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Department of Biological and Medical Sciences
Faculty of Health and Life Sciences
Gipsy Lane Campus, Sinclair Annex SNA 101
I am an independent Research Fellow in Cell and Developmental Biology. I am mainly interested in synapse formation and factors that influence the correct spatial and temporal formation of synapses during the development of the nematode C. elegans. I use Confocal and Electron Microscopy to investigate synaptic patterns and the ultrastrutcure of synaptic terminals in mutants of synaptogenesis.
Male genital structures are among the most rapidly evolving morphological traits and are often the only features that can distinguish closely related species. This process is thought to be driven by sexual selection and may reinforce species separation. However, while the genetic bases of many phenotypic differences have been identified, we still lack knowledge about the genes underlying evolutionary differences in male genital organs and organ size more generally. The claspers (surstyli) are periphallic structures that play an important role in copulation in insects. Here, we show that divergence in clasper size and bristle number between Drosophila mauritiana and Drosophila simulans is caused by evolutionary changes in tartan (trn), which encodes a transmembrane leucine-rich repeat domain protein that mediates cell–cell interactions and affinity. There are no fixed amino acid differences in trn between D. mauritiana and D. simulans, but differences in the expression of this gene in developing genitalia suggest that cis-regulatory changes in trn underlie the evolution of clasper morphology in these species. Finally, analyses of reciprocal hemizygotes that are genetically identical, except for the species from which the functional allele of trn originates, determined that the trn allele of D. mauritiana specifies larger claspers with more bristles than the allele of D. simulans. Therefore, we have identified a gene underlying evolutionary change in the size of a male genital organ, which will help to better understand not only the rapid diversification of these structures, but also the regulation and evolution of organ size more broadly.
The endoplasmic reticulum (ER) is a highly dynamic polygonal membrane network composed of interconnected tubules and sheets (cisternae) that forms the first compartment in the secretory pathway involved in protein translocation, folding, glycosylation, quality control, lipid synthesis, calcium signalling, and metabolon formation. Despite its central role in this plethora of biosynthetic, metabolic and physiological processes, there is little quantitative information on ER structure, morphology or dynamics. Here we describe a software package (AnalyzER) to automatically extract ER tubules and cisternae from multi-dimensional fluorescence images of plant ER. The structure, topology, protein-localisation patterns, and dynamics are automatically quantified using spatial, intensity and graph-theoretic metrics. We validate the method against manually-traced ground-truth networks, and calibrate the sub-resolution width estimates against ER profiles identified in serial block-face SEM images. We apply the approach to quantify the effects on ER morphology of drug treatments, abiotic stress and over-expression of ER tubule-shaping and cisternal-modifying proteins.
The cytoskeleton is an early attribute of cellular life and its main components are composed of conserved proteins (Fletcher and Mullins, 2010). The actin cytoskeleton has a direct impact on cell size control in animal cells (Fletcher and Mullins, 2010; Faix et al., 1996), but its mechanistic contribution to cellular growth in plants remains largely elusive. Here, we reveal a role of actin in cell size regulation in plants. The actin cytoskeleton shows proximity to vacuoles, and the phytohormone auxin not only controls the organisation of actin filaments, but also impacts on vacuolar morphogenesis in an actin-dependent manner.
Pharmacological and genetic interference with the actin-myosin system abolishes the auxin effect on vacuoles and thus disrupts its negative influence on cellular growth. SEM-based 3D nanometre resolution imaging of the vacuoles revealed that auxin controls the constriction and luminal size of the vacuole. We show that this actin-dependent mechanism controls the relative cellular occupancy of the vacuole, thus proposing an unanticipated mechanism for cytosol homeostasis during cellular growth.
My expertise is electron microscopy, including various preparation methods (chemical fixation, High Pressure Freezing and Freeze Substitution, microwave fixation), EM tomography, serial sectioning, Serial Block Face SEM, Correlative microscopy and 3D reconstructions (using Imaris, Amira, iMod or Reconstruct). I have prepared and imaged a variety of organisms (Trichoplax, C. elegans, Drosophila, Zebrafish, plants) during my scientific career.
I have also experience in Confocal microscopy and standard molecular biology techniques as Western Blot, PCR, Cloning, in-situ-hybridisation, Yeast-2-Hybrid etc.
Royal Microscopy Society
European Microscopy Society
I studied Biology in the University of Goettingen, Germany where I obtained my Diploma . My Diploma thesis investigated the evolution of the nervous system and neurons using SNARE proteins as potential markers for neuronal anchestors in the early metazoan Trichoplax adhaerens.
For my PhD I joined Dr. Stefan Eimer at the European Neuroscience Institute in Goettingen and used the model organism C. elegans to understand how synaptic transmission is regulated through the presynaptic density which is thought to be involved in vesicle tethering and recruitment to the presynaptic fusion site.
As a post-doc I worked with Prof. Martin Goepfert at the University of Goettingen to understand how mechanical stimuli lead to the opening of mechanosensory ion channels to generate an electric signal in the sensory neurons. Using Electron Microscopy I visualized connecting structures between the ion channel containing cell membrane and the microtubules. Thise structures were lost when the ankyrin repeats of the mechanosensory ionchannel NOMPC were lost, but elongated when the Ankyrin repeats were doubled.