Specific COPII vesicles transport ER membranes to sites of autophagosome formation

Abstract

The endoplasmic reticulum (ER) is considered a prominent membrane source for the formation of autophagosomes. Recent results from our laboratory revealed a cellular mechanism for the contribution of the ER to autophagosomes in yeast: membranes, together with unconventional membrane fusion machinery, are delivered to sites of autophagosome formation by specific coat protein complex II (COPII) vesicles.

Keywords: Autophagy; SNARE proteins; membrane fusion; membrane traffic.

Figure 1.

Model for the contribution of endoplasmic reticulum (ER) membranes to autophagosome biogenesis via vesicular transport. Ufe1, an ER-resident Qa/t-SNARE protein, is incorporated into specific coat protein complex II (COPII) vesicles that form upon conditions that trigger autophagy. The COPII vesicles are targeted to sites of autophagosome formation where they fuse with other membrane sources, such as Atg9-containing vesicles, to form a phagophore that through continuous expansion will give rise to an autophagosome. Ufe1 itself might participate in such membrane fusions by forming complexes with distinct SNARE proteins that are present on other membranes. The identity of the individual partner SNARE proteins for the particular fusion reactions remains to be determined. A specific membrane fusion requires the participation of 3 to 4 distinct SNARE proteins but for simplicity fewer individual SNARE proteins are shown here.