Τρίτη 30 Ιανουαρίου 2018

Autophagy Controls Resource Allocations and Protein Storage Accumulation in Arabidopsis Seeds.

Autophagy Controls Resource Allocations and Protein Storage Accumulation in Arabidopsis Seeds.

J Exp Bot. 2018 Jan 25;:

Authors: Di Berardino J, Marmagne A, Berger A, Yoshimoto K, Cueff G, Chardon F, Masclaux-Daubresse C, Reisdorf-Cren M

Abstract
Autophagy is essential for nutrient recycling and plays a fundamental role in seed production and grain filling in plants. Autophagy participates in nitrogen remobilization at the whole plant level, and the seeds of autophagy mutants present abnormal C and N contents relative to wild type (WT). It is well known that autophagy genes are induced in leaves during senescence. The increased expression of autophagy genes in seeds has never been reported so far. We show here that most of the ATG genes are induced during seed maturation in Arabidopsis siliques and that ATG8f is the most highly expressed among them. PromoterATG8f::UIDA and promoterATG8f::GFP fusions confirmed the strong expression of ATG8f in the phloem companion cells of pericarps and funiculus and in the embryo. Expression was especially strong at the late stages of development. Many GFP-ATG8 autophagic structures resembling pre-autophagosomal structures (PAS) and autophagosomes confirmed the presence of autophagic activity in WT seed embryos. Seeds of atg5 and WT plants grown under low or high nitrate conditions were analysed. Nitrate-independent phenotypes were found with higher seed abortion in atg5 and higher total protein concentrations in the viable seeds of this mutant as compared to WT. The higher total protein accumulation in atg5 viable seeds was significant from early developmental stages onwards. In addition, relatively higher 12S globulin precursors and lower 12S mature forms were found in atg5 seeds. These two features led us to the conclusion that atg5 seed development is accelerated and that protein storage deposition pathway is somehow abnormal or incomplete.

PMID: 29378007 [PubMed - as supplied by publisher]



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