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The DEAD-box helicase Hlc regulates basal transcription and chromatin opening of stress-responsive genes

ABSTRACT: Stress-responsive genes are lowly transcribed under normal conditions and robustly induced in response to stress. The significant difference between basal and induced transcription indicates that the general transcriptional machinery requires a mechanism to distinguish each transcription state. However, what factors specifically function in basal transcription remains poorly understood. Using a classic model stress-responsive gene (Drosophila MtnA), we found that knockdown of the DEAD-box helicase Hlc resulted in a significant transcription attenuation of MtnA under normal, but not stressed, conditions. Mechanistically, Hlc directly binds to the MtnA locus to maintain the accessibility of chromatin near the transcriptional start site, which allows the recruitment of RNA polymerase II and subsequent MtnA transcription. Using RNA-seq, we then identified plenty of additional stress-responsive genes whose basal transcription was reduced upon knockdown of Hlc. Taken together, these data suggest that Hlc-mediated transcription regulation is an essential and widespread mechanism for precise control of stress-responsive genes.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE205804 | GEO | 2022/07/24

REPOSITORIES: GEO

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Drosophila melanogaster

Project description:The DEAD-box helicase Hlc regulates basal transcription and chromatin opening of stress-responsive genes

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2023-12-05 | GSE249051 | GEO

Differential Role of NKG2D in Recognition and Killing of Hepatic Lineage Cells Derived from Embryonic Stem Cells and Induced Pluripotent Stem Cells

Project description:Recent advances towards the efficient and reproducible differentiation of stem cells into hepatocyte-like cells (HLC) have created potential opportunities in clinical transplantation. For this approach to be successfully translated, however, it is necessary to understand the immune response to stem cell-derived cellular products. Whereas both embryonic stem cells and induced pluripotent stem cells have been utilized as cellular sources for differentiation and lineage specification, their relative ability to be recognized by immune effector cells is unclear. Here we determine the expression of immune recognition molecules on HLC generated from murine embryonic stem cells and induced pluripotent stem cells, compared to adult hepatocytes, and we evaluate the impact on recognition by NK cells. We report that HLC lack MHC class I expression, and that embryonic stem cell derived-HLC have higher expression of the NK cell activating ligands Rae1, H60, and Mult1 than induced pluripotent stem cell-derived HLC and adult hepatocytes. Moreover, the lack of MHC class I render embryonic stem cell derived-HLC, and induced pluripotent stem cell derived-HLC, susceptible to killing by syngeneic and allogeneic NK cells. Both embryonic stem cell derived-HLC, and induced pluripotent stem cell derived-HLC, are killed by NK cells at higher levels than adult hepatocytes. Finally, we demonstrate that the NK cell activation receptor, NKG2D, plays a key role in NK cell killing of embryonic stem cell derived-HLC, but not induced pluripotent stem cell-derived HLC. Hepatocytes were isolated from FVB/NJ mice and C57Bl/6 mice using a modification of the Seglen’s perfusion technique.

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bHLH Transcription Factors that Facilitate K+ Uptake During Stomatal Opening are Repressed by Abscisic Acid through Phosphorylation

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Extracellular matrix components HAPLN1, lumican and collagen I cause hyaluronic acid-dependent folding of the developing human neocortex

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Marchantia polymorpha

Project description:Salinity stress-responsive transcription factors in the liverwort Marchantia polymorpha

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