The consequences of stress effects on Drosophila melanogaster somatic cells in conditions of disturbed synthesis of heat shock proteins

Restoration of cell proliferation and repair of chromosome damage (chromatin 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 to 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]. The duration of heat treatment was selected according to the period of regression of heat shock puffs [3]. In both experimental systems, the period of HSP synthesis and the delay in resuming cell proliferation and recovering from mitotic chromosome stickiness increased similarly, compared to corresponding positive control. This suggests the involvement of HSPs in repairing chromatin protein damage leading to chromosome stickiness and in resuming cell proliferation. An increase in the number of cells with morphologically abnormal (pulverized or aggregated) chromatin was observed only after heat treatment for 30 min (rather than 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 treatment differed from one another. Different mechanisms responsible for induction of chromosome abnormalities (premature condensation of interphase chromosomes or disturbed condensation of mitotic chromosomes) and different roles of HSP in these processes are discussed.