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Genetic Basis For Skeletal Muscle Formation And Regeneration In Development And Disease
Funder
National Health and Medical Research Council
Funding Amount
$876,005.00
Summary
How does muscle grow and repair after injury or disease? This basic question in the focus of the research in this fellowship. Specific cells are put aside during development to generate the growth and provide stem cells required for regeneration. Using the advantages of the zebrafish system I will record the action of different stem cell populations during growth and disease. I will define the genes required for stem cell action and utilize this knowledge to create new therapeutic pathways.
Many human muscle diseases are caused by mutations in genes encoding skeletal muscle actin. Actin is a major building block of the sarcomere, the engine of muscle contraction. Our studies have identified a mutation in chaperonin, the main protein-folding complex responsible for actin folding, which results in a muscle defect. These results have led to a novel hypothesesis, which we test in this grant, namely that as the chaperonin complex can act as a modulator of of muscle disease.
Genetic Basis For Skeletal Muscle Formation In Development And Disease.
Funder
National Health and Medical Research Council
Funding Amount
$751,854.00
Summary
Inherited skeletal dystrophies and myopathies are devastating and debilitating disease for which there are no cures and general muscle wasting is major health problem for a significant number of older Australians. Understanding how muscles form, grow and are maintained in model system, the Zebrafish, will provide avenues for treatment of these diseases. We will create models of human muscle diseases in zebrafish and test the usefulness of different therapeutic approaches we develop.
Molecular And Cellular Basis For Muscle Regeneration In Zebrafish.
Funder
National Health and Medical Research Council
Funding Amount
$541,104.00
Summary
Muscle repair occurs via the use of muscle stem cells, which provide skeletal muscle with its regenerative capacity. Muscle stem cells are particularly important in muscle diseases such as muscular dystrophies where muscle regeneration is an important factor in disease progression. We will identify the processes controlling muscle regeneration utilising zebrafish as a model organism. We hope this research will lead to an understanding of how muscle stem cells are generated.
Mechanistic Characterisation Of The Epigenetic Modifier Smchd1
Funder
National Health and Medical Research Council
Funding Amount
$1,197,133.00
Summary
FSHD is a progressive muscular dystrophy that currently has no treatment or cure. SMCHD1 is known to play an important role in FSHD, where its usual function in switching genes off is imperfect, contributing to disease. In this project we will determine how SMCHD1 switches genes off and what SMCHD1 looks like at the molecular level, so that we can elucidate how to boost SMCHD1 function for FSHD therapy.
Defining The Role Of Glycosylation In Basement Membrane Failure During Muscular Dystrophy
Funder
National Health and Medical Research Council
Funding Amount
$824,664.00
Summary
This project aims to utilize mutations within the zebrafish fkrp gene to understand the pathogenic basis of the human diseases associated with mutation of this gene which results in a spectrum of muscular dystrophies. By generating models of alleles that represent the range of phenotypes seen in humans we will have a directly translatable model system to human pathology.
The Molecular Mechanisms Of Anabolic Androgen Actions In Skeletal Muscle
Funder
National Health and Medical Research Council
Funding Amount
$487,500.00
Summary
We are studying the role of male sex hormones, androgens, in controlling muscle function. Muscle wasting occurs in a variety of disorders, including cancer, burns and trauma, and also during normal ageing. Treatment with androgens helps prevent muscle wasting, and causes increased muscle size, although current therapies can also have side effects. Little is known about how androgens prevent wasting and promote muscle growth. Therefore, we propose to study the actions of male sex hormones in musc ....We are studying the role of male sex hormones, androgens, in controlling muscle function. Muscle wasting occurs in a variety of disorders, including cancer, burns and trauma, and also during normal ageing. Treatment with androgens helps prevent muscle wasting, and causes increased muscle size, although current therapies can also have side effects. Little is known about how androgens prevent wasting and promote muscle growth. Therefore, we propose to study the actions of male sex hormones in muscle. We will study the growth of mouse muscle cells in culture, and measure their rate of growth when treated with androgens. All cells contain certain factors that control their growth and replication, and we will test whether androgens activate these factors to increase growth. We will also study the effect of androgens on muscle in mice, to investigate complex effects that only occur in real muscle. We will neuter male mice, which causes muscle wasting. Neutered mice will then be treated with androgens or placebo, and we will compare the muscle growth effect of androgen treatment versus placebo. We will measure muscle strength, size, and the number of muscle cells in treated and placebo mice. We will also see if the effects of androgen require a particular protein, the androgen receptor, which acts as a lock-key mechanism in cells, to allow them to respond to androgens. We will make a strain of mouse with a non-functional version of the androgen receptor only in muscle cells. This will determine if the muscle growth effects of androgens occur through a direct action on muscle, or indirectly through acting on other tissues in the body. This information will ultimately allow us to design more targeted androgen therapies for muscle wasting, that act only on muscle.Read moreRead less
Targeting Beta-adrenergic Signalling To Improve Muscle Regeneration In Muscular Dystrophy
Funder
National Health and Medical Research Council
Funding Amount
$473,224.00
Summary
Duchenne muscular dystrophy (DMD) is the most common and severe form of muscular dystrophy, caused by a lack of a protein called dystrophin. Dystrophic muscles are fragile, prone to injury, and have a compromised ability to regenerate after damage. Modulating pathways regulating beta-adrenergic signalling has potential to attenuate the dystrophic pathology and to delay the onset or slow the progression of the muscle wasting and weakness in muscular dystrophy.
Molecular Mechanisms That Generate And Activate Muscle Stem Cells During Growth And Disease.
Funder
National Health and Medical Research Council
Funding Amount
$596,086.00
Summary
This study aims answer long standing questions in the field of muscle stem cells. Understanding how stem cell-driven muscle repair occurs has profound implications for our understanding of the pathology and treatment of muscle disease. Muscular dystrophies and myopathies are amongst the largest group of inherited disorders to afflict the human condition. It is our hope that the results of this research will lead to a better understanding of how treatments, stem cell based or otherwise, could be ....This study aims answer long standing questions in the field of muscle stem cells. Understanding how stem cell-driven muscle repair occurs has profound implications for our understanding of the pathology and treatment of muscle disease. Muscular dystrophies and myopathies are amongst the largest group of inherited disorders to afflict the human condition. It is our hope that the results of this research will lead to a better understanding of how treatments, stem cell based or otherwise, could be employed to correct such disorders.Read moreRead less
Modeling Emery-Dreifuss Muscular Dystrophy In Zebrafish
Funder
National Health and Medical Research Council
Funding Amount
$460,190.00
Summary
Emery-Dreifuss muscular dystrophy (EDMD) is a muscle degenerative disease characterised by specific muscle degeneration. Human genetic studies have identified specific genes that are mutated in patients with EDMD. We have generated zebrafish models of the most common forms of EDMD and propose to use these models to determine how mutations in these genes contributes to a lack of muscle integrity in this muscular dystrophy.