Open AccessChanges in cell morphology and actin organization during heat shock in Dictyostelium discoideum : does HSP70 play a role in acquired thermotolerance?
Author(s) -
Xiang Wei,
Rensing Ludger
Publication year - 1999
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.1999.tb13764.x
Subject(s) - dictyostelium discoideum , actin , pseudopodia , microbiology and biotechnology , cytoskeleton , hsp70 , actin cytoskeleton , phalloidin , biophysics , biology , shock (circulatory) , heat shock , heat shock protein , colocalization , cell , biochemistry , medicine , gene
Abstract In response to heat shock (34°C, 30 min), cell morphology and actin organization in Dictyostelium discoideum are drastically changed. Loss of pseudopodia and disappearance of F‐actin‐containing structures were observed by using fluorescence microscopy. These changes were paralleled by a rapid decrease of the F‐actin content measured by a TRITC‐phalloidin binding assay. The effects of heat shock on cell morphology and actin organization are transient: After heat shock (34°C) or during a long‐term heat treatment (30°C), cell morphology, F‐actin patterns and F‐actin content recovered/adapted to a state which is characteristic for untreated cells. Because F‐actin may be stabilized by increased amounts of heat shock proteins, their response and interaction with F‐actin was analyzed. After a 1 h heat treatment (34°C), the major heat shock protein of D. discoideum (HSP70) showed maximally increased synthesis rates and levels. During recovery from a 34°C shock or during a continuous heat treatment at 30°C, the HSP70 content first increased and then declined slowly toward normal levels. Pre‐treatment of cells with a short heat shock of 30 min at 34°C stabilized the F‐actin content when the cells were exposed to a second heat shock. Furthermore, a transient colocalization of HSP70 and actin was observed at the beginning of heat treatment (30°C) using immunological detection of HSP70 in the cytoskeletal actin fraction.