P-393 - Is autophagy involved in the response to oxidative stress of tobacco BY-2 cells overexpressing thioredoxin o1?

Abstract

Autophagy is a catabolic process for cellular remodeling and macromolecular recycling of cytoplasmic components and organelles. Interestingly, autophagy appears as a key mechanism to cope with adverse conditions by removing damaged cellular components, although less information exists about this process in plants. In this sense, little is known about the possible role of redox regulation through thiol oxidoreductases thioredoxins (Trxs), specifically the mitochondrial/nuclear Trxo1. We have previously described a protective role of pea thioredoxin (PsTrxo1) overexpressed in TBY-2 cells treated with H2O2, thus increasing their viability via antioxidants, delaying cell death. In this work, we analyze the possible implication of autophagy as a protective mechanism operating in the PsTrxo1 transformed TBY-2 cells. For this, together with cell viability, different markers such as autophagy-related proteins ATGs are analyzed by Western blot, in parallel to autolysosomes and autophagosomes formation by fluorescence microscopy. The results have shown significant changes in ATG4 and ATG8 contents as well as presence of both lytic structures in H2O2-treated overexpressing PsTrxo1 cells, which suggest that Trxo1 may be also involved in the redox control of some autophagy components.