Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Ca2+ levels in the cell play an important role in both animals and plants. Abnormalities in these Ca2+ levels are related to several cancers. Therefore, many studies focus on Ca2+ concentrations in the cell. Often, proteins that light up when binding to Ca2+ are used to observe the presence of Ca2+. This light is then detected for imaging. This technique works fine for superficial imaging, but not if you want to image processes that happen deeper into the tissue. Photoacoustic (PA) imaging gets around this problem by detecting ultrasonic waves. To create such a signal, these Ca2+ binding proteins should radiate warmth instead of emitting light. To achieve this we introduced mutations into existing Ca2+ sensors. The main aim of these mutations was to stop this sensor from emitting light and make it radiate warmth instead. Due to Covid19-measures, we miss essential data to conclude if the created mutants are better candidates than the original senor for use in PA. We propose possible mutations for further research that might dim the original sensor. The second part of the project focuses on monitoring Ca2+ levels in cells that are induced by ErbB receptors on the cell membrane. ErbB receptors can give the cell signals to increase cell survival, growth or to start processes that will lead to the cell’s death. Abnormalities in these receptors are related to many cancers. These receptors need to be activated before the signal can travel further into the cell. Activation starts after a small molecule (ligand) binds to the receptor. This changes the shape of the receptor and makes it more likely to form pairs with other receptors or with itself (dimers). One receptor of this family, ErbB3, is not very active. For this reason, it is assumed that ErbB3 always needs to pair up with another family member before it is able to send signals down the cell. Some mutations in ErbB3 are found regularly in cancer. In this work, we wanted to observe if these mutations in ErbB3 have an influence on Ca2+ levels in cells. We found that some cells containing the normal ErbB3 receptor enhance Ca2+ levels, in contrast with cells containing the mutant receptor. This indicates that ErbB3 mutants do not the receptor more active. We then monitored Ca2+ concentrations in cells containing the normal ErbB3 receptor and other ErbB family members. We found that these kinds of cells could influence signals more than cells containing only the mutant ErbB3 receptor. Because of the Covid-19 outbreak, planned experiments involving cells containing the mutant ErbB3 receptor and normal other receptors were not carried out.

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Diseases such as Alzheimer’s- or Parkinson’s disease that cause the degeneration of the nervous system are on the rise, especially as the global population grows older and older. A better understanding of how the brain works is required to expand the therapeutic options available to treat these diseases. Previous decades have seen many advances in the field of neurology, but scientists still struggle to combine their knowledge into a full understanding of how the brain works and more importantly, how it deals with degeneration and disease. To facilitate such an understanding, better models are needed which mimic how the brain functions but in a way that is easier to visualize and investigate. Animals such as mice and rats are often used as models for the brain. Unfortunately, research animals are often subjected to unpleasant experiences and killed after the research has concluded. Moreover, animals are not always similar enough to humans to allow us to model complex diseases. Therefore, scientists have aimed to replace animals with models of the brain that can be produced without their intervention. These in-lab models often rely on the use of cells that can grow indefinitely outside of the individual from which they were initially isolated. Historically, these cells have been grown on flat, two-dimensional surfaces which are easy to use and inexpensive. However, scientists have recently realised that the behaviour of cells grown in such a way is very different from how they would grow inside of our body. Dimension possibly plays a crucial role in this. Consequently, scientists are suspending cells into an environment that surrounds them from all sides, allowing them to grow and contact each other in all directions. Cells that grow in our body, live under similar circumstances. It is therefore assumed that such a model can more closely imitate the functioning of our brain in the lab. Like many other body tissues, the brain must organise itself to function. An important way how the brain organizes the behaviour of cells within is through long stretches of fibre. Cells cling onto these fibres and as the fibres change shape and align themselves in a certain direction, the cells are likely to follow. Such behaviour potentially impacts the development and outcome of several diseases in the brain and across the human body. Mimicking this interaction between fibres and cells in the lab requires a model where the shape and behaviour of the fibres can be controlled and the impact on the behaviour of the cells investigated. For this reason, researchers have developed a new method to control the behaviour of the fibres in a controlled and reproducible fashion. Human cells that can grow indefinitely were used here to develop neurons, the primary cell type of the brain which was suspended in a solution of fibres. In other methods, the neurons degrade quickly and return to their native form, preventing a proper investigation of the effects of fibre behaviour on neuronal cells over a longer time. Here, for this reason, a new method is proposed by us which is able to longer sustain the developed neurons, without using expensive factors normally used by others. This finding allows us to potentially investigate in further work how controlling fibre behaviour impacts neuronal behaviour over a longer period.

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

When we go running, or go to work, we navigate without using Google maps on our smartphones. The process that enables us to navigate relies on a cognitive map inside the brain, and is referred to as spatial navigation. This map represents the individual’s knowledge of the relationship of the environment to space. Several brain regions are known to be involved. The cognitive map of the environment requires constant updating with the incoming sensory information. However, the different brain regions involved in this process do not directly encode for sensory information. It is stated that the retrosplenial cortex (RSC), a subdivision of the cortex located caudally around the corpus callosum, could encoded for this information. Recently, more research has been devoted to the anatomical and functional characteristics of the RSC, in spatial navigation. Several researchers reported (reciprocal) connections between the RSC and other spatially involved brain regions, such as the hippocampal and parahippocampal formation, and the posterior parietal cortex. Connections between sensory areas and the RSC have also been described, and include the primary visual -, primary motor -, and primary somatosensory cortices. The RSC appears to play a role in spatial memory and learning, and in encoding and storing of spatial information. Furthermore, a recent finding at the Bonin’s lab supports a functional difference in the RSC along the rostro-caudal axis. More spatially selective cells are found in the anterior RSC, whereas more visually selective cells are found in the posterior RSC. We optimized a retrograde dual labeling approach to investigate if this functional difference is mediated by an anatomical difference between the long-range input pathways along the rostro-caudal axis. We injected Cholera toxin subunit B (CTB) tracers conjugated to Alexa Fluor (AF) fluorescent probes (CTB 488, CTB 555) into the RSC of mice, to label individual neurons in the areas that provide input. This individual retrogradely-labeled cells were quantified to map out all the brain regions that provide anterior and/or posterior input to the RSC. We hypothesized that the anterior RSC receives spatial inputs, while the posterior RSC receives visual inputs. However, our findings did not confirm this hypothesis. We found that the somatosensory and motor cortices provided most of the inputs to the anterior RSC, while the spatial areas provided mainly spatial inputs to the posterior RSC. Nevertheless, projections from spatial areas to the anterior RSC were also observed, but to a lesser extent. Visual areas also provided some projections to the posterior RSC, which is consistent with our hypothesis. However, only one mouse was used to obtain these results, which means that only preliminary conclusions can be drawn so far. More data, along with further optimization of the protocol, would result in more reliable results that would fit the hypothesis.

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

In the face of climate change, carbon storage and sequestration are becoming more and more important by the day. Natural Climate Solutions are the most promising method for realizing negative emissions, with forests and wetlands as the most performant ecosystems considering carbon storage and sequestration. Peatlands have the highest carbon stocks of all wetlands, but can become carbon sources rather than sinks when drained. After drainage, tree invasion is possible, which often results in a succession to willow or alder carrs. Though these forests sequester and store carbon as living biomass, they might reduce the carbon stock in the soil. In this research, we aimed to quantify the SOC stocks in 13 Flemish fens, using a coupled design of plots invaded and not invaded by trees. We used vegetation analysis to assess differences in plant communities. Different fen types were accounted for, we sampled quaking fens, sloping fens and alkaline fens. Our results show that tree cover reduces the soil organic carbon, as well as plant diversity. However, a study considering the total carbon stock including living tree biomass is needed to compare invaded and non-invaded situations. However, our results give an indication that open fens might be delivering more ecosystem services than fens invaded by trees.

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Age-related neurodegenerative diseases are predominating our aging society, decreasing the life quality of older patients. Indeed, adult mammals lack the ability to regenerate their central nervous system (CNS) and therefore cannot repair and recover once damage or injury has been sustained. Nowadays, modern medicine has not caught up with the progression of these age-related pathologies, and there is yet to see a cure for them. Consequently, a rise in research focusing on finding the molecular players and signalling pathways involved in successful neuroregeneration is manifesting. Importantly, despite the clear correlation between age and occurrence of neurodegenerative disease, most of the research is performed in young laboratory animals. Unfortunately, age has a significant impact on the CNS and its regenerative ability, leading to a failure in many of the promising neuroregenerative strategies in an aging CNS. This calls for the necessity of a well characterised aging model organism where new promising and efficient neuroregenerative strategies can be observed and explored. This thesis points out the African turquoise killifish as a very promising model to investigate the negative aging effects on axonal regeneration in the adult CNS. The killifish is the shortest living vertebrate that can be bred in captivity, living to approximately 6 months of age in the facility of the host lab. Despite their limited lifespan, killifish display molecular and cellular changes that are parallel to those observed in aging humans over several decades. However, unlike humans, and to our advantage, the adult killifish can repair and regenerate its damaged CNS, making it the ideal model to study axonal regeneration, whether or not in an aging environment. This study follows the regeneration process of retinal ganglion cell (RGC) axons after optic nerve crush (ONC) in the killifish. Indeed, the visual system is used as a template to study axonal regeneration in the adult CNS. As an extension of the CNS, the retina and optic nerve display similarities to the brain and spinal cord in terms of its anatomy, functionality, response to injury and immunology. Our results suggest that aging severely reduces the regeneration process as the ability of old fish to regenerate and functionally recover is impaired after ONC. In order to investigate when, where, and what goes wrong and impairs this spontaneously regenerating ability, the regeneration process was spatiotemporally evaluated, focusing on the regenerating RGC soma in the retina as well as on their axons reinnervating the optic tectum (OT) and other retinofugal brain areas. Some first results show that regeneration is already delayed in early stages of the repair process in aged fish, finally resulting in an impaired/absent repair and functional recovery with age. Interestingly, despite being able to fully reinnervate their OT and regain certain vision-related reflexes, even young fish do not seem to fully recover from an ONC. Therefore, we additionally focused on the young adult killifish in particular, who appear to have an impaired regeneration of non-image forming RGCs, that results in a reduced reinnervation of other RGC projection areas in the brain, apart from the OT.