International Mammalian Genome Society

The 14th International Mouse Genome Conference (2000)

B4. Identification of A Novel RING Finger Protein Associated with Pallidin

Liping Huang1 and Jane Gitschier2
Western Human Nutrition Research Center, University of California Davis;
Howard Hughes Medical Institute, University of California San Francisco.

We have recently reported the identification of the gene that underlies the defect for the pallid mutant. Pallid is one of thirteen platelet storage pool deficiency (SPD) mouse mutants. Pallid animals are characterized by abnormal structures/functions of subcellular organelles including platelet dense granules, melanosomes as well as lysosomes and abnormal metabolisms of manganese and zinc ions. The pallid gene encodes a protein (pallidin) that interacts with syntaxin 13, a t-SNARE protein involved in intracellular vesicle docking and fusion. The interaction between pallidin and syntaxin 13 suggests a role for pallidin in the vesicle-docking and fusion process in cells.

Here we describe the identification of another novel protein that interacts with pallidin, Paint 1 (pallidin interactor 1), a mammalian protein with homology to a yeast protein involved in protein transport to the yeast vacuoles. The homology suggests that Paint 1 may play a role in intracellular protein trafficking in mammals. An approximately 3.7-kb transcript of Paint 1 was detected in mouse tissues of liver, brain, kidney, spleen, intestine and heart with abundant expression in brain by northern blot assay. The full-length open reading frame of 2919-bp predicts a hydrophilic protein of 973 amino acids. Paint 1 has a ring finger zinc-binding motif at the C-terminus of the protein identical to its yeast homologue. By immunohistochemistry analysis, Paint 1 was detected in the cytoplasm of the rat fibroblasts using an antibody raised against a peptide near C-terminus of Paint 1. The precious intracellular localization of Paint 1 will be further studied. The possible functions of Paint 1 and its yeast homologue in intracellular manganese and zinc homeostasis will be discussed as the pallid mutant exhibit abnormal manganese and zinc metabolisms.


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