Abstract
Endophytic colonization of Arabidopsis thaliana by the beneficial root endophyte Serendipita indica is characterized by an initial biotrophic phase followed by a restricted host cell death-associated phase. This latter phase involves regulated cell death (RCD) for fungal accommodation. However, the host molecular pathways that limit S. indica colonization and govern symbiosis remain largely unknown. Our study demonstrates that autophagy, a major cellular degradation pathway, is activated during S. indica colonization and is required to restrict fungal colonization in Arabidopsis. Independent Arabidopsis knockout (KO) mutants deficient in autophagosome formation are more susceptible to deoxyadenosine (dAdo), a cell death inducer produced by two secreted S. indica effectors at the onset of the cell death-associated phase. In the atg5 autophagy mutant background, impaired dAdo uptake prevents dAdo-induced and symbiosis-mediated cell death. Based on our data, we propose that autophagy-mediated pro-survival responses in the host are crucial for maintaining a balanced symbiotic interaction between S. indica and Arabidopsis.
In a Nutshell Our study reveals that during colonization of Arabidopsis thaliana roots by the beneficial root endophyte Serendipita indica, autophagy, a key cellular degradation pathway, is activated to limit fungal colonization. Autophagy-deficient Arabidopsis mutants are more susceptible to deoxyadenosine (dAdo), a cell death inducer produced by S. indica. We propose that autophagy-mediated pro-survival responses are essential for maintaining a balanced symbiotic interaction between S. indica and Arabidopsis.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
Main Figure 4 was updated with new data. The model in Figure 5 was slightly adapted. Supplemental figures were updated
