scholarly journals HMGB Proteins from Yeast to Human. Gene Regulation, DNA Repair and Beyond

2017 ◽  
Author(s):  
Vizoso-Vázquez Ángel ◽  
Barreiro-Alonso Aida ◽  
Rico-Díaz Agustín ◽  
Lamas-Maceiras Mónica ◽  
Rodríguez-Belmonte Esther ◽  
...  
Keyword(s):  
Dna Repair ◽  
Gene Regulation ◽  
Human Gene ◽  
Hmgb Proteins

The ArabidopsisRAD51paralogsRAD51B,RAD51DandXRCC2play partially redundant roles in somatic DNA repair and gene regulation

2013 ◽  
Vol 201 (1) ◽  
pp. 292-304 ◽  
Author(s):  
Yingxiang Wang ◽  
Rong Xiao ◽  
Haifeng Wang ◽  
Zhihao Cheng ◽  
Wuxing Li ◽  
...  
Keyword(s):  
Dna Repair ◽  
Gene Regulation

scholarly journals Mechanisms of Nucleosome Reorganization by PARP1

2021 ◽  
Vol 22 (22) ◽  
pp. 12127
Author(s):  
Natalya V. Maluchenko ◽  
Dmitry K. Nilov ◽  
Sergey V. Pushkarev ◽  
Elena Y. Kotova ◽  
Nadezhda S. Gerasimova ◽  
...  
Keyword(s):  
Molecular Dynamics ◽  
Dna Repair ◽  
Gene Regulation ◽  
Transcription Initiation ◽  
Histone H1 ◽  
Linker Histone ◽  
Gene Promoters ◽  
Linker Histone H1 ◽  
Nucleosomal Dna ◽  
Dna Ends

Poly(ADP-ribose) polymerase 1 (PARP1) is an enzyme involved in DNA repair, chromatin organization and transcription. During transcription initiation, PARP1 interacts with gene promoters where it binds to nucleosomes, replaces linker histone H1 and participates in gene regulation. However, the mechanisms of PARP1-nucleosome interaction remain unknown. Here, using spFRET microscopy, molecular dynamics and biochemical approaches we identified several different PARP1-nucleosome complexes and two types of PARP1 binding to mononucleosomes: at DNA ends and end-independent. Two or three molecules of PARP1 can bind to a nucleosome depending on the presence of linker DNA and can induce reorganization of the entire nucleosome that is independent of catalytic activity of PARP1. Nucleosome reorganization depends upon binding of PARP1 to nucleosomal DNA, likely near the binding site of linker histone H1. The data suggest that PARP1 can induce the formation of an alternative nucleosome state that is likely involved in gene regulation and DNA repair.

Intronic microRNAs: a crossroad in gene regulation

2012 ◽  
Vol 40 (4) ◽  
pp. 759-761 ◽  
Author(s):  
Natalia Gromak
Keyword(s):  
Gene Regulation ◽  
Human Gene ◽  
Mrna Splicing ◽  
Translational Repression ◽  
Mirna Biogenesis ◽  
Mrna Transcript ◽  
Rna Pol Ii ◽  
Pol Ii ◽  
Human Genes ◽  
Non Coding Rnas

Most human genes transcribed by RNA Pol II (polymerase II) contain short exons separated by long tracts of non-coding intronic sequences. In addition to their role in generating proteomic diversity through the process of alternative splicing, intronic sequences host many ncRNAs (non-coding RNAs), involved in various gene regulation processes. miRNAs (microRNAs) are short ncRNAs that mediate either mRNA transcript translational repression and/or degradation. Between 50 and 80% of miRNAs are encoded within introns of host mRNA genes. This observation suggests that there is co-regulation between the miRNA biogenesis and pre-mRNA splicing processes. The present review summarizes current advances in this field and discusses possible roles for intronic co-transcriptional cleavage events in the regulation of human gene expression.

scholarly journals High-Resolution Mapping of Expression-QTLs Yields Insight into Human Gene Regulation

PLoS Genetics ◽  
2008 ◽  
Vol 4 (10) ◽  
pp. e1000214 ◽  
Author(s):  
Jean-Baptiste Veyrieras ◽  
Sridhar Kudaravalli ◽  
Su Yeon Kim ◽  
Emmanouil T. Dermitzakis ◽  
Yoav Gilad ◽  
...  
Keyword(s):  
Gene Regulation ◽  
High Resolution ◽  
Human Gene ◽  
High Resolution Mapping ◽  
Resolution Mapping ◽  
Insight Into

Genomic features underlie the co-option of SVA transposons as cis-regulatory elements in human pluripotent stem cells

2022 ◽  
Author(s):  
Samantha M. Barnada ◽  
Andrew Isopi ◽  
Daniela Tejada-Martinez ◽  
Clement Goubert ◽  
Sruti Patoori ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Gene Regulation ◽  
Stem Cell ◽  
Pluripotent Stem Cells ◽  
Binding Sites ◽  
Human Gene ◽  
Regulatory Elements ◽  
Neighboring Gene ◽  
Genomic Features

Domestication of transposable elements (TEs) into functional cis-regulatory elements is a widespread phenomenon. However, the mechanisms behind why some TEs are co-opted as functional enhancers while others are not are underappreciated. SINE-VNTR-Alus (SVAs) are the youngest group of transposons in the human genome, where ~3,700 copies are annotated, nearly half of which are human-specific. Many studies indicate that SVAs are among the most frequently co-opted TEs in human gene regulation, but the mechanisms underlying such processes have not yet been thoroughly investigated. Here, we leveraged CRISPR-interference (CRISPRi), computational and functional genomics to elucidate the genomic features that underlie SVA domestication into human stem-cell gene regulation. We found that ~750 SVAs are co-opted as functional cis-regulatory elements in human induced pluripotent stem cells. These SVAs are significantly closer to genes and harbor more transcription factor binding sites than non-co-opted SVAs. We show that a long DNA motif composed of flanking YY1/2 and OCT4 binding sites is enriched in the co-opted SVAs and that these two transcription factors bind consecutively on the TE sequence. We used CRISPRi to epigenetically repress active SVAs in stem cell-like NCCIT cells. Epigenetic perturbation of active SVAs strongly attenuated YY1/OCT4 binding and influenced neighboring gene expression. Ultimately, SVA repression resulted in ~3,000 differentially expressed genes, 131 of which were the nearest gene to an annotated SVA. In summary, we demonstrated that SVAs modulate human gene expression, and uncovered that location and sequence composition contribute to SVA domestication into gene regulatory networks.

The Theoretical Basis of Transcriptional Therapy of Cancer: Can It Be Put Into Practice?

2005 ◽  
Vol 23 (17) ◽  
pp. 3957-3970 ◽  
Author(s):  
Ari M. Melnick ◽  
Kerin Adelson ◽  
Jonathan D. Licht
Keyword(s):  
Dna Repair ◽  
Gene Regulation ◽  
Chromatin Remodeling ◽  
Transcriptional Repression ◽  
Theoretical Basis ◽  
Critical Role ◽  
Therapeutic Agents ◽  
Epigenetic Silencing ◽  
Frequent Event ◽  
Aberrant Gene

Aberrant gene silencing is a frequent event in cancer and plays a critical role in the molecular pathogenesis of malignant transformation. The two major mechanisms of silencing in cancer include transcriptional repression by mutated or aberrantly expressed transcription factors, and aberrant epigenetic silencing by hypermethylation of tumor suppressor or DNA repair–related genes. Both of these mechanisms require the activities of multiprotein chromatin remodeling and modifying machines, several of which may be mutated in cancer. The end result is genetic reprogramming of cells to express combinations of genes that confer the neoplastic phenotype. Recent discoveries in transcriptional biochemistry and gene regulation indicate that therapeutic agents can be engineered to specifically target these mechanisms. We provide a framework for the clinical or translational scientist to consider how such drugs might be developed and what their impact might be on restoring cells to normal genetic programming.

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