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 ◽  
...  
1998 ◽  
Vol 8 (9) ◽  
pp. 533-S2 ◽  
Author(s):  
Danielle Vermaak ◽  
Oliver C. Steinbach ◽  
Stephan Dimitrov ◽  
Ralph A.W. Rupp ◽  
Alan P. Wolffe

Diabetes ◽  
2012 ◽  
Vol 61 (5) ◽  
pp. 969-975 ◽  
Author(s):  
Frans Schuit ◽  
Leentje Van Lommel ◽  
Mikaela Granvik ◽  
Lotte Goyvaerts ◽  
Geoffroy de Faudeur ◽  
...  

2017 ◽  
Author(s):  
Aniket V. Gore ◽  
Kelly A. Tomins ◽  
James Iben ◽  
Li Ma ◽  
Daniel Castranova ◽  
...  

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.


2017 ◽  
Author(s):  
Alicia Nevers ◽  
Antonia Doyen ◽  
Christophe Malabat ◽  
Bertrand Néron ◽  
Thomas Kergrohen ◽  
...  

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.


Science ◽  
2020 ◽  
Vol 367 (6473) ◽  
pp. 96-100 ◽  
Author(s):  
Candace S. Britton ◽  
Trevor R. Sorrells ◽  
Alexander D. Johnson

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.


2018 ◽  
Vol 46 (12) ◽  
pp. 6009-6025 ◽  
Author(s):  
Alicia Nevers ◽  
Antonia Doyen ◽  
Christophe Malabat ◽  
Bertrand Néron ◽  
Thomas Kergrohen ◽  
...  

2019 ◽  
Author(s):  
Candace S. Britton ◽  
Trevor R. Sorrells ◽  
Alexander D. Johnson

AbstractWhile changes in both the coding-sequence of transcriptional regulators and in the cis-regulatory sequences recognized by them have been implicated in the evolution of transcriptional circuits, little is known of how they evolve in concert. We describe an evolutionary pathway in fungi where a new transcriptional circuit (a-specific gene repression by Matα2) evolved by coding changes in an ancient master regulator, followed millions of years later by cis-regulatory sequence changes in the genes of its future regulon. We discerned this order of events by analyzing a group of species in which the coding changes in the regulator are present, but the cis-regulatory changes in the target genes are not. In this group we show that the coding changes became necessary for the regulator’s deeply conserved function and were therefore preserved. We propose that the changes first arose without altering the overall function of the regulator (although changing the details of its mechanism) and were later co-opted to “jump start” the formation of the new circuit.


2009 ◽  
Vol 119 (10) ◽  
pp. 3138-3148 ◽  
Author(s):  
Nicolas Leuenberger ◽  
Sylvain Pradervand ◽  
Walter Wahli

Genetics ◽  
1995 ◽  
Vol 140 (1) ◽  
pp. 79-90 ◽  
Author(s):  
M Wahi ◽  
A D Johnson

Abstract Transcriptional repression of the a-specific genes in Saccharomyces cerevisiae alpha cells involves the concerted action of several proteins. The homeodomian protein alpha 2, together with MCM1, recruits two general transcriptional repressors, SSN6 and TUP1, to the promoters of a-specific genes. SSN6 and TUP1 then mediate repression of the a-specific genes. SIN4, another general negative regulator, is required for this repression, but unlike tup1 or ssn6 deletions, sin4 deletions cause only partial loss of repression. We have screened for other genes required for a-specific gene repression in alpha cells. In addition to recovering multiple alleles of previously identified genes required for this process (referred to as alpha 2 repression), we have identified four other genes, designated ARE1, ARE2, ARE3, and ARE4 (for alpha 2 repression). Recessive mutations in the ARE genes cause partial loss of a-specific gene repression and cause pleiotropic phenotypes similar to those resulting from mutations in SSN6, TUP1, or SIN4, suggesting that the ARE genes are general negative regulators. Based on our initial analysis, we propose that two distinct classes of general negative regulators cooperate to bring about full levels of alpha 2 repression. The sequence of ARE1 revealed that it encodes a CDC28-related protein kinase, identical to UME5, and thus suggests that protein phosphorylation plays a role in alpha 2 repression.


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