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Updated: May 24, 2026

Visualizing Clathrin-mediated Endocytosis of G Protein-coupled Receptors at Single-event Resolution via TIRF Microscopy
Published on: October 20, 2014
The clathrin assembly protein PICALM is required for erythroid maturation and transferrin internalization in mice
Mai Suzuki1, Hirokazu Tanaka, Akira Tanimura
1Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
Abstract:
Phosphatidylinositol binding clathrin assembly protein (PICALM), also known as clathrin assembly lymphoid myeloid leukemia protein (CALM), was originally isolated as part of the fusion gene CALM/AF10, which results from the chromosomal translocation t(10;11)(p13;q14). CALM is sufficient to drive clathrin assembly in vitro on lipid monolayers and regulates clathrin-coated budding and the size and shape of the vesicles at the plasma membrane. However, the physiological role of CALM has yet to be elucidated. Here, the role of CALM in vivo was investigated using CALM-deficient mice. CALM-deficient mice exhibited retarded growth in utero and were dwarfed throughout their shortened life-spans. Moreover, CALM-deficient mice suffered from severe anemia, and the maturation and iron content in erythroid precursors were severely impaired. CALM-deficient erythroid cells and embryonic fibroblasts exhibited impaired clathrin-mediated endocytosis of transferrin. These results indicate that CALM is required for erythroid maturation and transferrin internalization in mice.
Insights
Phosphatidylinositol binding clathrin assembly protein (CALM) is essential for mouse growth and survival. CALM deficiency causes severe anemia and impaired transferrin uptake, highlighting its critical role in erythroid maturation.
Area of Science:
- Cell Biology
- Molecular Biology
- Hematology
Background:
- Phosphatidylinositol binding clathrin assembly protein (PICALM), also known as clathrin assembly lymphoid myeloid leukemia protein (CALM), is involved in clathrin assembly and vesicle formation.
- Its precise physiological function in vivo remained largely unknown.
Purpose of the Study:
- To investigate the in vivo physiological role of CALM using a mouse model.
Main Methods:
- Generation and analysis of CALM-deficient mice.
- Assessment of growth, lifespan, erythroid maturation, and iron content.
- Evaluation of clathrin-mediated endocytosis in erythroid cells and fibroblasts.
Main Results:
- CALM-deficient mice displayed growth retardation, dwarfism, and shortened lifespans.
- Severe anemia was observed, with impaired erythroid precursor maturation and iron content.
- Impaired transferrin internalization via clathrin-mediated endocytosis was evident in CALM-deficient cells.
Conclusions:
- CALM is crucial for normal erythroid maturation in mice.
- CALM plays a vital role in transferrin internalization, essential for erythroid development.
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