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Dr. Dorota Rybaczek

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Department of Cytophysiology, University of Lodz, 90-136 Lodz, Poland
Interests: genomics

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Dear Colleagues,

Genomic instability is a major cause of cancer cell formation in multicellular organisms and is one criterion for the diagnosis of cancer, as a significant proportion of mutations leading to tumourigenesis can be caused by the dysregulation of the mechanisms responsible for normal DNA segregation in mitosis. The regulatory systems of these processes impose different metabolic specificities on each phase of the cell cycle and, by supervising the correct chronology of events, condition the maintenance of the structural and functional integrity of the eu- and heterochromatin sequences.

The effect of many chemical agents can be to 'bypass' (overriding) or disrupt the surveillance of genome integrity. The course of the subsequent phases of nuclear division is then aberrant and can lead to cell death. Disabling the function of internal S-phase checkpoints leads to the sensitisation of tumour cells to anticancer agents and the effects of ionising radiation. It represents not only an important fundamental problem in cell cycle biology, but also an important issue in terms of potential medical applications.

We invite the submission of studies related to the molecular dynamics of replication and mitosis and cellular stress in eukaryotic cells. Since IJMS is a journal of molecular science, pure clinical studies will not suitable for our journal. However, clinical or pure model submissions with biomolecular experiments are welcome.

Dr. Dorota Rybaczek
Guest Editor

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Keywords

genomic instability
chromosomal instability
premature mitoses
premature chromosome condensation
cell death
replication stress
DNA damage
cell cycle checkpoints
synthetic lethality
chromothripsis
eukaryotic cells

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Research

14 pages, 1435 KiB

Open AccessArticle

The Upstream 1350~1250 Nucleotide Sequences of the Human ENDOU-1 Gene Contain Critical Cis-Elements Responsible for Upregulating Its Transcription during ER Stress

by Hung-Chieh Lee, Hsuan-Te Chao, Selina Yi-Hsuan Lee, Cheng-Yung Lin and Huai-Jen Tsai

Int. J. Mol. Sci. 2023, 24(24), 17393; https://doi.org/10.3390/ijms242417393 - 12 Dec 2023

Cited by 1 | Viewed by 724

Abstract

ENDOU-1 encodes an endoribonuclease that overcomes the inhibitory upstream open reading frame (uORF)-trap at 5′-untranslated region (UTR) of the CHOP transcript, allowing the downstream coding sequence of CHOP be translated during endoplasmic reticulum (ER) stress. However, transcriptional control of ENDOU-1 remains enigmatic. To address this, we cloned an upstream 2.1 kb (−2055~+77 bp) of human ENDOU-1 (pE2.1p) fused with reporter luciferase (luc) cDNA. The promoter strength driven by pE2.1p was significantly upregulated in both pE2.1p-transfected cells and pE2.1p-injected zebrafish embryos treated with stress inducers. Comparing the luc activities driven by pE2.1p and −1125~+77 (pE1.2p) segments, we revealed that cis-elements located at the −2055~−1125 segment might play a critical role in ENDOU-1 upregulation during ER stress. Since bioinformatics analysis predicted many cis-elements clustered at the −1850~−1250, we further deconstructed this segment to generate pE2.1p-based derivatives lacking −1850~−1750, −1749~−1650, −1649~−1486, −1485~−1350 or −1350~−1250 segments. Quantification of promoter activities driven by these five internal deletion plasmids suggested a repressor binding element within the −1649~−1486 and an activator binding element within the −1350~−1250. Since luc activities driven by the −1649~−1486 were not significantly different between normal and stress conditions, we herein propose that the stress-inducible activator bound at the −1350~−1250 segment makes a major contribution to the increased expression of human ENDOU-1 upon ER stresses. Full article

(This article belongs to the Special Issue Cellular Stress and Genomics in Eukaryotes)

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