids.
Nprl31 as well as Nprl31/Df(3L)ED4515 mutants are partially lethal (majority die at the pupae/pharate adult stage) but the Nprl31/Df(3L)ED4515 transheterozygotes eclose at significantly higher rate (though majority die as pharate adults) than the Nprl31 homozygotes - likely due to additional negative impact of their genetic background. Nprl31/Df(3L)ED4515 adults show reduced climbing ability.
The size of cells in the Nprl31 somatic follicle cell clones is significantly increased compared to adjacent heterozygous cells and the egg chambers containing Nprl31 mutant germline clones are also increased in size.
Nprl31 mutants - Nprl31/Df(3L)ED4515 transheterozygotes or homozygotes - display reduced survival rates under nutrient-liming conditions (complete starvation or amino acid starvation, respectively) and fail to activate autophagy (assessed by LysoTracker staining in larval fat body) upon starvation.
Nprl31 has partially lethal - majority die phenotype, non-enhanceable by Nprl21
Df(3L)ED4515/Nprl31 has partially lethal - majority die phenotype, suppressible | partially by Tor[+]/mTorA948V
Nprl31 is a non-enhancer of partially lethal - majority die phenotype of Nprl21
Nprl31, Wdr241 has embryonic/larval fat body | third instar larval stage phenotype
Nprl31, Wdr241 has lysosome | third instar larval stage phenotype
Fat bodies from Wdr241/Wdr241;Nprl31/Nprl31 third instar larvae accumulate large numbers of late endosomes or lysosomes (not autolysosomes); these are not observed in single Nprl31/Nprl31 mutants, and autolysosomes in Wdr241/Wdr241 single mutants are larger (and activate autophagy) rather than the than puncta in the double mutants (do not activate autophagy).
Df(3L)ED4515/Nprl31 is rescued by Scer\GAL4da.G32/Nprl3UASp.Tag:FLAG,Tag:HA
Nprl31 is rescued by Scer\GAL4da.G32/Nprl3UASp.Tag:FLAG,Tag:HA
Nprl31 is rescued by Scer\GAL4Cg.PA/Nprl3UASp.Tag:FLAG,Tag:HA
Df(3L)ED4515/Nprl31 is partially rescued by Scer\GAL4G14/Nprl3UASp.Tag:FLAG,Tag:HA
Df(3L)ED4515/Nprl31 is partially rescued by Nprl3UASp.Tag:FLAG,Tag:HA/Scer\GAL4elav.PLu
The partial lethality as well as reduced survival rates and failure to activate autophagy (assessed by LysoTracker staining in larval fat body) under nutrient-limiting conditions characteristic for Nprl31 mutants (Nprl31 homozygotes or Nprl31/Df(3L)ED4515 transheterozygotes) is rescued by expression of Nprl3Scer\UAS.P\T.T:Zzzz\FLAG,T:Ivir\HA1 under the control of Scer\GAL4da.G32. Expression under the Scer\GAL4Cg.PA driver also rescues the increased lethality and climbing defects of Nprl31/Df(3L)ED4515 animals and the latter is partially suppressed also by Scer\GAL4G14 and Scer\GAL4elav.PLu-driven expression of Nprl3Scer\UAS.P\T.T:Zzzz\FLAG,T:Ivir\HA1.