Arabidopsis flowering integrator SOC1 transcriptionally regulates autophagy in response to long-term carbon starvation.

Abstract

Autophagy is a highly conserved, self-digestion process that is essential for plant adaptations to various environmental stresses. Although the core components of autophagy in plants have been well established, the molecular basis for its transcriptional regulation remains to be fully characterized. In this study, we demonstrate that SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1 (SOC1), a MADS-box family transcription factor that determines flowering transition in Arabidopsis, functions as a transcriptional repressor of autophagy. EMSAs, ChIP-qPCR assays, and dual-luciferase receptor assays showed that SOC1 can bind to the promoters of ATG4b, ATG7, and ATG18c via the conserved CArG box. qRT-PCR analysis showed that the three ATG genes ATG4b, ATG7, and ATG18c were up-regulated in the soc1-2 mutant. In line with this, the mutant also displayed enhanced autophagy activity, as revealed by increased autophagosome formation and elevated autophagic flux compared with the wild type. More importantly, SOC1 negatively affected the tolerance of plants to long-term carbon starvation, and this process requires a functional autophagy pathway. Finally, we found that SOC1 was repressed upon carbon starvation at both the transcriptional and protein levels. Overall, our study not only uncovers an important transcriptional mechanism that contributes to the regulation of plant autophagy in response to nutrient starvation, but also highlights novel cellular functions of the flowering integrator SOC1.