The distributions of tau short and long isoforms fused with EGFP in cultured cells.
Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) are caused by mutations of the TAU gene. Many such mutations are located near the splicing site of exon 10 and affect the splicing ratio of 3-repeat/4-repeat tau isoforms (referred to as 3R-tau and 4R-tau) which contain 3 and 4 microtubule-binding domains, respectively. Little is known, however, concerning cellular localization of 3R-tau and 4R-tau. We examined the subcellular localization of tau isoforms in IMR-32 cells under differentiated conditions using the fusion proteins of tau isoforms probed with fluorescent protein (EGFP). 3R-tau was observed in spotty and rarely linear distributions while 4R-tau was observed in linear and sometimes spotty distributions. Together with findings of phase-contrast microscopy of cultured cells, these results indicated that 3R- and 4R-tau were predominantly localized at growth tips/branching points and along neurite processes, respectively. Due to their different localizations, balanced expression of 3R- and 4R-tau may coordinate plastic morphogenesis and stabilization of neurite processes.
Kosaka
Satoru
S
Department of Neuroscience, Osaka City University Medical School, Japan.
Takuma
Hiroshi
H
Tomiyama
Takami
T
Mori
Hiroshi
H
D045744:Cell Line, Tumor; D049452:Green Fluorescent Proteins / Q000032:analysis*; D006801:Humans; D008870:Microtubules / Q000737:chemistry; D020033:Protein Isoforms; D011993:Recombinant Fusion Proteins / Q000032:analysis*; D016875:tau Proteins / Q000032:analysis*
D020033:Protein Isoforms; D011993:Recombinant Fusion Proteins; D016875:tau Proteins; D049452:Green Fluorescent Proteins