[Frontiers in Bioscience 18, 862-891, June 1, 2013]

Clathrin, adaptors and disease: Insights from the yeast Saccharomyces cerevisiae

Margaret D. Myers1, Gregory S. Payne1

1Department of Biological Chemistry, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095

TABLE OF CONTENTS

1. Abstract
2. Introduction
2. Introduction
3. Clathrin
3.1. Endocytosis
3.2. TGN-endosome traffic
4. Multimeric Adaptors
4.1. AP-1
4.2. AP-2
4.3. AP-3
5. Monomeric endocytic adaptors
5.1. Sla1p
5.2. Ent1p, Ent2p, Ede1p, Yap1801p, Yap1802p
5.2.1. Ent1p and Ent2p
5.2.2. Ede1p
5.2.3. Yap1801p and Yap1802p
5.3. Syp1p
6. Monomeric TGN-endosome adaptors
6.1. Gga1p and Gga2p
6.2. Ent3p and Ent5p
7. Clathrin adaptors and disease
7.1. Sorting signal mutations
7.2. AP mutations
7.3. Monomeric adaptor mutations
7.4. Functions of adaptors in trafficking of Alzheimer's disease-related proteins
7.5. Microbial pathogenesis
7.6. Yeast models for disease
8. Perspectives
9. References

1. ABSTRACT

Since the identification of clathrin as a vesicular coat protein, numerous studies have contributed to our understanding of the role of clathrin and clathrin-mediated trafficking pathways in cell function. The budding yeast, Saccharomyces cerevisiae, offers a wealth of highly developed approaches that have been applied to study clathrin-mediated trafficking events, most of which are conserved in mammalian cells. Here we review the function of clathrin and clathrin adaptors in yeast. We also discuss the role of these proteins in human disease and how certain pathogens have co-opted trafficking pathways for their own use. These studies highlight the advantages of studying complex trafficking events using yeast as a model.