Effect of pH and Cell Cycle Progression on Development and Decay of Thermotolerance

Holahan, Patricia K.; Dewey, William C.

doi:10.2307/3576566

Cited by 15 publications

(2 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1). This latter result agrees with our earlier observation that the heat-induced cell cycle delay was similar for the clonogenic and nonclonogenic cells (Holahan and Dewey, 1986;Vidair and Dewey, 1991). Thus, the nonclonogenic and clonogenic cells behaved similarly until the cells entered mitosis, a t which time thermal damage was expressed in the nonclonogenic cells as both a longer duration of prophase-metaphase and multinucleation.…”

Section: Discussionsupporting

confidence: 92%

Heat shock alters centrosome organization leading to mitotic dysfunction and cell death

Vidair

Doxsey

Dewey

1993

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

To identify the cellular target(s) responsible for thermal killing in the G1 phase of the cell cycle, synchronous cultures of Chinese hamster ovary cells (CHO) were heat shocked and studied for one cell cycle by time-lapse videomicroscopy and immunocytochemistry. At the first mitosis post-heating, the fraction of cells giving rise to multinucleated progeny approximately equaled the nonclonogenic fraction. In addition, the cells yielding multinucleated progeny were delayed in prophase-metaphase relative to the cells yielding two uninucleated progeny (clonogenic cells). To study the basis for the delay in prophase-metaphase and subsequent formation of multinucleated cells, cells in mitosis were examined by immunofluorescence for spindle abnormalities. Multipolar mitotic spindles and chromosome misalignment were induced by heat. All multiple spindle poles induced by heat stained for pericentriolar material (PCM), the microtubule nucleating material of centrosomes. Heated cells in mitosis also contained additional foci of PCM which were not associated with the spindle. Cells made thermotolerant by a nonlethal heat shock were resistant to both thermal killing and the induction of multiple foci of PCM. Quantitative analysis revealed a good correlation between the fraction of cells with multipolar spindles, the fraction with more than two foci of PCM, and the nonclonogenic fraction. These data indicate that heat-induced alterations to the PCM of centrosomes resulted in multipolar mitotic spindles, delay in prophase-metaphase, and formation of multinucleated cells which were nonclonogenic. These results identify the centrosome as a G1 target for cell killing.

show abstract

Section: Discussionsupporting

confidence: 92%

Heat shock alters centrosome organization leading to mitotic dysfunction and cell death

Vidair

Doxsey

Dewey

1993

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In fact, the treatment at 43°C increased the amount of thermotolerance compared with thermotolerance after pretreatment with PUR only (compare curves 2 and A). This increase in thermotolerance cannot be attributed to heating at 43°C selectively killing heat-sensitive S cells, thus leaving heat-resistant G1 cells, because the expression of thermotolerance is very similar in asynchronous cells and G1 cells (Holahan and Dewey, 1986). Also note that the amount of thermotolerance was similar for pretreatment with PUR only (curve A for 20 pglml followed by 2-5 h r a t 37°C) and for the high concentration of PUR administered during and immediately before heating at 43°C (curves 5 and 6).…”

Section: Heat Protection Induced By Chm or Pur Compared With Thermotomentioning

confidence: 99%

Induction of heat shock proteins in Chinese hamster ovary cells and development of thermotolerance by intermediate concentrations of puromycin

Lee

Dewey

1987

Journal Cellular Physiology

View full text Add to dashboard Cite

During 4 hr after puromycin (PUR: 20 micrograms/ml) treatment, the synthesis of three major heat shock protein families (HSPs: Mr = 110,000, 87,000, and 70,000) was enhanced 1.5-fold relative to that of untreated cells, as studied by one-dimensional gel electrophoresis. The increase of unique HSPs, if studied with two-dimensional gels, would probably be much greater. In parallel, thermotolerance was observed at 10(-3) isosurvival as a thermotolerance ratio (TTR) of either 2 or greater than 5 after heating at either 45.5 degrees C or 43 degrees C, respectively. However, thermotolerance was induced by only intermediate concentrations (3-30 micrograms/ml) of puromycin that inhibited protein synthesis by 15-80%; a high concentration of PUR (100 micrograms/ml) that inhibited protein synthesis by 95% did not induce either HSPs or thermotolerance. Also, thermotolerance was never induced by any concentration (0.01-10 micrograms/ml) of cycloheximide that inhibited protein synthesis by 5-94%. Furthermore, after PUR (20 micrograms/ml) treatment, the addition of cycloheximide (CHM: 10 micrograms/ml), at a concentration that reduces protein synthesis by 94%, inhibited both thermotolerance and synthesis of HSP families. Thus, thermotolerance induced by intermediate concentrations of PUR correlated with an increase in newly synthesized HSP families. This thermotolerance phenomenon was compared with another phenomenon termed heat resistance and observed when cells were heated at 43 degrees C in the presence of CHM or PUR immediately after a 2-hr pretreatment with CHM or PUR. Heat protection increased with inhibition of synthesis of both total protein and HSP families. Moreover, this heat protection decayed rapidly as the interval between pretreatment and heating increased to 1-2 hr, and did not have any obvious relationship to the synthesis of HSP families. Therefore, there are two distinctly different pathways for developing thermal resistance. The first is thermotolerance after intermediate concentrations of PUR treatment, and it requires incubation after treatment and apparently the synthesis of HSP families. The second is resistance to heat after CHM or PUR treatment immediately before and during heating at 43 degrees C, and it apparently does not require synthesis of HSP families. This second pathway not requiring the synthesis of HSP families also was observed by the increase in thermotolerance at 45.5 degrees C caused by heating at 43 degrees C after cells were incubated for 2-4 hr following pretreatment with an intermediate concentration of PUR.

show abstract

Biochemistry of the cell cycle

Lloyd¹

1987

Biochemical Journal

View full text Add to dashboard Cite

Effect of pH and Cell Cycle Progression on Development and Decay of Thermotolerance

Cited by 15 publications

References 7 publications

Heat shock alters centrosome organization leading to mitotic dysfunction and cell death

Heat shock alters centrosome organization leading to mitotic dysfunction and cell death

Induction of heat shock proteins in Chinese hamster ovary cells and development of thermotolerance by intermediate concentrations of puromycin

Biochemistry of the cell cycle

Contact Info

Product

Resources

About