European Regional Development Fund(GINOP-2.3.2-15-2016-00006) Támogató: GINOP
(GINOP-2.3.2-15-2016-00032)
(KKP129797) Támogató: NKFIH
(K119842) Támogató: NKFIH
Lysosomal degradation, the common destination of autophagy and endocytosis, is one
of the most important elements of eukaryotic metabolism. The small GTPases Rab39A
and B are potential new effectors of this pathway, as their malfunction is implicated
in severe human diseases like cancer and neurodegeneration. In this study, the lysosomal
regulatory role of the single Drosophila Rab39 ortholog was characterized, providing
valuable insight into the potential cell biological mechanisms mediated by these proteins.
Using a de novo CRISPR-generated rab39 mutant, we found no failure in the early steps
of endocytosis and autophagy. On the contrary, we found that Rab39 mutant nephrocytes
internalize and degrade endocytic cargo at a higher rate compared to control cells.
In addition, Rab39 mutant fat body cells contain small yet functional autolysosomes
without lysosomal fusion defect. Our data identify Drosophila Rab39 as a negative
regulator of lysosomal clearance during both endocytosis and autophagy.