Intracellular Ca super(2+) Release Triggers Translocation of Membrane Marker FM1-43 from the Extracellular Leaflet of Plasma Membrane into Endoplasmic Reticulum in T Lymphocytes

• Published in: The Journal of biological chemistry Vol. 280; no. 16; pp. 16377 - 16382
• Main Authors: Dadsetan, Sepehr, Shishkin, Vyacheslav, Fomina, Alla F
• Format: Journal Article
• Language: English
• Published: 01.04.2005
• ISSN: 0021-9258; 1083-351X

Stimulation of T cell receptor in lymphocytes enhances Ca super(2+) signaling and accelerates membrane trafficking. The relationships between these processes are not well understood. We employed membrane-impermeable lipid marker FM1-43 to explore membrane trafficking upon mobilization of intracellular Ca super(2+) in Jurkat T cells. We established that liberation of intracellular Ca super(2+) with T cell receptor agonist phytohemagglutinin P or with Ca super(2+)-mobilizing agents ionomycin or thapsigargin induced accumulation of FM1-43 within the lumen of the endoplasmic reticulum (ER), nuclear envelope (NE), and Golgi. FM1-43 loading into ER-NE and Golgi was not mediated via the cytosol because other organelles such as mitochondria and multivesicular bodies located in close proximity to the FM1-43-containing ER were free of dye. Intralumenal FM1-43 accumulation was observed even when Ca super(2+) signaling in the cytosol was abolished by the removal of extracellular Ca super(2+). Our findings strongly suggest that release of intracellular Ca super(2+) may create continuity between the extracellular leaflet of the plasma membrane and the lumenal membrane leaflet of the ER by a mechanism that does not require global cytosolic Ca super(2+) elevation.