Arabidopsis cargo receptor NBR1 contributes to protein quality control by promoting the formation of protein aggregates and mediating their clearance via selective autophagy.

Autophagy is an intracellular trafficking mechanism by which cytosolic macromolecules and organelles are sequestered into autophagosomes for degradation inside the vacuole. In various eukaryotes including yeast, metazoans, and plants, the precursor of the autophagosome, termed the phagophore, nucleates in the vicinity of the endoplasmic reticulum (ER) with the participation of phosphatidylinositol 3-phosphate (PI3P) and the coat protein complex II (COPII). Here we show that Arabidopsis thaliana FYVE2, a plant-specific PI3P-binding protein, provides a functional link between the COPII machinery and autophagy. FYVE2 interacts with the small GTPase SAR1, which is essential for the budding of COPII vesicles. FYVE2 also interacts with ATG18A, another PI3P effector on the phagophore membrane. Fluorescently tagged FYVE2 localized to autophagic membranes near the ER and was delivered to vacuoles. SAR1 fusion proteins were also targeted to the vacuole via FYVE2-dependent autophagy. Either mutations in FYVE2 or the expression of dominant-negative mutant SAR1B proteins resulted in reduced autophagic flux and the accumulation of autophagic organelles. We propose that FYVE2 regulates autophagosome biogenesis through its interaction with ATG18A and the COPII machinery, acting downstream of ATG2.

Kikuchi-Fujimoto disease (KFD) is a benign, self-limiting disease, with a specific histopathology. It can be diagnosed clinically, and specific symptoms include fever and cervical lymphadenopathy. The histological finding of KFD in cervical lymph nodes includes necrotizing lymphadenitis. KFD needs conservative treatments. If KFD persists for a long period, steroids or nonsteroidal antiinflammatory drugs can be used to control symptoms. Previous studies have reported the treatment of KFD with hydroxychloroquine (HC) in patients unresponsive to steroids. Herein, we report a case of a 25-year-old female patient diagnosed with KFD unresponsive to steroids, and was successfully treated with HC.

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