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Active Transport Of Calcium Across Dental Enamel Cells - Testing A New Paradigm
Funder
National Health and Medical Research Council
Funding Amount
$258,000.00
Summary
Dental enamel defects and tooth loss affect over half our population, resulting in substantial suffering and economic costs. It is likely that many enamel defects could be prevented, and replacement teeth made more lifelike, if more was known about the cells responsible for producing enamel. A particular problem is our lack of understanding about how enamel-forming cells avoid overdosing on calcium, which can lead to cellular toxicity. The overall aim of this research is to use the latest cell b ....Dental enamel defects and tooth loss affect over half our population, resulting in substantial suffering and economic costs. It is likely that many enamel defects could be prevented, and replacement teeth made more lifelike, if more was known about the cells responsible for producing enamel. A particular problem is our lack of understanding about how enamel-forming cells avoid overdosing on calcium, which can lead to cellular toxicity. The overall aim of this research is to use the latest cell biology and biochemical techniques to elucidate the mechanisms of calcium handling in enamel cells, with developing teeth from rat as the experimental model. Our focus is on calcium transport mechanisms, a field where past theories were overturned by our recent findings with gene-knockout animals. We will test a new theory that has arisen from our investigations, using drugs and gene-silencing techniques to interfere with the cellular machinery now thought to be crucial for transporting calcium. By providing strong physiological evidence for this new mechanism, our expected results will define specific proteins that might be targeted by drugs and nutrition, and provide important information about how dietary fluoride and caffeine affect enamel quality. These findings would change thinking about how enamel defects can be prevented and provide a solid foundation to the exciting new field of dental bioengineering, whose goal is to coax stem cells to make natural replacement teeth.Read moreRead less
The Role Of Intersectin-1 In Endocytic Anomalies: Implications For Down Syndrome And Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$510,500.00
Summary
Individuals with Down syndrome have three copies of human chromosome 21, rather than the normal two. We have discovered a gene called Intersectin-1, located on human chromosome 21, that is expressed at higher levels than normal in individuals with Down syndrome. Intersectin-1 has a role in endocytosis, a process whereby cells take up molecules from the outside. Endocytosis occurs in all cells but is highly specialised in the brain where chemical transmitters are released and then rapidly recover ....Individuals with Down syndrome have three copies of human chromosome 21, rather than the normal two. We have discovered a gene called Intersectin-1, located on human chromosome 21, that is expressed at higher levels than normal in individuals with Down syndrome. Intersectin-1 has a role in endocytosis, a process whereby cells take up molecules from the outside. Endocytosis occurs in all cells but is highly specialised in the brain where chemical transmitters are released and then rapidly recovered by endocytosis in a process enabling neurones to pass signals to one another. A disturbance in endocytosis has been reported as the earliest hallmark of Alzheimer's disease in both non-Down syndrome and Down syndrome individuals. This disturbance is characterised by the presence of enlarged endosomes (small packages in neuronal cells containing chemical neurotransmitters formed during endocytosis). These enlarged endosomes are present long before the characteristic plaques of Alzheimer's disease appear. Since all individuals with Down syndrome develop Alzheimer's-like neuropathology, there must be a common disease mechanism that can be traced to the extra gene dosage from chromosome 21. We propose that a malfunctioning of Intersectin-1 is this common mechanism and we aim to test our hypothesis by the generation and analysis of mouse models of disrupted endocytosis.Read moreRead less
Regulation Of Pre-mRNA And MRNA Processing By The Neuron-specific Hu RNA-binding Proteins
Funder
National Health and Medical Research Council
Funding Amount
$477,750.00
Summary
The precise control of protein expression is absolutely critical in biology, and the key decisions about which genes are turned on or off at any one moment control the proper growth and maturation of an organism during development, and are responsible for the organism's homeostasis and proper response to environmental changes as an adult. Many gene expression programs are highly complex and controlled by regulating the activation of individual genes as they are copied from DNA to RNA. However, t ....The precise control of protein expression is absolutely critical in biology, and the key decisions about which genes are turned on or off at any one moment control the proper growth and maturation of an organism during development, and are responsible for the organism's homeostasis and proper response to environmental changes as an adult. Many gene expression programs are highly complex and controlled by regulating the activation of individual genes as they are copied from DNA to RNA. However, this activation is just the start of the process to produce an active protein. In higher organisms, these RNA copies almost always contain interruptions called introns, which must be excised from the RNA. Also, protein factors bound to specific RNAs can dictate whether the RNA is used to make protein or not, and these factors can also affect the localisation of the RNA to a specific sub-cellular destination, giving rise to highly localised protein expression. Evidence suggests that neurons are a cell type that rely heavily on mechanisms of RNA regulation. During development neurons become highly polarised, acquiring an axon which can elongate and find distant synaptic targets. While much is known about how axon growth cones respond to various guidance cues, the mechanisms by which the axon is able to translate this guidance cue information into structural changes which allow the growth cone to expand or collapse is largely unexplored. Recent evidence suggests that accurate growth cone guidance is absolutely dependent upon local protein synthesis. The functional corollary of this finding is that axon guidance requires RNA localisation and control of protein synthesis of RNAs in the growth cone. This phenomenon of spatial gene regulation within an individual cell is a central research interest for understanding how the brain functions.Read moreRead less