Search Rutherford Discovery Fellowship awards 2010–2017

Public Summary: Human language and our ability to cooperate in large groups of unrelated individuals are perhaps our two most important survival strategies. Yet the language we speak and whether we choose to cooperate are not coded in our genes, but are determined by the speech and social norms of those around us – these are inherently cultural phenomena that require a cultural explanation. Since Darwin, it has been recognized that, like species, cultures evolve. The power of Darwin’s theory was to link micro-scale processes of survival and reproduction to macro-scale trends in evolution over many generations. This research programme takes a Darwinian approach to two aspects of human culture, using methods and thinking from population genetics and evolutionary biology to answer questions about the cultural evolution of language and cooperation. On a micro scale, I will investigate how new sounds and words (in the case of language) and prosocial norms and behaviours (in the case of cooperation) spread through populations to become established in a broader cultural system. On a macro scale, language family trees will be used to trace genealogical relationships between cultures. By modelling the evolution of linguistic and cultural traits along these trees, I will identify general laws governing language change and the evolution of cooperative norms and institutions. More broadly, this work promises a better understanding of how words, behaviours, ideas, technologies, and ideologies spread through groups, and how complex cultural systems, like language or religion, emerge and evolve through time.

Public Summary: Background & Motivation: Bioelectrical event is associated with every muscular contraction in the human body. Interpreting and control the timing, pattern and shape of these bioelectrical events underpin a major new US National Institute of Health (NIH) programme on developing “electroceuticals”. Gastrointestinal (GI) motility is also governed by many factors, among which is a bioelectrical event called slow waves, generated by a network of pacemaker cells called the interstitial cells of Cajal (ICC). Significant losses of ICC have been associated with prominent chronic GI disorders, e.g., gastroparesis, diabetes-related digestive dysfunctions, and slow transit constipation, and are linked to persistent slow wave dysrhythmias. These diseases often present non-specific symptoms that are difficult to diagnose and expensive to manage. Therefore, an improved foundation for understanding ICC structure-function relationships and slow wave dysrhythmias will offer more specific avenues targeted at the underlying patho-electrophysiological mechanisms to develop diagnostic and electroceuticals for GI disorders. Vision: To establish a world-class, highly inter-disciplinary programme with the aim to determine how slow waves coordinate digestion through an integrated use of experimental analysis, medical device instrumentation, and mathematical modelling. Track-record: The PI has a strong emerging record in instrumentation, experimentation, and modelling of GI electrophysiology. Since PhD conferral in 2012, the PI has independently attracted more than $NZD 580k in contestable external funding and is lead or co-supervising six postgraduate students. During the proposal, the PI will be supported by an existing collaborative network of world-leading experimental physiologists and clinicians in NZ, USA, and Belgium. Approach: The overall strategy of this programme is to employ a joint experimental-modelling approach to integrate novel and existing experimental data of GI electrophysiology, tissue micro-structure, and motility function in a unifying mathematical modelling framework. The experimental data will involve high-resolution electrical mapping of slow waves from Auckland City Hospital and University of Louisville, KY, USA. These two locations will offer clinical trials of recording devices from control subjects and patients with motility disorders. Detailed images of a tissue-scale ICC network will be obtained using a unique extended-imaging acquisition setup in Université Libre de Bruxelles, Belgium. A series of numerical metrics will be developed and applied to quantify the micro-structural changes in ICC networks spanning healthy to diseased states. Functional calcium transient data will be obtained through collaboration with a group based at Mayo Clinic, Rochester, MN, USA. Validated mathematical models will then be developed to link the structures of ICC network to propagation of slow waves, calcium transients, and motility. The models will be applied to identify the mechanisms of how ICC loss relates to diminished digestive functions. Finally, a commercial arm of the programme will be focused on securing intellectual properties for novel instrumentation and analysis systems, toward building a medical technology-based company in NZ. The first major product line will be a commercial package of a non-invasive tool for mapping gastric slow waves - “enhanced electrogastrography (EGG)”.

Public Summary: Ice flows from the interior of Antarctica’s ice sheets before entering the world’s oceans and melting from the base of floating ice shelves or calving as ice bergs. Changing the flow speed of the grounded ice sheet can therefore change the rate of sea level rise. Estimates of sea level rise this century vary widely. The Intergovernmental Panel on Climate Change (2013) predicts less than a meter global mean sea level rise by 2100. However, the latest model simulations show that Antarctica alone may contribute more than this. Uncertainty in our ability to predict sea level rise is primarily due to difficulties estimating how changes at the boundaries of ice sheets affect the speed at which they flow into the ocean. Although satellite observations show increasing ice loss from the Antarctic, observations of the physical processes thought to be rate-determining, such as ice shelf disintegration, ice cliff failure, or runaway glacier retreat, are rare or difficult to adequately observe at all. Despite these challenges, key ice sheet processes are considered to warrant closer scrutiny. One of these processes is the role played by liquid water at the base of ice sheets. Ice sheets are underlain by considerable networks of liquid water. This water can be concentrated in subglacial lakes, in channels that connect lakes, or be distributed across the base of the ice. The quantity and distribution of this water is a primary control on the flow velocity of the overriding ice. Major ice streams that drain the interior of West Antarctica have stopped flowing, or accelerated, due to changes in the way water is routed beneath the ice. This research programme will examine the role of water beneath ice sheets at a variety of scales. The first step will be to map the extent of water bodies beneath the Antarctic Ice Sheet using satellite data, detecting surface elevation changes due to the water’s presence. That information will then be combined with airborne and ground based observations to provide a large-to-medium scale view of the subglacial hydrology beneath the ice. The main phase of the research will include a unique series of observations that we will make by drilling through the West Antarctic Ice Sheet and directly sampling the underlying water and sediments. The initial stages of this programme are already underway as part of a collaborative international Ross Ice Shelf Project. Using hot water drilling technology under construction at Victoria University of Wellington our research programme will instrument a subglacial water conduit beneath the ice sheet. Thus it will be possible to constrain the volume, history, and role of water beneath the ice sheet, as well as helping to reveal the history of the ice sheet itself. Our comprehensive study of subglacial water will then be used to inform numerical models of ice flow, addressing a major shortcoming in our ability to predict the rate at which sea level will rise.

Public Summary: A New Zealand first space industry Rocket Lab has recently emerged giving the potential for low-cost, public access to space. The challenge is to understand and control highly complex dynamics of rockets travelling at speeds from supersonic to hypersonic (> Mach 6) and up to 150 km in altitude for high accuracy pointing. Standard control methods have long development times and high cost due to the large number of launches required. The major problem is that at these high speeds, shock waves and turbulence can occur, so that small asymmetries and design differences in the rocket can give completely different and unexpected control responses and dynamics. There are also random disturbances affecting the rocket from the atmosphere which are virtually impossible to predict prior to launch. This proposal will build a mathematical model of the rocket as it's travelling through space, including directly identifying random wind loads to allow prediction and stabilization of the rocket. This approach will avoid the need for costly trial and error type runs to tune the control systems and significantly reduce the typically long turn around time required to launch and accurately position a payload. Data will be obtained from smaller scale launch vehicles developed at the University of Canterbury and the larger scale launches of Rocket Lab. There will also be wind tunnel testing with controlled turbulence to test the control algorithms on conditions not previously 'seen'. The solutions developed will be applicable in many other areas of aerospace and industry automation in general. The knowledge gained will develop unique capability in New Zealand for training both undergraduate and postgraduates to enter cutting edge space industry research and development.

Public Summary: Atmospheric carbon dioxide levels are due to reach 400 parts per million in the next two years. These are some of the highest levels the Earth has experienced in the past 23 million years, and the most elevated since the Pliocene epoch 3 million years ago. These modern elevated levels are the consequence of man-made greenhouse gas emissions. Recent geological studies have indicated that when atmospheric carbon dioxide levels exceed the 350-400 ppm range in the geological past, the West Antarctic and Greenland Ice Sheet melted, and combined with some melting of the East Antarctic Ice Sheet, contributed to sea levels between 10-20 m higher than present. However, the consequences of Antarctic warming are more far reaching than sea level rise alone. Changes in the Southern Ocean sea ice belt around Antarctic would affect the primary plankton productivity in the Southern Ocean. Just as critical is that warming of the Antarctic weakens the temperature gradient between the poles and equators, as this changes the location and strength of the westerly winds that pass over the Southern Ocean and New Zealand latitudes. These winds help drive global ocean circulation, and regulate the relative location where Antarctic and tropical-sourced water masses meet. These waters currently meet in the latitude of New Zealand, and as we have a strongly maritime-influenced climate, changes in the Southern Ocean and Antarctic will have a profound impact on our climate. This research aims to reconstruct past Antarctic Ice Sheet variability and associated oceanographic change in the Southern Ocean and offshore of New Zealand using geological drill core data. These high resolution reconstructions will be conducted during selected time slices in the past 23 million years when carbon dioxide levels exceeded 400-450 parts per million. Intervals of interest include the Pliocene Warm Period (5.3 to 3.6 million years ago) and the Middle Miocene Climatic Optimum (~18 to 15 million years ago) - the two most recent periods when atmospheric CO2 levels exceeded modern-day levels of 400 ppm. As such, this study aims to address the following fundamental question 'How did the Antarctica Ice Sheet and the Southern Ocean respond to elevated levels of atmospheric greenhouse gases and global warming events during these past warmer climates, and what were the impacts to the oceans offshore of New Zealand?'. Specifically it will investigate 1) mechanisms for the high sensitivity of the Antarctic Ice sheets melting during moderately elevated levels of atmospheric carbon dioxide; 2) environmental forcings and responses in the Southern Ocean related to changes in ice sheet and sea ice extent; and 3) provide improved boundary conditions (i.e. inputs) for numerical computer models of greenhouse climates in the past and the future.

Public Summary: Chemical weathering of silicate minerals (the majority of Earth's crust) consumes CO2 and is the ultimate long-term control on the concentration of CO2 in the atmosphere. The warm climates associated with greenhouse conditions enhance weathering, thereby reducing atmospheric CO2 and lowering mean global temperature in a negative feedback loop. Weathering feedbacks have long been invoked to explain concurrent global cooling and increased erosion rates during the past few million years. Understanding these feedbacks is vital for accurately predicting global climate response to accumulating atmospheric CO2. Weathering feedbacks imply that the onset of global ice ages resulted in increased physical erosion rates which, due to more fresh minerals available for weathering, reduced CO2 through silicate mineral weathering. While this sequence is logically consistent and intuitive, recent work has cast doubt on two critical linkages in this system, raising two important questions; 1) Did erosion rates accelerate significantly over the past few million years, and 2) Does chemical weathering speed up with faster erosion. In this project, we will apply a new suite of analytical methods to one of the fastest eroding landscapes on Earth in order to determine the roles of weathering and erosion on soil production, and ultimately on long-term climate stability. We will use new methods based on the radioactive decay of uranium and thorium to measure the first ever in-situ soil ages for New Zealand, allowing us to calculate the speed of soil production and how long soil can last in our rapidly eroding mountains and hillcountry. Total landsurface lowering rates will be measured using terrestrial cosmogenic nuclides (TCNs), which are rare atoms that are formed when cosmic rays collide with atoms in Earth's atmosphere and surface materials. We will combine these lowering rates with trace element concentrations in soils and rock to separately calculate chemical weathering rates and physical erosion rates, allowing us to answer the question if chemical weathering rates increase indefinitely with physical erosion rates. A novel mineral luminescence thermochronometer will measure the time required to erode the upper ~1km of Earth's surface. This will provide a long-term measurement of surface lowering, allowing us to determine if denudation rates have indeed increased in the recent geologic past. These methods are only beginning to be deployed globally, and this project will be the first time in which the entire suite has been applied. Victoria University of Wellington is uniquely suited to accomplish this project, with the entire infrastructure already in place to perform all analyses. This project will make use of the School of Geography, Environment and Earth Science's mulitcollector ICP mass spectrometer, the new cosmogenic nuclide laboratory and the luminescence laboratory. TCN measurements will be made in collaboration with the National Isotope Centre at GNS Science in Wellington. This project will result in development of unique-to-New Zealand methods with broad applicability. Uranium decay methods can be used to measure soil age and sustainability. TCNs can date fault ruptures and landslides, and measure erosion rates, while luminescence thermochronometry can determine the long-term evolution of New Zealand's active landscape.

Public Summary: Disorders of the Autism Spectrum are life-long, and estimated to affect approximately 1% of New Zealanders. This high prevalence combined with the associated demands on social and educational care, represents a major issue in human health. Furthermore, Autism Spectrum Disorders (ASD) are a hidden burden on families and society as affected individuals largely disappear from the medical landscape after their diagnosis early in life. The development of DNA sequencing technologies is enabling the identification of some of the genetic causes of ASD, revealing a strong, but complex genetic basis. Identifying a genetic trait that predisposes to the development of disease can give insight into disease biology, aid diagnosis and enable discrimination among patients, which can subsequently lead to better targeted treatment options. However, there is only a very limited molecular diagnostic service, and no mutation discovery research program in place in New Zealand. Consequently, there is a lack of information to help shape the relevant educational and health support systems for patients and families.
Our aim is to establish a genetic research paradigm focused on uncovering underlying genetic causes of ASD in the New Zealand population, helping develop the discovery methodology that will eventually be transferred to the clinic. Using an approach generalizable to other genetic disorders, we will use the latest sequencing technologies to search for variations in the DNA of patients that cause the disease. We suspect some of these variations will be specific to New Zealand. Once our sequencing and analysis approach is in place, we can extend our studies to look at the next biological step: how these variations affect how cells in the brain communicate with one another during development. The results of this study will help contribute to the international effort to genetically define the disease, ultimately translating to therapeutics and a more specific health and educational support system for patients and family members.

Public Summary: Alpine environments have steep climatic gradients and therefore represent ever-changing battlegrounds. Here, species' interactions and responses to changing climatic conditions are played out in small arenas. There are well documented examples of species changing their geographic distribution in response to changing climate conditions over geological and recent time scales. Although climate sets the baseline conditions for life on Earth, the rate at which species respond to changing climatic conditions is mediated by interactions with neighbouring species.
Temperature decreases with elevation; therefore, in a warming climate the expectation is that species will shift their distribution upslope. The combination of aspect, slope and shading within mountainous landscapes gives, at any given elevation, a variety of cooler and warmer microclimates. On a local scale, this landscape heterogeneity creates safe havens and invasion springboards, short-term ecological refugia which mediate the rate of species' range shifts. On a regional scale, locations with climatic conditions that are consistently suitable for a species act as long-term evolutionary refugia which accumulate higher genetic diversity. In contrast, founder effects mean that recently colonised locations tend to have lower genetic diversity. Using ecological niche models to locate climatically suitable areas through time we will identify potential past, present and future thermal refugia. Using genetic data we will assess how these modelled refugia coincide with hotspots of current genetic diversity on a local and regional scale.
It is not individual species but communities of interacting species that govern the ecosystem services, (e.g. carbon storage), upon which humanity relies. A key challenge in theoretical and applied ecology is understanding how species shift or adapt to changing climatic conditions and how this affects communities. We will use plant community abundance and co-occurrence data to test for patterns in community structure along climatic gradients and for evidence of the impact of species-species interactions on species distributions. This will allow us to better understand the composition and distribution of alpine communities and how these are reshuffled under changing climatic conditions.
It is not possible to conserve the entire range for every species. Conservation prioritization aims to conserve the most valuable areas for biodiversity and or ecosystem services. Usually this is taken to mean the most species rich areas. A better approach is to trade off less valuable parts from the range of one species for more valuable parts of the range of that species or another species. This raises the question of what we consider valuable to mean. Should we prioritize areas within the range of a species that: a) currently have higher abundance or climatic suitability; or b) have higher genetic diversity or have been occupied for longer; or c) are more likely to stay or become climatically suitable under future climate change? We will address this question in the New Zealand context and assess the relative merit of these prioritization metrics.
This research brings together ecological niche modelling, population genetics and community ecology: balancing advances in ecological modelling with new empirical data to bring significant applied benefits to the New Zealand conservation community.

Public Summary: Currently the incidence of type 2 diabetes (T2D) is being described as a worldwide epidemic, and is usually attributed to metabolic imbalance resulting in obesity. T2D and associated diseases are one of the greatest causes of early mortality and put significant strain on New Zealand’s healthcare resources. As such effective therapeutic approaches to prevent and treat T2D need to be found. T2D is characterized by the impaired ability for insulin to stimulate glucose transport into the cell (insulin resistance) and failure of the pancreatic beta-cells to secrete sufficient insulin to maintain normal blood glucose levels. This ensuing chronic elevation in blood glucose is associated with the increased risk of developing diseases such as cancer, heart disease, neuropathy and kidney and liver failure. The mechanisms regulating glucose transport and beta-cell insulin secretion, and how they are modified by metabolic imbalance leading to the development of T2D are not well understood. However, it is known that intracellular vesicles need to insert and be maintained at the cell membrane for glucose to be transported into the cell (via glucose transporters (GLUTs)) and for beta-cells to release insulin (from insulin vesicles), and that this process is impaired during the development of T2D. In this proposal we will investigate whether the scaffolding protein beta-catenin, which is dynamically regulated by glucose and insulin signaling intermediates, is involved with the insertion and maintenance of GLUTs and insulin vesicles at the cell membrane of skeletal muscle and pancreatic beta-cells, respectively. Our preliminary data from cell culture models suggest that deletion of beta-catenin impairs normal glucose stimulated insulin secretion and insulin induced glucose transport. Furthermore, polymorphisms in the TCF7L2 gene (binding partner of beta-catenin) are associated with T2D suppression of beta-cell function, and the deletion of proteins that degrade beta-catenin enhance insulin sensitivity and prevent diet-induced T2D. We hypothesize that beta-catenin plays a regulatory role in glucose transport and glucose stimulated insulin secretion by facilitating and maintaining the insertion of insulin vesicles and GLUT4 into the cell membrane. Furthermore, dysregulation of beta-catenin during metabolic imbalance contributes to impairments in peripheral insulin sensitivity and beta-cell function associated with T2D. To investigate this hypothesis we will utilize loss and gain of beta-catenin function (deletion, overexpression and chemical manipulation) cell culture and transgenic mouse models. We will also employ the high fat diet mouse model of T2D to study the effect the metabolic imbalance has on beta-catenin function as a chaperone to facilitate GLUT and insulin vesicle insertion and maintenance at the cell membrane. Finally, we will assess whether altering beta-catenin expression levels is a viable target to treat or prevent the development of T2D. This research will provide evidence, for the first time, that a defect in the machinery facilitating the insertion and maintenance of GLUTs and insulin vesicles at the cell membrane is a common mechanism that links beta-cell dysfunction and insulin resistance during the development of T2D. In addition, we will identify beta-catenin as a novel pharmacological target for the treatment and prevention of T2D.

Public Summary: Together with proteins, fats, sugars and DNA, RNA is a member of the selected group of molecules that play a major role in life's chemical machinery. RNA has long been known to act as a carrier of information from DNA to proteins and is essential for translating DNA into proteins. Recent scientific advances have shown that RNAs are important for turning genes on and off in response to different signals. For example, RNAs can sense the presence of other molecules, changes in temperature and changes in pH. These are thrilling discoveries suggesting we have only scratched the surface of RNA's potential functions. We are discovering the importance of RNA in many different areas. In the area of human health we have discovered that different RNAs are involved in the progress of and susceptibility to cancer, progressive hearing loss, Prader-Willi syndrome and many other diseases. Disease-causing bacteria use sensors built of RNA to detect temperature changes due to ingestion by a host. In agriculture, a mutation involving an RNA gene has been linked to the increased muscularity of Texel sheep. The computational study of RNA is difficult compared to protein and DNA. We want to develop ways that will enable more researchers to make fascinating discoveries in this field.