scholarly journals Antisense transcriptional interference mediates condition-specific gene repression in budding yeast

2017 ◽  
Author(s):  
Alicia Nevers ◽  
Antonia Doyen ◽  
Christophe Malabat ◽  
Bertrand Néron ◽  
Thomas Kergrohen ◽  
...  
Keyword(s):  
Budding Yeast ◽  
Underlying Mechanism ◽  
Antisense Transcription ◽  
Exponential Phase ◽  
Gene Repression ◽  
Specific Gene ◽  
Gene Promoters ◽  
Mrna Transcription ◽  
Pervasive Transcription ◽  
Transcription Interference

ABSTRACTPervasive transcription generates many unstable non-coding transcripts in budding yeast. The transcription of such noncoding RNAs, in particular antisense RNAs (asRNAs), has been shown in a few examples to repress the expression of the associated mRNAs. Yet, such mechanism is not known to commonly contribute to the regulation of a given class of genes. Using a mutant context that stabilised pervasive transcripts, we observed that the least expressed mRNAs during the exponential phase were associated with high levels of asRNAs. These asRNAs also overlapped their corresponding gene promoters with a much higher frequency than average. Interrupting antisense transcription of a subset of genes corresponding to quiescence-enriched mRNAs restored their expression. The underlying mechanism acts in cis and involves several chromatin modifiers. Our results convey that transcription interference represses up to 30% of the 590 least expressed genes, which includes 163 genes with quiescence-enriched mRNAs. We also found that pervasive transcripts constitute a higher fraction of the transcriptome in quiescence relative to the exponential phase, consistent with gene expression itself playing an important role to suppress pervasive transcription. Accordingly, the HIS1 asRNA, normally only present in quiescence, is expressed in exponential phase upon HIS1 mRNA transcription interruption.

scholarly journals Antisense transcriptional interference mediates condition-specific gene repression in budding yeast

2018 ◽  
Vol 46 (12) ◽  
pp. 6009-6025 ◽  
Author(s):  
Alicia Nevers ◽  
Antonia Doyen ◽  
Christophe Malabat ◽  
Bertrand Néron ◽  
Thomas Kergrohen ◽  
...  
Keyword(s):  
Budding Yeast ◽  
Gene Repression ◽  
Specific Gene ◽  
Transcriptional Interference

scholarly journals Antisense-mediated repression of SAGA-dependent genes involves the HIR histone chaperone

2021 ◽  
Author(s):  
Julien Soudet ◽  
Nissrine Beyrouthy ◽  
Anna Marta Pastucha ◽  
Andrea Maffioletti ◽  
Zahra Bakir ◽  
...  
Keyword(s):  
Rna Polymerase Ii ◽  
Transcription Initiation ◽  
De Novo ◽  
Antisense Transcription ◽  
Histone Chaperone ◽  
Gene Promoters ◽  
Genome Wide ◽  
Chaperone Complex ◽  
Histone Deposition ◽  
Transcription Interference

Eukaryotic genomes are pervasively transcribed by RNA polymerase II (RNAPII), and transcription of long non-coding RNAs often overlaps with coding gene promoters. This might lead to coding gene repression in a process named Transcription Interference (TI). In Saccharomyces cerevisiae (S. cerevisiae), TI is mainly driven by antisense non-coding transcription and occurs through re-shaping of promoter Nucleosome-Depleted Regions (NDRs). In this study, we developed a genetic screen to identify new players involved in Antisense-Mediated Transcription Interference (AMTI). Among the candidates, we found the HIR histone chaperone complex known to be involved in de novo histone deposition. Using genome-wide approaches, we reveal that HIR-dependent histone deposition represses the promoters of SAGA-dependent genes via antisense non-coding transcription. However, while antisense transcription is enriched at promoters of SAGA-dependent genes, this feature is not sufficient to define the mode of gene regulation. We further show that the balance between HIR-dependent nucleosome incorporation and transcription factor binding at promoters directs transcription into a SAGA- or TFIID-dependent regulation. This study sheds light on a new connection between antisense non-coding transcription and the nature of coding transcription initiation.

scholarly journals BisMapR: a strand-specific, nuclease-based method for genome-wide R-loop detection

2021 ◽  
Author(s):  
Phillip Wulfridge ◽  
Kavitha Sarma
Keyword(s):  
Genome Stability ◽  
Antisense Transcription ◽  
Gene Promoters ◽  
Normal Cells ◽  
Disease States ◽  
Detection Strategy ◽  
Genome Wide ◽  
Loop Detection ◽  
Nucleic Acid Structures ◽  
Nuclear Processes

AbstractR-loops are three stranded nucleic acid structures with essential roles in many nuclear processes. However, their unchecked accumulation as seen in some neurodevelopmental diseases and cancers and is associated with compromised genome stability. Genome-wide profiling of R-loops in normal cells and their comparison in disease states can help identify precise locations of pathogenic R-loops and advance efforts to attenuate deviant R-loops while preserving biologically important ones. Toward this, we have developed an antibody-independent R-loop detection strategy, BisMapR, that combines nuclease-based R-loop isolation with non-denaturing bisulfite chemistry to produce high-resolution, genome-wide R-loop profiles that retain strand information. Furthermore, BisMapR achieves greater resolution and is faster than existing strand-specific R-loop profiling strategies. We applied BisMapR to reveal discrete R-loop behavior at gene promoters and enhancers. We show that gene promoters exhibiting antisense transcription form R-loops in both directions. and uncover a subset of active enhancers that, despite being bidirectionally transcribed, form R-loops exclusively on one strand. Thus, BisMapR reveals a previously unnoticed feature of active enhancers and provides a tool to systematically examine their mechanisms in gene expression.

scholarly journals Long Noncoding RNA HOXA-AS3 Integrates NF-κB Signaling To Regulate Endothelium Inflammation

2019 ◽  
Vol 39 (19) ◽  
Author(s):  
Xinxing Zhu ◽  
Duchu Chen ◽  
Yanli Liu ◽  
Jinjin Yu ◽  
Liang Qiao ◽  
...  
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Vascular Diseases ◽  
Specific Gene ◽  
Gene Promoters ◽  
Inhibitor Protein ◽  
Functional Importance ◽  
Acetylation Status ◽  
Clinicopathological Analysis ◽  
Promising Therapeutic Target

ABSTRACT The long noncoding RNA HOXA-AS3 has recently been reported to act as a critical regulator in inflammation-linked lung adenocarcinoma. However, the roles of HOXA-AS3 in endothelium inflammation and related vascular disorders remain poorly defined. In the current study, we identified HOXA-AS3 to be a critical activator to promote NF-κB-mediated endothelium inflammation. HOXA-AS3, a chromatin-associated regulator which colocalizes with NF-κB at specific gene promoters, was found to interact with NF-κB and positively regulate its activity through control of the expression of the NF-κB inhibitor protein IκBα and the acetylation status at the K310 site of p65. More importantly, clinicopathological analysis showed that HOXA-AS3 expression has a significant positive correlation with atherosclerosis. Thus, we conclude that HOXA-AS3 may serve as a crucial biomarker for the clinical diagnosis of atherosclerosis, as well as a promising therapeutic target for the treatment of multiple inflammatory vascular diseases. In addition, this study suggests the functional importance of HOXA-AS3 in the regulation of inflammatory disorders.

scholarly journals The environmental stress response causes ribosome loss in aneuploid yeast cells

2020 ◽  
Vol 117 (29) ◽  
pp. 17031-17040 ◽  
Author(s):  
Allegra Terhorst ◽  
Arzu Sandikci ◽  
Abigail Keller ◽  
Charles A. Whittaker ◽  
Maitreya J. Dunham ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Stationary Phase ◽  
Environmental Stress ◽  
Budding Yeast ◽  
Expression Patterns ◽  
Yeast Cells ◽  
Specific Gene ◽  
Environmental Stress Response ◽  
Cellular Stresses

Aneuploidy, a condition characterized by whole chromosome gains and losses, is often associated with significant cellular stress and decreased fitness. However, how cells respond to the aneuploid state has remained controversial. In aneuploid budding yeast, two opposing gene-expression patterns have been reported: the “environmental stress response” (ESR) and the “common aneuploidy gene-expression” (CAGE) signature, in which many ESR genes are oppositely regulated. Here, we investigate this controversy. We show that the CAGE signature is not an aneuploidy-specific gene-expression signature but the result of normalizing the gene-expression profile of actively proliferating aneuploid cells to that of euploid cells grown into stationary phase. Because growth into stationary phase is among the strongest inducers of the ESR, the ESR in aneuploid cells was masked when stationary phase euploid cells were used for normalization in transcriptomic studies. When exponentially growing euploid cells are used in gene-expression comparisons with aneuploid cells, the CAGE signature is no longer evident in aneuploid cells. Instead, aneuploid cells exhibit the ESR. We further show that the ESR causes selective ribosome loss in aneuploid cells, providing an explanation for the decreased cellular density of aneuploid cells. We conclude that aneuploid budding yeast cells mount the ESR, rather than the CAGE signature, in response to aneuploidy-induced cellular stresses, resulting in selective ribosome loss. We propose that the ESR serves two purposes in aneuploid cells: protecting cells from aneuploidy-induced cellular stresses and preventing excessive cellular enlargement during slowed cell cycles by down-regulating translation capacity.

Improved transgenic sexing strains for genetic control of the Australian sheep blow fly Lucilia cuprina using embryo-specific gene promoters

2019 ◽  
Vol 295 (2) ◽  
pp. 287-298 ◽  
Author(s):  
Ying Yan ◽  
Megan E. Williamson ◽  
Rebecca J. Davis ◽  
Anne A. Andere ◽  
Christine J. Picard ◽  
...  
Keyword(s):  
Genetic Control ◽  
Lucilia Cuprina ◽  
Specific Gene ◽  
Gene Promoters ◽  
Blow Fly ◽  
Australian Sheep

scholarly journals The globular domain of histone H1 is sufficient to direct specific gene repression in early Xenopus embryos

1998 ◽  
Vol 8 (9) ◽  
pp. 533-S2 ◽  
Author(s):  
Danielle Vermaak ◽  
Oliver C. Steinbach ◽  
Stephan Dimitrov ◽  
Ralph A.W. Rupp ◽  
Alan P. Wolffe
Keyword(s):  
Histone H1 ◽  
Gene Repression ◽  
Specific Gene ◽  
Globular Domain ◽  
Xenopus Embryos

scholarly journals Basonuclin 1 deficiency causes testicular premature aging: BNC1 cooperates with TAF7L to regulate spermatogenesis

2019 ◽  
Vol 12 (1) ◽  
pp. 71-83 ◽  
Author(s):  
Jing-Yi Li ◽  
Yi-Feng Liu ◽  
Hai-Yan Xu ◽  
Jun-Yu Zhang ◽  
Ping-Ping Lv ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Binding Protein ◽  
Premature Aging ◽  
Specific Gene ◽  
Obstructive Azoospermia ◽  
Gene Promoters ◽  
Binding Studies ◽  
Truncation Mutation ◽  
Tata Box Binding Protein

Abstract Basonuclin (BNC1) is expressed primarily in proliferative keratinocytes and gametogenic cells. However, its roles in spermatogenesis and testicular aging were not clear. Previously we discovered a heterozygous BNC1 truncation mutation in a premature ovarian insufficiency pedigree. In this study, we found that male mice carrying the truncation mutation exhibited progressively fertility loss and testicular premature aging. Genome-wide expression profiling and direct binding studies (by chromatin immunoprecipitation sequencing) with BNC1 in mouse testis identified several spermatogenesis-specific gene promoters targeted by BNC1 including kelch-like family member 10 (Klhl10), testis expressed 14 (Tex14), and spermatogenesis and centriole associated 1 (Spatc1). Moreover, biochemical analysis showed that BNC1 was associated with TATA-box binding protein-associated factor 7 like (TAF7L), a germ cell-specific paralogue of the transcription factor IID subunit TAF7, both in vitro and in testis, suggesting that BNC1 might directly cooperate with TAF7L to regulate spermatogenesis. The truncation mutation disabled nuclear translocation of the BNC1/TAF7L complex, thus, disturbing expression of related genes and leading to testicular premature aging. Similarly, expressions of BNC1, TAF7L, Y-box-binding protein 2 (YBX2), outer dense fiber of sperm tails 1 (ODF1), and glyceraldehyde-3-phosphate dehydrogenase, spermatogenic (GAPDHS) were significantly decreased in the testis of men with non-obstructive azoospermia. The present study adds to the understanding of the physiology of male reproductive aging and the mechanism of spermatogenic failure in infertile men.

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