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

Soudet, Julien; Beyrouthy, Nissrine; Pastucha, Anna Marta; Maffioletti, Andrea; Menéndez, Dario; Bakir, Zahra; Stutz, Françoise

doi:10.1093/nar/gkac264

Cited by 6 publications

(11 citation statements)

References 70 publications

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“…In such culture conditions, the Pho4 transcriptional activator is rarely located in the nucleus [19]. Thus, as we proposed in [46] for the SAGA-dependent gene class to which PHO5 belongs, the steady-state chromatin structure of the promoter NDR might be maintained tightly closed by ongoing AS transcription. What may also be relevant to this mechanism is the recently discovered autoregulatory mechanism of the SAGA complex, which is induced in response to environmental changes such as phosphate starvation conditions [67].…”

Section: Discussionmentioning

confidence: 88%

“…The right panel represents RNAPII PAR-CLIP signal or nascent transcription signal in the same conditions. Data were retrieved from [ 46 ] and [ 47 ], respectively. (C) Levels of PHO5 mRNA in wild-type BMA41 (wt) and corresponding rrp6Δ mutant cells upon induction through phosphate starvation.…”

Section: Resultsmentioning

confidence: 99%

“…For RNA-seq and RNAPII PAR-CLIP, data were retrieved from [ 46 ] (GEO: GSE175991) and from [ 47 ] (GEO: GSE56435). Data of MNase-seq, ATAC-seq and Sth1 ChEC-seq were reanalyzed from [ 13 ] (GEO: GSE130946).…”

Section: Methodsmentioning

confidence: 99%

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Antisense non-coding transcription represses the PHO5 model gene at the level of promoter chromatin structure

Novačić

Menéndez²,

Ljubas³

et al. 2022

PLoS Genet

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Pervasive transcription of eukaryotic genomes generates non-coding transcripts with regulatory potential. We examined the effects of non-coding antisense transcription on the regulation of expression of the yeast PHO5 gene, a paradigmatic case for gene regulation through promoter chromatin remodeling. A negative role for antisense transcription at the PHO5 gene locus was demonstrated by leveraging the level of overlapping antisense transcription through specific mutant backgrounds, expression from a strong promoter in cis, and use of the CRISPRi system. Furthermore, we showed that enhanced elongation of PHO5 antisense leads to a more repressive chromatin conformation at the PHO5 gene promoter, which is more slowly remodeled upon gene induction. The negative effect of antisense transcription on PHO5 gene transcription is mitigated upon inactivation of the histone deacetylase Rpd3, showing that PHO5 antisense RNA acts via histone deacetylation. This regulatory pathway leads to Rpd3-dependent decreased recruitment of the RSC chromatin remodeling complex to the PHO5 gene promoter upon induction of antisense transcription. Overall, the data in this work reveal an additional level in the complex regulatory mechanism of PHO5 gene expression by showing antisense transcription-mediated repression at the level of promoter chromatin structure remodeling.

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Section: Discussionmentioning

confidence: 88%

Section: Resultsmentioning

confidence: 99%

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Antisense non-coding transcription represses the PHO5 model gene at the level of promoter chromatin structure

Novačić

Menéndez²,

Ljubas³

et al. 2022

PLoS Genet

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“…We first tested the importance of Reb1 TF in resetting promoter NDR architecture after replication. Reb1 depletion only affects the expression of a minority of genes that was previously defined [40, 41]. Thus, we performed our analyses by making the distinction between Reb1 ‘target’ and ‘non-target’ genes.…”

Section: Resultsmentioning

confidence: 99%

“…3). Highly transcribed and lowly transcribed genes were retrieved from the RNA-seq in an Nrd1-AA strain in the absence of Rap [41].…”

Section: -1/+1 Annotations and Gene/replication Origins Listsmentioning

confidence: 99%

Refined mechanism of promoter Nucleosome-Depleted Regions resetting after replication

Zencir,

Gill,

Stutz

et al. 2024

Preprint

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Replication disrupts chromatin organization. Thus, the rapid resetting of nucleosome positioning is essential to maintain faithful gene expression. The initial step of this reconfiguration occurs at Nucleosome-Depleted Regions (NDRs). While studies have elucidated the role of Transcription Factors (TFs) and Chromatin Remodelers (CRs) in vitro or in maintaining NDRs in vivo, none has addressed their in vivo function shortly after replication. Through purification of nascent chromatin in yeast, we dissected the choreography of events governing the proper positioning of the -1/+1 nucleosomes flanking promoter NDRs. Our findings reveal that CRs are the primary contributors of -1/+1 repositioning post-replication, with RSC acting upstream of INO80. Surprisingly, while Reb1 and Abf1 TFs are not essential for NDR resetting, they are required for NDR maintenance via the promotion of H3 acetylations. Altogether, we propose a two-step model for NDR resetting in S. cerevisiae: first, CRs alone reset promoter NDRs after replication, while a combination of TFs and CRs is required for subsequent maintenance.

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Novel insights on the positive correlation between sense and antisense pairs on gene expression

Das,

Zea Rojas,

Tran

2024

WIREs RNA

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A considerable proportion of the eukaryotic genome undergoes transcription, leading to the generation of noncoding RNA molecules that lack protein‐coding information and are not subjected to translation. These noncoding RNAs (ncRNAs) are well recognized to have essential roles in several biological processes. Long noncoding RNAs (lncRNAs) represent the most extensive category of ncRNAs found in the human genome. Much research has focused on investigating the roles of cis‐acting lncRNAs in the regulation of specific target gene expression. In the majority of instances, the regulation of sense gene expression by its corresponding antisense pair occurs in a negative (discordant) manner, resulting in the suppression of the target genes. The notion that a negative correlation exists between sense and antisense pairings is, however, not universally valid. In fact, several recent studies have reported a positive relationship between corresponding cis antisense pairs within plants, budding yeast, and mammalian cancer cells. The positive (concordant) correlation between anti‐sense and sense transcripts leads to an increase in the level of the sense transcript within the same genomic loci. In addition, mechanisms such as altering chromatin structure, the formation of R loops, and the recruitment of transcription factors can either enhance transcription or stabilize sense transcripts through their antisense pairs. The primary objective of this work is to provide a comprehensive understanding of both aspects of antisense regulation, specifically focusing on the positive correlation between sense and antisense transcripts in the context of eukaryotic gene expression, including its implications towards cancer progression.This article is categorized under: RNA Processing > 3′ End Processing Regulatory RNAs/RNAi/Riboswitches > Regulatory RNAs

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

Cited by 6 publications

References 70 publications

Antisense non-coding transcription represses the PHO5 model gene at the level of promoter chromatin structure

Antisense non-coding transcription represses the PHO5 model gene at the level of promoter chromatin structure

Refined mechanism of promoter Nucleosome-Depleted Regions resetting after replication

Novel insights on the positive correlation between sense and antisense pairs on gene expression

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