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A New Paradigm For The Control Of Cellular Function: The Dynamic Reshaping Of The Epigenome By Histone Variants
Funder
National Health and Medical Research Council
Funding Amount
$672,735.00
Summary
Our DNA is packaged and partitioned into stable identities, chromosomes, which is critical for proper cell function and the inheritance of our genetic material from one cell generation to the next. Loss of chromosome integrity leads to cancer and therefore the cell must ensure that this does not happen. We have uncovered a new mechanism whereby different components of chromosomes can dynamically move from one location to another to ensure chromosomes remain stable when they are challenged.
H2A.Z Acetylation: Deregulation Of Enhancer Activity And 3D Chromatin In Prostate Cancer
Funder
National Health and Medical Research Council
Funding Amount
$859,350.00
Summary
DNA is not linear but packaged in the cell nucleus in a three-dimensional (3D) structure in such a way that distal regulatory regions can interact to control gene expression. Our new data suggests that a chemical modification of the histone variant H2A.Z plays a critical role in the formation of the 3D chromatin structure. This project is aimed to dissect the role of H2A.Z in prescribing 3D structure, which will provide a more precise understanding of gene deregulation in cancer.
The Role Of The Chaperone NASP In Regulating Histone Dynamics During DNA Replication And Repair
Funder
National Health and Medical Research Council
Funding Amount
$371,602.00
Summary
To fit inside our cells, DNA is intricately packaged with histone proteins into chromatin. All aspects of cell function are regulated by this packaging. My research will help us to understand how the cellular life of histones is controlled by a protein called NASP to ensure the packaging is correctly maintained and reorganised during normal genome function.
The Role Of Moz, An Epigenetic Regulator, In The Pathogenesis Of Leukaemia
Funder
National Health and Medical Research Council
Funding Amount
$713,872.00
Summary
We are studying the oncogene and epigenetic regulator MOZ, (monocytic leukaemia zinc finger protein), with the aim firstly of better understanding the pathogenesis of cancer and secondly developing a new class of anti-cancer drugs.
The Role Of Somatic Mutations In CCCTC-binding Factor (CTCF) Binding Sites In Cancer
Funder
National Health and Medical Research Council
Funding Amount
$371,114.00
Summary
The three dimensional organisation of genomic DNA has been recognised to play a crucial role in maintaining the stability and function of human cells. In cancer this organisation is often perturbed as a result of mutations to proteins that govern this process. This project will examine how mutations in the DNA may potentially alter the three dimensional organisation of cancer genomes and will identify links between these mutations with cancer development and patient prognosis.
We have recently discovered that MOZ (monocytic leukaemia zinc finger gene), a gene first identified in rmutations leading to a particularly aggressive form of leukaemia, is a major regulator of senescence. In the absence of MOZ cells exit the cell cycle and become senescent, independently of DNA damage. These obsevations are very important for understanding cancer development because for cancer to grow and spread the cells must avoid senescence.
Dissecting Spatial, Regional And Temporal Aspects Of The Cancer Epigenome
Funder
National Health and Medical Research Council
Funding Amount
$690,216.00
Summary
Epigenetic deregulation occurs commonly in cancer, and can affect not only single genes but can encompass large chromosomal domains, leading to altered expression of oncogenes and tumour suppressor genes, and genomic instability. We will investigate the role of epigenetic remodeling, how spacial reorganisation of the genome, nuclear architecture, chromatin looping and replication timing may affect long range epigenetic deregulation, and ultimately contribute to cancer formation and progression.
Regulation Of Ribosomal RNA Gene Chromatin During Malignant Transformation.
Funder
National Health and Medical Research Council
Funding Amount
$882,486.00
Summary
The overarching goal of this proposal is to determine the molecular basis for tumour cell dependence on activated ribosomal RNA gene repeats (rDNA). Our working model posits that rDNA repeats become activated through changes in rDNA chromatin structure that include increased binding of the RNA Polymerase I transcription factor UBF.
Understanding How Defects In Chromosome Structure Can Cause Disease
Funder
National Health and Medical Research Council
Funding Amount
$546,557.00
Summary
The correct folding of DNA is critical to a cell's survival. This is orchestrated by a special class of proteins called the condensins. Defects in condensin lead to aberrant chromosome folding and disease. We aim to understand how condensin folds chromosomes and why mutations in condensin are increasingly associated with disease.