Cellular heat stress can cause damage, and significant changes, to a variety of cellular structures. When exposed to chronically high temperatures, yeast cells invaginate vacuolar membranes. In this study, we found that the expression of Atg8, an essential autophagy factor, is induced after chronic heat stress. In addition, without Atg8, vacuolar invaginations are induced conspicuously, beginning earlier and invaginating vacuoles more frequently after heat stress. Our results indicate that Atg8’s invagination-suppressing functions do not require Atg8 lipidation, in contrast with autophagy, which requires Atg8 lipidation. Genetic analyses of vps24 and vps23 further suggest that full ESCRT machinery is necessary to form vacuolar invaginations irrespective of Atg8. In contrast, through a combined mutation with the vacuole BAR domain protein Ivy1, vacuoles show constitutively enhanced invaginated structures. Finally, we found that the atg8Δivy1Δ mutant is sensitive against agents targeting functions of the vacuole and/or plasma membrane (cell wall). Collectively, our findings revealed that Atg8 maintains vacuolar membrane homeostasis in an autophagy-independent function by coordinating with other cellular factors.

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We evaluated the effectiveness of using an indigenous generalist predatory mite, Neoseiulus barkeri (Hughes ) ( Acari: Phytoseiidae ) , to control Thrips palmi Karny(Thysanoptera: Thripidae )in greenhouse melons.In a growth chamber experiment, the density of T. palmi was lower on plants exposed to 20 N. barkeri per plant than on plants grown without a biological control. In a greenhouse experiment, the density of T. palmi was lower in the N. barkeri release plots than in the no-release plots. These results suggest that N. barkeri is an effective biological control agent against T. palmi.