TY - JOUR
T1 - The clathrin assembly protein PICALM is required for erythroid maturation and transferrin internalization in mice
AU - Suzuki, Mai
AU - Tanaka, Hirokazu
AU - Tanimura, Akira
AU - Tanabe, Kenji
AU - Oe, Natsuko
AU - Rai, Shinya
AU - Kon, Syunsuke
AU - Fukumoto, Manabu
AU - Takei, Kohji
AU - Abe, Takaya
AU - Matsumura, Itaru
AU - Kanakura, Yuzuru
AU - Watanabe, Toshio
PY - 2012/2/21
Y1 - 2012/2/21
N2 - 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.
AB - 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.
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U2 - 10.1371/journal.pone.0031854
DO - 10.1371/journal.pone.0031854
M3 - Article
C2 - 22363754
AN - SCOPUS:84857375101
SN - 1932-6203
VL - 7
JO - PLoS One
JF - PLoS One
IS - 2
M1 - e31854
ER -