ArticleMolecular and cellular biology2008
Disrupting vesicular trafficking at the endosome attenuates transcriptional activation by Gcn4.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- SAGA subunits Spt3 and Spt8 act directly and non-redundantly with TFIID in TBP recruitment in the Gcn4 transcriptome.Nucleic acids research · 2025Article
- Differential requirements for Gcn5 and NuA4 HAT activities in the starvation-induced versus basal transcriptomes.Nucleic acids research · 2023Article
- Differential requirements for P stalk components in activating yeast protein kinase Gcn2 by stalled ribosomes during stress.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Distinct functions of three chromatin remodelers in activator binding and preinitiation complex assembly.PLoS genetics · 2022Article
- Gcn4 Binding in Coding Regions Can Activate Internal and Canonical 5' Promoters in Yeast.Molecular cell · 2018Article
- A Lipid Transfer Protein Signaling Axis Exerts Dual Control of Cell-Cycle and Membrane Trafficking Systems.Developmental cell · 2018Article
- Identification of Genes inG3 (Bethesda, Md.) · 2017Article
- Genome-wide cooperation by HAT Gcn5, remodeler SWI/SNF, and chaperone Ydj1 in promoter nucleosome eviction and transcriptional activation.Genome research · 2016Article
- Genomic Analysis of ATP Efflux in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2015Article
- Control of Plasma Membrane Permeability by ABC Transporters.Eukaryotic cell · 2015Article
- Accumulation of a threonine biosynthetic intermediate attenuates general amino acid control by accelerating degradation of Gcn4 via Pho85 and Cdk8.PLoS genetics · 2014Article
- The balance of protein expression and degradation: an ESCRTs point of view.Current opinion in cell biology · 2013Review
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- An upstream ORF with non-AUG start codon is translated in vivo but dispensable for translational control of GCN4 mRNA.Nucleic acids research · 2011Article
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- Activator Gcn4 employs multiple segments of Med15/Gal11, including the KIX domain, to recruit mediator to target genes in vivo.The Journal of biological chemistry · 2010Article
- Autophagy and amino acid homeostasis are required for chronological longevity in Saccharomyces cerevisiae.Aging cell · 2009Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
Abstract
The late endosome (MVB) plays a key role in coordinating vesicular transport of proteins between the Golgi complex, vacuole/lysosome, and plasma membrane. We found that deleting multiple genes involved in vesicle fusion at the MVB (class C/D vps mutations) impairs transcriptional activation by Gcn4, a global regulator of amino acid biosynthetic genes, by decreasing the ability of chromatin-bound Gcn4 to stimulate preinitiation complex assembly at the promoter. The functions of hybrid activators with Gal4 or VP16 activation domains are diminished in class D mutants as well, suggesting a broader defect in activation. Class E vps mutations, which impair protein sorting at the MVB, also decrease activation by Gcn4, provided they elicit rapid proteolysis of MVB cargo proteins in the aberrant late endosome. By contrast, specifically impairing endocytic trafficking from the plasma membrane, or vesicular transport to the vacuole, has a smaller effect on Gcn4 function. Thus, it appears that decreasing cargo proteins in the MVB through impaired delivery or enhanced degradation, and not merely the failure to transport cargo properly to the vacuole or downregulate plasma membrane proteins by endocytosis, is required to attenuate substantially transcriptional activation by Gcn4.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.