Autophagy induced by rapamycin and carbon-starvation have distinct proteome profiles in Aspergillus nidulans

It is hypothesized that autophagy, a global catabolic pathway which is highly conserved from yeast to man, plays an important role in many bioprocesses. Though autophagy is known to be induced by either nutrient starvation or treatment with the drug rapamycin, it is not clear whether the two modes of induction have the same long-term impact in the cell, particularly in the biotechnologically important filamentous fungi. Here, we compare the overall proteomes from the carbon-starved (G-) and rapamycin treated (R+) model fungus Aspergillus nidulans. From about 1,100 visualized protein spots, we conservatively selected a total of 26 proteins with significant different expression. To highlight, increased levels of glucosidases and decreased levels of N-acetylglucosamine pyrophosphorylase were observed, suggesting degradation of the fungal cell wall as an alternate carbon source for both modes of induction. Cdc37 was reduced in expression while 14-3-3 ArtA was increased, implying regulation of polar growth, while also potentially regulating autophagy negatively via PKA or Tor. Other proteins included aspartate transaminase, tryptophan synthase B (TrpB), glycylpeptide N-tetradecanoyltransferase (Nmt1), and aldehyde dehydrogenase (aldA). More interestingly, the majority of the identified proteins (16 of 26) were uniquely expressed in elevated levels in G-. A novel predicted protein from AN8223 which has no sequence homology to other organisms is also implicated to be involved in carbon-starvation. Thus, proteomic data here show that in A. nidulans, rapamycin-induced autophagy and carbon-starvation induced autophagy share some effectors for cell survival, but predominantly involve different long-term effectors.