Development and Cell Biology Theme Day Talks and Photos
sarah de val: Transcriptional regulation of vascular patterning
Associate Professor Sarah De Val kicked off the day with a presentation on her lab's work in collaboration with Associate Professor Nicola Smart. After the heart is damaged by a heart attack it needs to form new blood vessels. However, humans don't produce enough new blood vessels to supply the remaining tissue; to regenerate the tissue we need to grow new blood vessels as well. Researchers have tried to augment natural vessel formation in damaged hearts with Vascular Endothelial Growth Factor (VEGF), but while VEGF can stimulate new vessels in healthy tissue, existing results suggest it doesn’t work in the damaged adult heart. The longstanding idea is that the way blood vessels form in the heart during development will also be the way they form after injury. If we can understand how a blood vessel in the heart forms, we can then make it form again in the damaged adult heart. In her talk, Sarah presented the various regulatory pathways that control 4 different types of blood vessels in the developing heart, and discussed how her research has investigated whether any of these pathways “switch on” when the heart is injured.
Clive Wilson: Signalling by parcel post: identifying disease-related mechanisms of signal packaging and release in Drosophila
Next up Prof Clive Wilson, Professor of Cell and Development Genetics, presented his group's work on exploring the fundamental mechanisms behind how cells communicate with one another. By studying the signals that go from cell to cell in Drosophila, Clive's team try to work out how one signal gets passed from one cell to another using genetics by blocking gene function. In his talk, Clive focused on an area where those signals are much more complicated than just one signal, and are in fact multiple signals packaged up into a particular structure that is released from one cell to another. "We can genetically affect individual components of those structures and that will go on to affect the individual structures and how they function. By doing that we can work out what the different steps are in making these signals and then how they work." (Prof Wilson).
anna schneider: Abolition of activity dependent synaptic vesicle release of layer V glutamatergic cortical projection neurons changes the distribution of GABAergic interneurons in the cerebral cortex
The third talk was presented by DPhil Student Anna Schneider from the Molnar Group. The background to her presentation is that communication within the brain occurs through synaptic connections between various neurons numbering in the billion. Proper brain function requires a balance between excitation and inhibition, which means a balance between glutamatergic pyramidal cells and GABAergic interneurons. "The objective of our research was to understand how glutamatergic pyramidal cells influence the distribution of GABAergic interneurons in the cerebral cortex and striatum for which we were using a conditional knockout mouse model to block vesicular neurotransmitter release from selected pyramidal cells." (Anna Schneider).
filipa simoes: Macrophages directly contribute collagen to scar formation during zebrafish heart regeneration
After a short break, the audience returned to hear from BHF CRE Intermediate Transition Research Fellow Dr Filipa Simões from the Riley Group. Her talk focused on her research into Macrophages, which are important cells that normally fight infections in the body. Her team is looking at them as important players after heart injury. "What our work is showing is that macrophages are incredibly plastic and can directly contribute to the scar that is formed after you have a heart attack. The reason why this is quite relevant is because after heart injury the adult human heart can't really repair itself, and it forms a permanent scar. So the more we understand how the scar is formed; which new players are involved, which new genes are involved, the better we could try to manipulate the presence of this scar, to make it a more transient scar and to perhaps help the heart to regenerate as other organisms do like the zebrafish." (Dr Simões).
matthew stower: Imaging Epithelial Tissue Dynamics in the Mouse Embryo
Next up was Dr Matthew Stower, a Postdoctoral Researcher from the Srinivas Group, a lab that works on understanding how cells in an epithelial context move. Epithelia are a type of structure which form a critical part of all different types of tissues in order to form organs in the body. Epithelial cells make a range of structures and in order to do that, the cells have to move around, reorganise themselves and form the characteristic shape and structure of that particular organ or tissue. Matthew is keen to understand how that is controlled and how those cells move in order to make all the different shapes of the tissues in the body. To do that, he and his team are using a very early stage of embryonic development where there is an epithelium called the visceral endoderm, and within it, a group of cells called the "AVE". He then presented a fascinating display of the different types of live imaging they use; confocal and light-sheet microscopy which enables the imaging of whole volumes of embryo rapidly over the course of 10 – 20 hours. "We are also working on different ways of computationally tracking the cells from our live imaging in to understand the movement of the cells in the tissue. This imaging will give us an insight as to the cell behaviours that take place, and in the future we'd like to know what genes are controlling those cell behaviours. This will potentially serve as a model to understand these kind of movements in larger, less accessible organs." (Dr Stower).
SARAH DE VAL: ATHENA SWAN IN DPAG
Just before lunch, the audience once again heard from Sarah De Val in her capacity as the Athena SWAN Academic Lead. In this talk, she reminded the Department's Researchers of the Athena SWAN initiatives in place and how these can help and support them. She also encouraged everyone to get involved with the newly established departmental working groups designed to enrich staff and student experiences at DPAG.
After lunch, everyone gathered for a poster session, where 9 Postdoctoral researchers and Students informally presented posters of their work. The posters were presented by Osama Al-Dalahmah (Szele Group), Rita Alonazian (Carr / Smart Group), Holly Hathrell (Srinivas Group), Zhilian Hu (Mommersteeg Group), Konstantinos Klaourakis (Riley Group), John Mason (Goberdhan Group), Svanhild Nornes (De Val Group), Aashika Sekar (Wilson Group) and Jacinta Kalisch-Smith (Sparrow Group).
anjali kusumbe: age-related angiocrine signals in homeostasis and disease
After the poster session, the audience reconvened to hear from an Oxford University speaker external to the theme, Professor Anjali Kusumbe from the Kennedy Institute of Rheumatology. Before becoming a group leader, Anjali's postdoctoral research on endothelial cell heterogeneity in bone led to identification of a specialised blood vessel subtype in bone and represents a very fundamental advancement in the understanding of bone vasculature and the links between blood vessel growth, bone formation and bone ageing. She has received multiple awards including the Werner-Risau Memorial Award for her work. The goal of her group in Oxford is to elucidate the niche functions of blood vessels in normal and tumour tissues. Her group utilizes high-resolution three-dimensional imaging, advanced intravital imaging, RNA-sequencing and cell-specific inducible genetic approaches in Mus musculus to identify novel interactions between blood vessels and tissue cells.
mathilda mommersteeg: Pleiotropic roles during zebrafish heart regeneration
Next up was Prof Mathilda Mommersteeg, Associate Professor of Developmental and Regenerative Medicine. Her talk both referenced key research she published in Cell Reports last year, and outlined their ongoing research into the issue of the adult human heart being unable to regenerate itself. Heart muscle that dies is replaced by scar tissue and that tissue is never replaced by heart muscle,"so the heart can't pump as well anymore and even if it will survive a heart attack, it causes heart failure to happen, and long-term the heart can't improve anymore. We know the zebrafish is the most wellknown model that can regenerate its heart; it can injure its heart and it can regenerate itself." (Prof Mommersteeg). Her team has now identified a model that may be better at regenerating than even the zebrafish.
deborah goberdhan: Stress-induced exosome signalling: a new mechanism in cancer progression
After a short break, researchers heard from Prof Deborah Goberdhan, Associate Professor of Cell Signalling. Her talk overviewed her group's work on characterising a new mechanism in cancer biology involving secreted vesicles known as exosomes, which signal between cells. In collaboration with the Harris group (WIMM) and the Wilson group (DPAG); her team has identified a new conserved site of exosome formation inside the cell. "Stressing cancer cells by reducing levels of key nutrients or the activity of the nutrient sensing signaling complex, mTORC1, leads to a switch in exosome production from this new site. The ‘switched’ exosomes have different protein content to the classically produced exosomes and can drive cancer cell turnover, potentially promoting tumour cell adaptation." (Prof Goberdhan). They are currently trying to work out how to selectively block their production in the long-term, alongside working on non-invasive ways to improve the early diagnosis of cancer in the shorter-term. This work is in collaboration with Dr Elizabeth Bird-Lieberman and Prof Jason Davis (Chemistry).
emma rawlins: Stem cell strategies for lung growth, maintenance and repair
The final talk of the day was given by external speaker Professor Emma Rawlins from the Gurdon Institute, University of Cambridge. Her laboratory works on lung developmental and stem cell biology and regeneration. Specific questions addressed include: How are our lungs built and maintained? How does this go wrong in disease? Can we use our insights from developmental biology to induce effective lung regeneration? Or to promote improved maturation of premature lungs? The laboratory uses a combination of human embryonic lung organoids and mouse genetics as model systems. They perform multiple techniques including, in vitro and mouse genetics, lineage-tracing, microscopy, live-imaging, cellular and molecular techniques.