Theautophagy-related genes AtATG5andAtATG7influence reserve mobilisation and responses to ABA during seed germination inArabidopsis thaliana

Author:

Contreras EstefaníaORCID,Pastor-Mora Elena,Aylón-Rodríguez Mar,González-Ceballos Mar,Delgado-Gutiérrez Miguel Ángel,Sánchez-Vicente InmaculadaORCID,Lorenzo ÓscarORCID,Vicente-Carbajosa JesúsORCID,Iglesias-Fernández RaquelORCID

Abstract

ABSTRACTAutophagy is a cell recycling mechanism that degrades cytoplasmic components. Although classically considered a non-selective bulk degradation mechanism, autophagy also functions selectively. Here, we investigate the impact of autophagy on seed development by studying the autophagy-related (ATG) genesAtATG5andAtATG7in Arabidopsis, focusing on their role in ABA responses. Seeds ofatg5andatg7mutants germinate significantly slower than Col-0, especially in the presence of ABA. Transcriptomic analyses comparing imbibedatg7and Col-0 seeds reveal differences in gene expression associated with lipid storage and seed maturation ontology categories. Germinating seeds ofatgmutants show histochemical alterations in the organisation of lipid droplets and protein storage vacuoles (PSV) in the emerging radicle. Notably, immunolocalization of ATG8 is observed in PSV in Col-0, but not inatgmutants. In the presence of ABA, approximately 10% of the transcriptome induced inatg7and repressed in Col-0 has been reported to be under control of the transcription factors ABI3 and ABI5, master regulators of ABA signaling in the seed. Yeast-two hybrid assays confirmed their direct interaction with the autophagy machinery through ATG8. Interestingly, the decrease in ABI5 observed in Col-0 seeds after imbibition is delayed inatgmutants, which also show altered accumulation in developing seeds of the ABI5 homolog bZIP67 that regulates reserve biosynthesis. Taken together, our data highlight the relevance of autophagy in controlling seed reserve mobilisation, its impact on seed germination, and the perception of environmental signals through ABA responses that include a transcription factor decay mechanism.

Publisher

Cold Spring Harbor Laboratory

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