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Biology subjects

Sahu, R. K.

Publications and source records attributed to Sahu, R. K..

2 recordsLinked to original sources

Transgenic resources for functional studies on the hsrω gene in Drosophila

The hsr{omega} gene of Drosophila melanogaster, an early discovered non-coding developmentally active and stress-inducible gene, has pleiotropic actions through its multiple nuclear and cytoplasmic non-coding transcripts. With a view to understand this diverse functions and mechanisms of actions of this gene, we generated a series of transgenic lines for over-expression or RNAi of different transcripts and CRISPR-Cas9 mediated deletion alleles. These are described here.

genetics↗

The SWI/SNF and RSC Cooperatively Remodel the Promoters of Unfolded Protein Response Targets and Heat Shock Genes

The ATP-dependent chromatin remodelling complexes maintain the chromatin dynamics, enabling the gene expression or its silencing. The SWI/SNF subfamily remodelers (SWI/SNF and RSC) generally promote gene expression by displacing or evicting nucleosomes at the promoter regions. Their action creates a nucleosome-depleted region where transcription machinery accesses the DNA. Their involvement has been shown critical for the induction of stress-responsive transcription programs. Although the role of SWI/SNF and RSC complexes in transcription regulation of heat shock responsive genes is well studied, their involvement at other pathway genes such as UPR, HSP and PQC is less known. In this study, we showed that the SWI/SNF occupies promoters of UPR, HSP and PQC genes in response to the unfolded protein stress, and its recruitment at UPR promoters is dependent on the Hac1 transcription factor and other epigenetic factors like Ada2 and Ume6. Disruption of SWI/SNFs activity does not affect the remodelling of these promoters or gene expression. However, inactivation of both RSC and SWI/SNF complexes diminishes expression of most of the UPR, HSP and PQC genes tested. Altogether these results suggest that these two remodelers work together or one compensates the loss of the other to ensure optimal induction of the stress-responsive genes.

molecular biology↗