Aug 2026· PLoS ONE· Vol 21, pp. e0355681 - e0355681· 0 citations· 53 references
Medicine
TL;DR
Investigation of the regulatory mechanisms underlying nutrition-deprivation-responsive changes in gene expression in YGP1 revealed that the Puf5-mediated regulation contributes to the acid stress responses, and YGP1 expression supports cell survival in the puf5Δ background.
Abstract
Cells adapt to fluctuating nutrient conditions by dynamically regulating gene expression, ensuring survival under stress. Ygp1, a secretory yeast glycoprotein, is one such gene that is induced by nutrition deprivation, particularly glucose starvation. In this study, we investigated the regulatory mechanisms underlying nutrition-deprivation-responsive changes in gene expression, focusing on YGP1 expression. Under glucose-rich conditions, YGP1 expression was positively regulated by the RNA-binding protein Puf5, a member of the Puf family. This regulation ensured rhythmic YGP1 expression during M phase of the cell cycle. The Puf5-mediated control targeted a specific 60-nucleotide region in the YGP1 promoter (−600 to −540 from the start codon), and this regulation was partly mediated by the acid stress-responsive transcriptional activator Haa1. In addition, upon glucose exhaustion (diauxic shift), YGP1 expression was strongly induced by the stress-responsive transcription factors Msn2 and Msn4 through the stress-response elements in the YGP1 promoter. Further analysis of the physiological significance of YGP1 expression revealed that the Puf5-mediated regulation contributes to the acid stress responses, and YGP1 expression supports cell survival in the puf5Δ background. In summary, YGP1 expression is regulated by two distinct factors in a glucose availability-dependent manner: Puf5 under glucose-rich conditions and the Msn2/Msn4 during glucose starvation. Especially, Puf5-mediated regulation contributes to the acid stress responses and subsequently supports long-term cell survival.
Cellular adaption to glucose availability requires precise coordination between signaling pathways and gene expression. In Saccharomyces cerevisiae, the vacuole serves as a metabolic hub whose protein composition and activity are dynamically regulated to nutrient availability. Additionally, the Protein Kinase A (PKA) pathway is a central mediator of glucose stress response, acting through the transcriptional factor Msn2. However, how PKA-Msn2 axis connects environmental cues to vacuolar gene expression remains poorly understood.
In this study, we investigate how PKA regulates Msn2 subcellular localization and its impact on expression of PRC1, a representative vacuolar lumenal hydrolase. By combining Msn2 subcellular localization and gene expression analysis, we found glucose limitation induces PRC1 expression, which reduced after deletion of Msn2/4 and disruption of Stress Response Elements (STRE) in PRC1 promoter. Furthermore, reduced PKA activity is associated with nuclear accumulation of Msn2 and enhanced PRC1 expression, whereas deletion of Msn2/4 attenuates this effect. Results reveal that PKA-mediated regulation of Msn2 is essential for glucose stress responses and provide insight into how signaling pathways control PRC1 expression in yeast.
Together, the findings establish hY3 as a ribosome-bound regulator of translation and stress responses, positioning it as a determinant of cell fate under metabolic stress.
The mesophyll protoplast transient expression system is an essential and robust methodology for examining gene expression regulation. Despite its potential, it has not been effectively employed to elucidate the genetic regulatory pathways and networks underlying plant responses to nutrient starvation, such as those involving phosphorus (Pi) and iron (Fe). In this study, we identified differentially expressed genes in response to Pi starvation in Arabidopsis using transcriptome analysis and RT-qPCR validation. Our findings revealed that Pi starvation significantly upregulated the expression of Pi-starvation induced (PSI) genes, including SPX1, SPX3, IPS1, and PS2, while simultaneously downregulating the expression of Fe starvation-responsive genes, such as FIT, IRT1, and FRO2. Additionally, through a dual luciferase transient expression assay in mesophyll protoplasts, we demonstrated that the transcription factor PHR1 serves as a crucial transcriptional regulator, modulating the expression of phosphate starvation response (PSR) genes. This regulation significantly enhances the transcriptional activity of the SPX1, SPX2, SPX3, IPS1, PS2, and PHT1;4 promoters. Upon the addition of the SPX1 protein, the activation of these gene promoters by PHR1 were alleviated. Concurrently, the transcriptional regulator FIT, which governs the expression of genes responsive to Fe starvation, markedly increased the transcriptional activity of the IRT1 and FRO2 promoters. Based on these findings, we propose the mesophyll protoplast transient expression system as a rapid and reliable method for investigating complex genetic networks. Overall, our study provides substantial evidence for understanding the role of the mesophyll protoplast transient expression system in elucidating the genetic regulatory pathways and networks involved in plant responses to nutrient starvation.
Yashan Tian, Jian-Ju She, Jin-Hui Lin et al.· Frontiers in Plant Science· 0 citations
The results of contrasting the Azf1- and Dep1-driven regulomes suggest that for efficient rProt secretion, upregulation in the vesicle-mediated transportation must co-occur, as in the case of Azf1-KO.
Maria Gorczyca, P. Kubiak, E. Celińska· Microbial Cell Factories· 0 citations
The budding yeast Saccharomyces cerevisiae is a well-established model organism to study cellular stress response and underlying mechanistic regulation. Although glucose starvation fundamentally alters gene regulation and cell behaviour, inconsistent deprivation protocols often trigger gross morphological artefacts. These non-specific changes confound findings by activating pathways independently of true glucose-signalling mechanisms. Furthermore, a thorough transcriptomic profile of glucose starvation using non-confounding conditions remains lacking. Consequently, the precise transcriptional impact of losing key metabolic regulators that mediate adaptation to glucose starvation remains undefined. Here we have employed a refined glucose starvation protocol, utilising raffinose exchange, which shows induction of vast transcriptional stress response with minimal impact on cellular morphology confirmed by label-free imaging. Transcriptomic profiling revealed shifts in metabolic regulation, ATP turnover, and cell-to-cell communication as acute glucose deprivation driving cells towards oxidation-driven metabolism. Additionally, we characterise transcriptional alterations seen in deletion mutants of SNF12 and SPT20, known regulators of cellular metabolism, showing previously unappreciated transcriptional conservation, in part mimicking glucose starvation response. Finally, we identified cargo and stress-specific expression related to both eisosome components and surface transporters that are critical for metabolic adaptation. Overall, this dataset provides a comprehensive transcriptomic resource for dissecting stress signalling and driving novel hypothesis generation.
Justas Stanislovas, K. Laidlaw, Katherine M. Paine et al.· bioRxiv· 0 citations
These findings confirm and extend the observations that SlBAG9 is a stress-responsive gene, and the characterized HSE1-dependent promoter module represents a promising candidate for genetic engineering aimed at enhancing thermotolerance in crops.
Fan Fei, Fan Yang, Yu-Cheng Peng et al.· International Journal of Mol...· 0 citations
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