India

Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.

The ecosystems of the dry tropics are in flux: the savannas, woodlands and dry forests that together cover a greater area of the globe than rainforests are both a source of carbon emissions due to deforestation and forest degradation, and also a sink due to the enhanced growth of trees. However, both of these processes are poorly understood, in terms of their magnitude and causes, and the net carbon balance and its future remain unclear. This gap in knowledge arises because we do not have a systematic network of observations of vegetation change in the dry tropics, and thus have not, until now, been able to use observations of how things are changing to understand the processes involved and to test key theories. Satellite remote sensing, combined with ground measurements, offers the ideal way to overcome these challenges, as it can provide regular, consistent monitoring at relatively low cost. However, most ecosystems in the dry tropics, especially savannas, comprise a mixture of grass and trees, and many optical remote sensing approaches (akin to enhanced versions of the sensors on digital cameras) struggle to distinguish changes between the two. Long wavelength radar remote sensing avoids this problem as it is insensitive to the presence of leaves or grass, and also is not affected by clouds, smoke or the angle of the sun, all of which complicate optical remote sensing. Radar remote sensing is therefore ideal to monitor tree biomass in the dry tropics. We have successfully demonstrated that such data can be used to accurately map woody biomass change for all 5 million sq km of southern Africa. In SECO we will create a network of over 600 field plots to understand how the vegetation of the dry tropics is changing. and complement this with radar remote sensing to quantify how the carbon cycle of the dry tropics has changed over the last 15 years. This will provide the first estimates of key carbon fluxes across all of the dry tropics, including the amount of carbon being released by forest degradation and deforestation and how much carbon is being taken up by the intact vegetation in the region. By understanding where these processes are happening, we will improve our knowledge of the processes involved. W will use these new data to improve the way we model the carbon cycle of the dry tropics, and test key theories. The improved understanding, formalised into a model, will be used to examine how the dry tropics will respond to climate change, land use change and the effects of increasing atmospheric CO2. We will then be able to understand whether the vegetation of the dry tropics will mitigate or exacerbate climate change, and we will learn what we need to do to maintain the structure of the dry tropics and preserve its biodiversity. Overall, SECO will allow us to understand how the vegetation of the dry tropics is changing, and the implications of this for the global carbon cycle, the ecology of savannas and dry forests, and efforts to reduce climate change. The data we create, and the analyses we conduct will be useful to other researchers developing methods to monitor vegetation from satellites, and also to those who model the response of different ecosystems to climate and other changes. Forest managers, ecologists and development practitioners can use the data to understand which parts of the world's savannas and dry forests are changing most, and how these changes might be managed to avoid negative impacts that threaten biodiversity and the livelihoods of the 1 billion, mostly poor, rural people who live in this region.

High blood pressure causes an increase in the size of the heart (cardiac hypertrophy) and is a major risk factor for the development of heart failure. One in five people die from this condition. Angiotensin II is a hormone that stimulates cardiac hypertrophy and it functions by binding to the Angiotensin II type I (ATI) receptor. A complex programme of intracellular signalling is initiated to stimulate hypertrophy and a new protein called ATRAP has been recently identified that protects against the effects of Angiotensin II. ATRAP was discovered because it binds to the ATI receptor but how ATRAP suppresses cardiac hypertrophy is not known. We have made an unexpected connection between ATRAP and a lipid binding protein, RdgB-beta. We propose to define the connection between the two proteins, ATRAP and RdgB-beta in the context of lipid signalling via enzymes called phospholipases that produce the 'signalling lipid', phosphatidic acid (PA). We will establish how this protein-lipid network operates during Angiotensin II signalling. The activity of phospholipases is stimulated when Angiotensin II binds to the receptor. RdgB-beta is uncharacterised and we have discovered that it has unusual lipid binding properties - it binds PA. Our concept is that RdgB-beta sequesters the 'PA' signal and therefore restrains the signalling cascade resulting in inhibition of cardiac hypertrophy. We will examine how RdgB-beta binds 'PA' and disposes of it. Because ATRAP binds RdgB-beta we think that a 'bridge' between two membranes is formed. This allows the 'PA' to be removed from the plasma membrane where signalling occurs and sent to the compartment where lipids are re-used for making new lipids. To form the bridge, RdgB-beta has to interact with ATRAP on one membrane and other proteins on the opposite membrane. We will therefore identify these proteins by using RdgB-beta as bait to fish for new proteins. We will also study the importance of RdgB-beta and ATRAP by increasing or decreasing the protein levels in the cells. This will inform us on how Angiotensin II signalling is affected. If RdgB-beta reinforces the restraint put by ATRAP on Angiotensin II signalling, this will provide strong evidence that the molecular mechanism used by ATRAP is to participate in the removal of the signalling lipid, PA. To further test the model, we will delete the gene for RdgB-beta in a model organism (Drosophila) and examine the phenotype in collaboration with our project partner in Bangalore, India. To determine the importance of PA binding to RdgB-beta, we will make mutant proteins that cannot bind PA. These mutants will be examined for rescue of the fly defect. The interaction between RdgB-beta and ATRAP together with the binding of PA to RdgB-beta could provide the molecular explanation of how ATRAP is able to suppress the function of Angiotensin II signalling and could therefore offer a novel therapeutic target for intervention in cardiovascular diseases. In the clinic, inhibition of Angiotensin II signalling by ACE inhibitors that prevents the production of Angiotensin II or drugs that prevent binding of Angiotensin II to its receptor are used for treatment for hypertension. Since most drugs have side-effects, drug combination that targets different systems are often used. Therefore the proposed research could well lead to a different molecular target which could provide a more effective treatment. Understanding how the endogenous inhibitor of Angiotensin II signalling, ATRAP, functions, may provide new strategies for drug targeting. Because ATRAP interacts with RdgB-beta, the possibility that targeting RdgB-beta may provide a unique opportunity to generate a new class of drugs that could be based on binding small hydrophobic molecules in the lipid binding pocket of RdgB-beta. The benefit derived from such drugs is huge as high blood pressure is one of the most common diseases that afflict humans.

Abstracts are not currently available in GtR for all funded research. This is normally because the abstract was not required at the time of proposal submission, but may be because it included sensitive information such as personal details.