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 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 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.

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 β-Cell–Specific Gene Repression: A Mechanism to Protect Against Inappropriate or Maladjusted Insulin Secretion?

Diabetes ◽  
2012 ◽  
Vol 61 (5) ◽  
pp. 969-975 ◽  
Author(s):  
Frans Schuit ◽  
Leentje Van Lommel ◽  
Mikaela Granvik ◽  
Lotte Goyvaerts ◽  
Geoffroy de Faudeur ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Gene Repression ◽  
Specific Gene ◽  
Β Cell

scholarly journals Specific Gene Repression by CRISPRi System Transferred through Bacterial Conjugation

2014 ◽  
Vol 3 (12) ◽  
pp. 929-931 ◽  
Author(s):  
Weiyue Ji ◽  
Derrick Lee ◽  
Eric Wong ◽  
Priyanka Dadlani ◽  
David Dinh ◽  
...  
Keyword(s):  
Gene Repression ◽  
Specific Gene ◽  
Bacterial Conjugation

scholarly journals An epigenetic mechanism for cavefish eye degeneration

2017 ◽  
Author(s):  
Aniket V. Gore ◽  
Kelly A. Tomins ◽  
James Iben ◽  
Li Ma ◽  
Daniel Castranova ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Eye Development ◽  
Phenotypic Diversity ◽  
Phenotypic Variability ◽  
Epigenetic Mechanism ◽  
Gene Repression ◽  
Specific Gene ◽  
Astyanax Mexicanus ◽  
Eye Disorders ◽  
Blind Cave

Coding and non-coding mutations in DNA contribute significantly to phenotypic variability during evolution. However, less is known about the role of epigenetics in this process. Although previous studies have identified eye development genes associated with the loss of eyes phenotype in the Pachón blind cave morph of the Mexican tetra Astyanax mexicanus1-6, no inactivating mutations have been found in any of these genes2,3,7-10. Here we show that excess DNA methylation-based epigenetic silencing promotes eye degeneration in blind cave Astyanax mexicanus. By performing parallel analyses in Astyanax mexicanus cave and surface morphs and in the zebrafish Danio rerio, we have discovered that DNA methylation mediates eye-specific gene repression and globally regulates early eye development. The most significantly hypermethylated and down-regulated genes in the cave morph are also linked to human eye disorders, suggesting the function of these genes is conserved across the vertebrates. Our results show that changes in DNA methylation-based gene repression can serve as an important molecular mechanism generating phenotypic diversity during development and evolution.

scholarly journals An insulator blocks access to enhancers by an illegitimate promoter, preventing repression by transcriptional interference

PLoS Genetics ◽  
2021 ◽  
Vol 17 (4) ◽  
pp. e1009536
Author(s):  
Miki Fujioka ◽  
Anastasiya Nezdyur ◽  
James B. Jaynes
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
P Element ◽  
Gene Repression ◽  
Transcriptional Interference ◽  
Promoter Specificity ◽  
Functional Units

Several distinct activities and functions have been described for chromatin insulators, which separate genes along chromosomes into functional units. Here, we describe a novel mechanism of functional separation whereby an insulator prevents gene repression. When thehomieinsulator is deleted from the end of a Drosophilaeven skipped(eve) locus, a flanking P-element promoter is activated in a partialevepattern, causing expression driven by enhancers in the 3’ region to be repressed. The mechanism involves transcriptional read-through from the flanking promoter. This conclusion is based on the following. Read-through driven by a heterologous enhancer is sufficient to repress, even whenhomieis in place. Furthermore, when the flanking promoter is turned around, repression is minimal. Transcriptional read-through that does not produce anti-sense RNA can still repress expression, ruling out RNAi as the mechanism in this case. Thus, transcriptional interference, caused by enhancer capture and read-through when the insulator is removed, repressesevepromoter-driven expression. We also show that enhancer-promoter specificity and processivity of transcription can have decisive effects on the consequences of insulator removal. First, a coreheat shock 70promoter that is not activated well byeveenhancers did not cause read-through sufficient to repress theevepromoter. Second, these transcripts are less processive than those initiated at the P-promoter, measured by how far they extend through theevelocus, and so are less disruptive. These results highlight the importance of considering transcriptional read-through when assessing the effects of insulators on gene expression.

scholarly journals Protein-coding changes preceded cis-regulatory gains in a newly evolved transcription circuit

Science ◽  
2020 ◽  
Vol 367 (6473) ◽  
pp. 96-100 ◽  
Author(s):  
Candace S. Britton ◽  
Trevor R. Sorrells ◽  
Alexander D. Johnson
Keyword(s):  
Transcriptional Regulators ◽  
Gene Repression ◽  
Specific Gene ◽  
Regulatory Sequence ◽  
Regulatory Sequences ◽  
Homeodomain Protein ◽  
Protein Coding ◽  
Evolutionary Pathway ◽  
Coding Sequence ◽  
Regulatory Sites

Changes in both the coding sequence of transcriptional regulators and in the cis-regulatory sequences recognized by these regulators have been implicated in the evolution of transcriptional circuits. However, little is known about how they evolved in concert. We describe an evolutionary pathway in fungi where a new transcriptional circuit (a-specific gene repression by the homeodomain protein Matα2) evolved by coding changes in this ancient regulator, followed millions of years later by cis-regulatory sequence changes in the genes of its future regulon. By analyzing a group of species that has acquired the coding changes but not the cis-regulatory sites, we show that the coding changes became necessary for the regulator’s deeply conserved function, thereby poising the regulator to jump-start formation of the new circuit.

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