THE CONSEQUENCES OF STRESS EFFECTS ON DRO SOPHILA-MELANOGASTER SOMATIC-CELLS IN CONDITIONS OF DISTURBED SYNTHESIS OF HEAT-SHOCK PROTEINS

Citation
Ya. Kutskova et La. Mamon, THE CONSEQUENCES OF STRESS EFFECTS ON DRO SOPHILA-MELANOGASTER SOMATIC-CELLS IN CONDITIONS OF DISTURBED SYNTHESIS OF HEAT-SHOCK PROTEINS, Genetika, 32(10), 1996, pp. 1406-1416
Citations number
50
Categorie Soggetti
Genetics & Heredity
Journal title
ISSN journal
00166758
Volume
32
Issue
10
Year of publication
1996
Pages
1406 - 1416
Database
ISI
SICI code
0016-6758(1996)32:10<1406:TCOSEO>2.0.ZU;2-R
Abstract
Restoration of cell proliferation and repair of chromosome damage (chr omatin agglutination, pulverization, or aggregation) in conditions of disturbed synthesis of heat shock proteins (HSPs) was studied in nerve ganglia of Drosophila melanogaster larvae. Two approaches were used t o suppress the heat shock response: (1) anaerobic heating of wild-type Canton S larvae at 37 degrees C for 13 min, which temporarily blocked HSP gene expression at the transcriptional level [1], and (2) aerobic heating of mutant l(1)ts403 larvae at 37 degrees C for 30 min, which disturbed HSP gene expression at the posttranscriptional level [2]. Th e duration of heat treatment was selected according to the period of r egression of heat shock puffs [3]. In both experimental systems, the p eriod of HSP synthesis and the delay in resuming cell proliferation an d recovering from mitotic chromosome stickiness increased similarly, c ompared to corresponding positive control. This suggests the involveme nt of HSPs in repairing chromatin protein damage leading to chromosome stickiness and in resuming cell proliferation. An increase in the num ber of cells with morphologically abnormal (pulverized or aggregated) chromatin was observed only after heat treatment for 30 min (rather th an for 13 min). However, the patterns of changes in the number of such cells in Canton S and l(1)ts403 larvae recovering from 30-min heat tr eatment differed from one another. Different mechanisms responsible fo r induction of chromosome abnormalities (premature condensation of int erphase chromosomes or disturbed condensation of mitotic chromosomes) and different roles of HSP in these processes are discussed.