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GTP Depletion and Genome Stability: Mechanistic Insights into Mycophenolic Acid-Induced Transcriptional and DNA Damage Responses

Aston University College of Health and Life Sciences
Partially Funded 🎓 Genetics 🎓 Molecular Biology 🎓 Nursing & Health gtp depletion mycophenolic acid transcriptional regulation dna damage response genome stability chromatin biology cancer therapy immunosuppressants

Explore how metabolic stress from mycophenolic acid affects genome stability and transcription. Investigate DNA repair and chromatin changes with direct relevance to cancer and transplant medicine. Employ molecular biology, microscopy, and bioinformatics to uncover novel cellular mechanisms under stress.

AI-generated overview

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Why This Research Matters

This research reveals broader effects of a widely prescribed immunosuppressant on genome stability, challenging assumptions about its selectivity. Insights will improve understanding of metabolic influences on DNA repair and transcription, with practical applications for enhancing cancer therapies and improving transplant patient outcomes.

Gene expression mRNA tRNA chromatin genomic instability

Project Description

Project Overview

Mycophenolic acid (MPA), an immunosuppressant active ingredient prescribed globally, disrupts essential cellular processes beyond immune suppression by depleting GTP. Recent findings indicate MPA impairs RNA polymerase III transcription and induces DNA damage at clinically relevant concentrations, challenging previous assumptions about its selectivity.

What You Will Do

This project aims to define molecular mechanisms linking MPA-induced metabolic stress to transcriptional dysregulation, chromatin architecture, and DNA damage responses. Using human cell lines, you will explore how MPA affects RNA polymerase II and III transcription, causes replication stress, influences DNA repair pathway choice, and compromises chromosome stability. A core focus includes studying MPA modulation of cellular responses to ionising radiation and chemotherapeutic agents.

Techniques involved include molecular and cellular biology methods (RNA-seq, qPCR, ChIP, CRISPR), genome stability assays (γH2AX, 53BP1, micronuclei quantification, EdU incorporation), fluorescence microscopy, and bioinformatic analyses of transcriptomic and genomic data.

Expected Outcomes

The project expects to elucidate how metabolic perturbation by MPA reshapes transcription and DNA repair, enhancing understanding of genome integrity maintenance under metabolic stress. It will also provide insights relevant to improving cancer treatments and transplant patient care by characterizing MPA’s broader cellular effects.

Why This Matters

The work challenges traditional views that MPA selectively targets lymphocytes by blocking GTP synthesis, revealing its wider impact on genome stability and transcriptional regulation. Understanding these mechanisms is critical for refining immunosuppressive therapies and advancing precision medicine approaches in oncology and transplant medicine.

Entry Requirements

Candidates should have either a First or Upper Second Class undergraduate degree in a relevant subject or a First or Upper Second Class undergraduate degree plus a Merit or Distinction in a Masters degree. Overseas qualifications will be considered if equivalent.

How to Apply

Applications require English language certified transcripts and certificates, a research statement, personal statement, CV, two academic references (on headed paper, signed and dated within 2 years), evidence of English proficiency, and a copy of your passport or settled/pre-settled status if applicable. Contact Dr Theo Kantidakis at t.kantidakis@aston.ac.uk for enquiries. Discussions with the supervisor about consumable costs should be uploaded with the application.

Eligibility

UK/Home
EU
International

Supervisor Profile

DT
Dr Theo Kantidakis
Aston University, College of Health and Life Sciences
1470 Citations
14 h-index
Google Scholar

Dr Theo Kantidakis is a specialist in transcriptional regulation and chromatin biology, with research focused on how metabolic and molecular stresses impact fundamental cellular processes. He co-supervises this project on MPA’s effects on transcription and genome stability, contributing expertise in molecular biology and gene expression mechanisms.

Key Publications

2010 302 citations
mTOR associates with TFIIIC, is found at tRNA and 5S rRNA genes, and targets their repressor Maf1
Identified the association of mTOR with TFIIIC and its role in targeting Maf1, linking mTOR signaling to tRNA and 5S rRNA gene regulation.
2014 245 citations
RECQL5 controls transcript elongation and suppresses genome instability associated with transcription stress
Showed RECQL5 regulates transcript elongation and protects genome stability under transcription stress conditions.
2017 237 citations
UV irradiation induces a non-coding RNA that functionally opposes the protein encoded by the same gene
Discovered a non-coding RNA induced by UV that antagonizes its co-encoded protein, revealing novel RNA-protein regulatory mechanisms.
2016 156 citations
Mutation of cancer driver MLL2 results in transcription stress and genome instability
Demonstrated that mutations in MLL2 cause transcription stress and genome instability linked to cancer development.
2006 131 citations
Activation by c-Myc of transcription by RNA polymerases I, II and III
Characterized how c-Myc activates multiple RNA polymerases, highlighting its role in gene expression regulation in cancer.

Research Contributions

Established the role of mTOR in regulating transcription of tRNA and 5S rRNA genes via Maf1.
This connected nutrient signaling pathways to RNA gene transcription control, impacting understanding of cellular growth regulation.
Elucidated mechanisms by which RECQL5 helicase maintains genome stability during transcription elongation.
Provided insight into preventing transcription-associated genome instability, relevant to cancer biology.
Demonstrated that mutations in the cancer driver MLL2 cause transcription stress leading to genome instability.
Advanced understanding of cancer pathogenesis related to transcriptional regulation disruptions.
Discovered a UV-induced non-coding RNA that antagonizes its co-expressed protein, revealing novel regulatory RNAs.
Opened new avenues in RNA biology and stress response mechanisms at the transcriptional level.

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Gene expression mRNA tRNA chromatin

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