PMID- 25436429 OWN - NLM STAT- MEDLINE DCOM- 20150310 LR - 20141224 IS - 1090-2104 (Electronic) IS - 0006-291X (Linking) VI - 456 IP - 1 DP - 2015 Jan 2 TI - Trans-Golgi protein p230/golgin-245 is involved in phagophore formation. PG - 275-81 LID - S0006-291X(14)02102-0 [pii] LID - 10.1016/j.bbrc.2014.11.071 [doi] AB - p230/golgin-245 is a trans-Golgi coiled-coil protein that is known to participate in regulatory transport from the trans-Golgi network (TGN) to the cell surface. We investigated the role of p230 and its interacting protein, microtubule actin crosslinking protein 1 (MACF1), in amino acid starvation-induced membrane transport. p230 or MACF1 knock-down (KD) cells failed to increase the autophagic flow rate and the number of microtubule-associated protein 1 light chain 3 (LC3)-positive puncta under starvation conditions. Loss of p230 or MACF1 impaired mAtg9 recruitment to peripheral phagophores from the TGN, which was observed in the early step of autophagosome formation. Overexpression of the p230-binding domain of MACF1 resulted in the inhibition of mAtg9 trafficking in starvation conditions as in p230-KD or MACF1-KD cells. These results indicate that p230 and MACF1 cooperatively play an important role in the formation of phagophore through starvation-induced transport of mAtg9-containing membranes from the TGN. In addition, p230 itself was detected in autophagosomes/autolysosome with p62 or LC3 during autophagosome biogenesis. Thus, p230 is an important molecule in phagophore formation, although it remains unclear whether p230 has any role in late steps of autophagy. CI - Copyright (c) 2014 Elsevier Inc. All rights reserved. FAU - Sohda, Miwa AU - Sohda M AD - Division of Oral Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Niigata 951-8514, Japan. FAU - Misumi, Yoshio AU - Misumi Y AD - Department of Cell Biology, Fukuoka University School of Medicine, Jonan-ku, Fukuoka 814-0180, Japan. Electronic address: misumi@fukuoka-u.ac.jp. FAU - Ogata, Shigenori AU - Ogata S AD - Joint Laboratory for Frontier Medical Science, Fukuoka University School of Medicine, Jonan-ku, Fukuoka 814-0180, Japan. FAU - Sakisaka, Shotaro AU - Sakisaka S AD - Department of Internal Medicine, Fukuoka University School of Medicine, Jonan-ku, Fukuoka 814-0180, Japan. FAU - Hirose, Shinichi AU - Hirose S AD - Department of Pediatrics, Fukuoka University School of Medicine, Jonan-ku, Fukuoka 814-0180, Japan. FAU - Ikehara, Yukio AU - Ikehara Y AD - Fukuoka Tenjin Medical Rehabilitation Academy, Chuo-ku, Fukuoka 810-0001, Japan. FAU - Oda, Kimimitsu AU - Oda K AD - Division of Oral Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Niigata 951-8514, Japan. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20141128 PL - United States TA - Biochem Biophys Res Commun JT - Biochemical and biophysical research communications JID - 0372516 RN - 0 (Actins) RN - 0 (Autoantigens) RN - 0 (GOLGA4 protein, human) RN - 0 (MACF1 protein, human) RN - 0 (Membrane Proteins) RN - 0 (Microfilament Proteins) RN - 0 (RNA, Small Interfering) SB - IM MH - Actins/metabolism MH - Autoantigens/*metabolism MH - *Autophagy MH - Biological Transport MH - Cell Membrane/metabolism MH - Golgi Apparatus/metabolism MH - HeLa Cells MH - Humans MH - Membrane Proteins/*metabolism MH - Microfilament Proteins/*metabolism MH - Microtubules/metabolism MH - Phagosomes/metabolism MH - Plasmids/metabolism MH - Protein Transport MH - RNA, Small Interfering/metabolism OTO - NOTNLM OT - Autophagy OT - Golgi OT - Immunochemistry OT - Membrane trafficking OT - siRNA EDAT- 2014/12/02 06:00 MHDA- 2015/03/11 06:00 CRDT- 2014/12/02 06:00 PHST- 2014/11/07 00:00 [received] PHST- 2014/11/19 00:00 [accepted] PHST- 2014/12/02 06:00 [entrez] PHST- 2014/12/02 06:00 [pubmed] PHST- 2015/03/11 06:00 [medline] AID - S0006-291X(14)02102-0 [pii] AID - 10.1016/j.bbrc.2014.11.071 [doi] PST - ppublish SO - Biochem Biophys Res Commun. 2015 Jan 2;456(1):275-81. doi: 10.1016/j.bbrc.2014.11.071. Epub 2014 Nov 28.