Yeast chromatin remodeling complexes and their roles in transcription

Lin, Aiyang; Du, Ying; Xiao, Wei

doi:10.1007/s00294-020-01072-0

Cited by 17 publications

(10 citation statements)

References 102 publications

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“…For example, most of the transcription factors involved in the heat stress response (Hsf1, Msn2, Msn4, and Aft2) showed significant increases in their accessibility because of nucleosome repositioning upon heat shock [32,33]. In this context, post-translational modifications of individual histones by histone modifiers (reviewed in [34,35]) and disassembly and removal of nucleosomes by ATP-dependent chromatin remodeling complexes [36] work in concert to regulate this process by rendering promoters accessible to Pol II [37][38][39]. Moreover, histone modifications can stimulate the recruitment of chromatin-modifying enzymes at specific genomic sites, allowing an increase or decrease in other histone modifications that can propagate to adjacent nucleosomes by several positive and negative feedbacks [40].…”

Section: Chromatin and Gene Expression In Response To Stressmentioning

confidence: 99%

Control of Gene Expression via the Yeast CWI Pathway

Sanz

García

Pavón-Vergés

et al. 2022

IJMS

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Living cells exposed to stressful environmental situations can elicit cellular responses that guarantee maximal cell survival. Most of these responses are mediated by mitogen-activated protein kinase (MAPK) cascades, which are highly conserved from yeast to humans. Cell wall damage conditions in the yeast Saccharomyces cerevisiae elicit rescue mechanisms mainly associated with reprogramming specific transcriptional responses via the cell wall integrity (CWI) pathway. Regulation of gene expression by this pathway is coordinated by the MAPK Slt2/Mpk1, mainly via Rlm1 and, to a lesser extent, through SBF (Swi4/Swi6) transcription factors. In this review, we summarize the molecular mechanisms controlling gene expression upon cell wall stress and the role of chromatin structure in these processes. Some of these mechanisms are also discussed in the context of other stresses governed by different yeast MAPK pathways. Slt2 regulates both transcriptional initiation and elongation by interacting with chromatin at the promoter and coding regions of CWI-responsive genes but using different mechanisms for Rlm1- and SBF-dependent genes. Since MAPK pathways are very well conserved in eukaryotic cells and are essential for controlling cellular physiology, improving our knowledge regarding how they regulate gene expression could impact the future identification of novel targets for therapeutic intervention.

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Section: Chromatin and Gene Expression In Response To Stressmentioning

confidence: 99%

Control of Gene Expression via the Yeast CWI Pathway

Sanz

García

Pavón-Vergés

et al. 2022

IJMS

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“…The SWI/SNF complex can be targeted to acetylated transcriptionally active chromatin, as it can bind acetylated histones (and non-histone proteins) through a bromodomain subunit [44]. Therefore, SWI/SNF activity generally correlates with transcriptional activation even if the complex has also been linked to transcriptional repression [46][47][48][49][50].…”

Section: Chromatin Remodelling Regulates Gene Expression and Chromatin Structurementioning

confidence: 99%

On and Off: Epigenetic Regulation of C. albicans Morphological Switches

2021

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The human fungal pathogen Candida albicans is a dimorphic opportunistic pathogen that colonises most of the human population without creating any harm. However, this fungus can also cause life-threatening infections in immunocompromised individuals. The ability to successfully colonise different host niches is critical for establishing infections and pathogenesis. C. albicans can live and divide in various morphological forms critical for its survival in the host. Indeed, C. albicans can grow as both yeast and hyphae and can form biofilms containing hyphae. The transcriptional regulatory network governing the switching between these different forms is complex but well understood. In contrast, non-DNA based epigenetic modulation is emerging as a crucial but still poorly studied regulatory mechanism of morphological transition. This review explores our current understanding of chromatin-mediated epigenetic regulation of the yeast to hyphae switch and biofilm formation. We highlight how modification of chromatin structure and non-coding RNAs contribute to these morphological transitions.

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“…These proteins include: (a) the enzymes that catalyze the post-translational modification of histone proteins, such as lysine (K) acetyl-transferases (KATs), and lysine (K) deacetylases (KDACs); (b) ATP-dependent chromatin remodelers which actively move nucleosomes in relation to the underlying DNA; and (c) histone variant proteins that are incorporated into non-canonical nucleosomes. There is an impressive body of work detailing the precise molecular consequences of many fungal chromatin modifiers [ 32 , 33 , 34 ]. However, in simplified terms, their collective action interferes with chromatin structure, regulating the accessibility of the DNA sequence for DNA-templated processes.…”

Section: Chromatin Structure and Anti-fungal Resistancementioning

confidence: 99%

Chromatin Structure and Drug Resistance in Candida spp.

O'Kane

Weild

Hyland

2020

JoF

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Anti-microbial resistance (AMR) is currently one of the most serious threats to global human health and, appropriately, research to tackle AMR garnishes significant investment and extensive attention from the scientific community. However, most of this effort focuses on antibiotics, and research into anti-fungal resistance (AFR) is vastly under-represented in comparison. Given the growing number of vulnerable, immunocompromised individuals, as well as the positive impact global warming has on fungal growth, there is an immediate urgency to tackle fungal disease, and the disturbing rise in AFR. Chromatin structure and gene expression regulation play pivotal roles in the adaptation of fungal species to anti-fungal stress, suggesting a potential therapeutic avenue to tackle AFR. In this review we discuss both the genetic and epigenetic mechanisms by which chromatin structure can dictate AFR mechanisms and will present evidence of how pathogenic yeast, specifically from the Candida genus, modify chromatin structure to promote survival in the presence of anti-fungal drugs. We also discuss the mechanisms by which anti-chromatin therapy, specifically lysine deacetylase inhibitors, influence the acquisition and phenotypic expression of AFR in Candida spp. and their potential as effective adjuvants to mitigate against AFR.

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Yeast chromatin remodeling complexes and their roles in transcription

Cited by 17 publications

References 102 publications

Control of Gene Expression via the Yeast CWI Pathway

Control of Gene Expression via the Yeast CWI Pathway

On and Off: Epigenetic Regulation of C. albicans Morphological Switches

Chromatin Structure and Drug Resistance in Candida spp.

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