ArticleMolecular biology of the cell2002
Dictyostelium LvsB mutants model the lysosomal defects associated with Chediak-Higashi syndrome.
Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 71 citations in OpenAlex.
- The lysosomal trafficking regulator "LYST": an 80-year traffic jam.Frontiers in immunology · 2024Review
- The old and the new about the contractile vacuole of Trypanosoma cruzi.The Journal of eukaryotic microbiology · 2022Review
- Review
- Deficiency in Lyst function leads to accumulation of secreted proteases and reduced retinal adhesion.PloS one · 2022Article
- The Ecology and Evolution of Amoeba-Bacterium Interactions.Applied and environmental microbiology · 2021Review
- The Polarized Redistribution of the Contractile Vacuole to the Rear of the Cell is Critical for Streaming and is Regulated by PI(4,5)P2-Mediated Exocytosis.Frontiers in cell and developmental biology · 2021Review
- Lysosomal trafficking regulator Lyst links membrane trafficking to toll-like receptor-mediated inflammatory responses.The Journal of experimental medicine · 2017Article
- Eat Prey, Live:Frontiers in immunology · 2017Review
- Physical, Functional and Genetic Interactions between the BEACH Domain Protein SPIRRIG and LIP5 and SKD1 and Its Role in Endosomal Trafficking to the Vacuole in Arabidopsis.Frontiers in plant science · 2017Article
- Using the social amoeba Dictyostelium to study the functions of proteins linked to neuronal ceroid lipofuscinosis.Journal of biomedical science · 2016Review
- Dictyostelium LvsB has a regulatory role in endosomal vesicle fusion.Journal of cell science · 2014Article
- Intracellular killing of bacteria: is Dictyostelium a model macrophage or an alien?Cellular microbiology · 2014Review
- Antagonistic control of lysosomal fusion by Rab14 and the Lyst-related protein LvsB.Traffic (Copenhagen, Denmark) · 2013Article
- Drosophila mauve mutants reveal a role of LYST homologs late in the maturation of phagosomes and autophagosomes.Traffic (Copenhagen, Denmark) · 2012Article
- Rab8a regulates the exocyst-mediated kiss-and-run discharge of the Dictyostelium contractile vacuole.Molecular biology of the cell · 2012Article
- The enlarged lysosomes in beige j cells result from decreased lysosome fission and not increased lysosome fusion.Traffic (Copenhagen, Denmark) · 2012Article
- Regulation of secretory granule size by the precise generation and fusion of unit granules.Journal of cellular and molecular medicine · 2010Review
- Dictyostelium finds new roles to model.Genetics · 2010Review
- Effect of starvation on the endocytic pathway in Dictyostelium cells.Eukaryotic cell · 2010Article
- Endosomal and secretory markers of the Legionella-containing vacuole.Communicative & integrative biology · 2009Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Chediak-Higashi syndrome is a genetic disorder caused by mutations in a gene encoding a protein named LYST in humans ("lysosomal trafficking regulator") or Beige in mice. A prominent feature of this disease is the accumulation of enlarged lysosome-related granules in a variety of cells. The genome of Dictyostelium discoideum contains six genes encoding proteins that are related to LYST/Beige in amino acid sequence, and disruption of one of these genes, lvsA (large volume sphere), results in profound defects in cytokinesis. To better understand the function of this family of proteins in membrane trafficking, we have analyzed mutants disrupted in lvsA, lvsB, lvsC, lvsD, lvsE, and lvsF. Of all these, only lvsA and lvsB mutants displayed interesting phenotypes in our assays. lvsA-null cells exhibited defects in phagocytosis and contained abnormal looking contractile vacuole membranes. Loss of LvsB, the Dictyostelium protein most similar to LYST/Beige, resulted in the formation of enlarged vesicles that by multiple criteria appeared to be acidic lysosomes. The rates of endocytosis, phagocytosis, and fluid phase exocytosis were normal in lvsB-null cells. Also, the rates of processing and the efficiency of targeting of lysosomal alpha-mannosidase were normal, although lvsB mutants inefficiently retained alpha-mannosidase, as well as two other lysosomal cysteine proteinases. Finally, results of pulse-chase experiments indicated that an increase in fusion rates accounted for the enlarged lysosomes in lvsB-null cells, suggesting that LvsB acts as a negative regulator of fusion. Our results support the notion that LvsB/LYST/Beige function in a similar manner to regulate lysosome biogenesis.
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