Downregulation of hsp22 gene expression in Drosophila melanogaster from sites located near chemical plants

Abstract

ABSTRACT.A common physiological response of organisms to environmental conditions is variation in gene expression, especially true for genes encoding for heat shock proteins. In insects, this process has been examined for induced heat or cold stress. The putative longterm imprinted/acquired heat shock protein response due to unfriendly environmental conditions has been far less studied. The Drosophila melanogaster hsp22 gene, which has been extensively reviewed as being sensitive to different changing life conditions, was examined by qRT-PCR, using carboxy-X-rhodamine. In the present study, we focused on the detection of hsp22 level of transcription in three D. melanogaster isolates, collected from sites located near different chemical plants in Romania and subjected to one-year adaptation to laboratory conditions. In all isolates, the hsp22 gene expression was determined using the housekeeping genes Gapdh1 and UbcD10 as internal controls. According to our experimental results, the D. melanogaster hsp22 gene was significantly downregulated compared to the same gene in w 1118 iso, used as a calibrator. We showed that hsp22 could play an important role in relation to stress resistance and adaptation. This study highlights the importance of in vivo studies to demonstrate genome plasticity to overcome different damages induced by any presumed source of stress.

Overexpression of Arabidopsis HsfA1a enhances diverse stress tolerance by promoting stress-induced Hsp expression

“…The molecular basis underlying the role of Hsfs in stress tolerance is still not clear. Expression of Hsps as chaperones, including Hsp18.2 and Hsp70, protects cells against injuries associated with various stressors (Simões-Araújo et al, 2003;de Azevedo et al, 2012;Magdalena et al 2012). On the other hand, HsfA1a can bind various promoter targets that are not limited to classical Hsp genes and also include other genes (Guo et al, 2008), implying a broad physiological basis for the stress tolerance role of HsfA1a.…”