||Professor, Principal Investigator
||1) The regulation and mechanism of autophagy (in yeast Saccharomyces cerevisiae)
2) Autophagy-pathogen interactions
- Research Profile
- Selected Publications
Fulvio Reggiori (1970) studied Biochemistry at University of Fribourg, Switzerland, and in 1997, he obtained his PhD in Biochemistry from the same Institution. Here, in the laboratory of Prof. Andreas Conzelmann, he has worked on the remodelling of the lipid moiety of GPI-anchored proteins and on sphingolipid biosynthesis in yeast Saccharomyces cerevisiae.
After staying one additional year in the same laboratory as a postodoctoral fellow, he moved to the MRC Laboratory of Molecular Biology in Cambridge, United Kingdom, in 1998. There, in the laboratory of Dr. Hugh Pelham, he has investigated the signals targeting integral membrane proteins into the internal vesicles of multivesicular bodies.
In 2001, he joined the laboratory of Prof. Daniel Klionsky at the Life Sciences Institute of the University of Michigan in Ann Arbor (USA). There, he started working on different aspects of the molecular mechanism of autophagy in yeast.
In 2005, Fulvio Reggiori was appointed as a tenured Assistant Professor at the Department of Cell Biology of the University Medical Center Utrecht, where he started is independent research career working on the molecular mechanism of autophagy. The laboratory interests also extended to pathogens that subvert autophagy to invade host cells. In 2011, he became an Associate professor at the same Institution.
In 2015, Fulvio Reggiori became Professor at the Department of Cell Biology of the University Medical Center Groningen, where he is contuining his investigation on the molecular mechanism of autophagy in yeast and on the interaction between pathogens and the ATG proteins.
- Mauthe M, Langereis M, Jung J, Zhou X, Jones A, Omta W, Tooze SA, Stork B, Paludan SR, Ahola T, Egan D, Behrends C, Mokry M, de Haan C, van Kuppeveld F, Reggiori F (2016), An siRNA screen for ATG depletion reveals the extent of unconventional functions of the autophagy proteome in virus replication, J Cell Biol, 214, 619-635. (pdf)
- Khaminets A, Heinrich T, Mari M, Grumati P, Huebner AK, Akutsu M, Liebmann L, Stolz A, Nietzsche S, Koch N, Mauthe M, Katon I, Qualmann B, Weis J, Reggiori F, Kurth I, Hübner CA, Dikic I (2015), Regulation of endoplasmic reticulum homeostasis by FAM134B-mediated selective autophagy, Nature, 522, 354-358. (pdf)
- Mari M, Geerts WJ, Reggiori F (2014), Immuno- and correlative light microscopy-electron tomography methods for 3D protein localization in yeast, Traffic, 15, 1164-78. (pdf)
- Hönscher C, Mari M, Auffarth K, Bohnert M, Griffith J, Geerts W, van der Laan M, Cabrera M, Reggiori F, Ungermann C (2014), Cellular metabolism regulates contact sites of vacuoles with mitochondria, Dev Cell, 30, 86-94. (pdf)
- Rieter E, Vinke F, Bakula D, Cebollero E, Ungermann C, Proikas-Cezanne T, Reggiori F (2013), Atg18 function in autophagy is regulated by specific sites within its β-propeller, J Cell Sci, 126, 593-604. (pdf)
- Cebollero E, van der Vaart A, Zhao M, Rieter E, Klionsky DJ, J. Helms B, Reggiori F (2012), Phosphatidylinositol-3-phosphate clearance plays a key role in autophagosome completion, Curr Biol, 22, 1545-1553. (pdf)
- Nair U, Jotwani A, Geng J, Gammoh N, Richerson D, Yen W-L, Griffith J, Nag S, Wang K, Moss T, Baba M, McNew JA, Jiang X, Reggiori F*, Melia TJ, Klionsky DJ (2011), SNARE proteins are required for macroautophagy, Cell, 146, 290-302. *co-corresponding author (pdf)
- Mari M, Griffith J, Rieter E, Krishnappa L, Klionsky DJ, Reggiori F (2010), An Atg9-containing compartment that functions in the early steps of autophagosome biogenesis, J Cell Biol, 190, 1005-1022. (pdf)
- van der Vaart A, Griffith J, Reggiori F (2010), Exit from the Golgi is required for the expansion of the autophagosomal phagophore in the yeast Saccharomyces cerevisiae, Mol Biol Cell, 21, 2270–2284. (pdf)
- Reggiori F, Monastyrska I, Verheije MH, Calì’ T, Ulasli M, Bianchi S, Bernasconi R, de Haan CAM, Molinari M (2010), Coronaviruses hijack LC3-I-positive EDEMosome membranes for replication, Cell Host Microbe, 7, 500-508. *co-corresponding author (pdf)