ArticleMolecular biology of the cell2012
Regulation of SREBP during hypoxia requires Ofd1-mediated control of both DNA binding and degradation.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- The axes of biology: a novel axes-based network embedding paradigm to decipher the functional mechanisms of the cell.Bioinformatics advances · 2024Article
- MfOfd1 is crucial for stress responses and virulence in the peach brown rot fungus Monilinia fructicola.Molecular plant pathology · 2020Article
- Oxygen-responsive transcriptional regulation of lipid homeostasis in fungi: Implications for anti-fungal drug development.Seminars in cell & developmental biology · 2018Review
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- ChIP-seq and in vivo transcriptome analyses of the Aspergillus fumigatus SREBP SrbA reveals a new regulator of the fungal hypoxia response and virulence.PLoS pathogens · 2014Article
- Casein kinase 1 regulates sterol regulatory element-binding protein (SREBP) to control sterol homeostasis.The Journal of biological chemistry · 2014Article
- Structural requirements for sterol regulatory element-binding protein (SREBP) cleavage in fission yeast.The Journal of biological chemistry · 2013Article
- Dsc orthologs are required for hypoxia adaptation, triazole drug responses, and fungal virulence in Aspergillus fumigatus.Eukaryotic cell · 2012Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cells adapt to changes in ambient oxygen by changing their gene expression patterns. In fission yeast, the sterol regulatory element-binding protein Sre1 is proteolytically cleaved under low oxygen, and its N-terminal segment (Sre1N) serves as a hypoxic transcription factor. When oxygen is present, the prolyl hydroxylase Ofd1 down-regulates Sre1N activity in two ways: first, by inhibiting its binding to DNA, and second, by accelerating its degradation. Here we use a mathematical model to assess what each of these two regulatory functions contributes to the hypoxic response of the cell. By disabling individual regulatory functions in the model, which would be difficult in vivo, we found that the Ofd1 function of inhibiting Sre1N binding to DNA is essential for oxygen-dependent Sre1N regulation. The other Ofd1 function of accelerating Sre1N degradation is necessary for the yeast to quickly turn off its hypoxic response when oxygen is restored. In addition, the model predicts that increased Ofd1 production at low oxygen plays an important role in the hypoxic response, and the model indicates that the Ofd1 binding partner Nro1 tunes the response to oxygen. This model quantifies our understanding of a novel oxygen-sensing mechanism that is widely conserved.
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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.