Doctor of Philosophy, University of Cambridge (2016)
Bachelor of Science, Istanbul Technical University (2011)
Michelle Monje-Deisseroth, Postdoctoral Faculty Sponsor
How Support of Early Career Researchers Can Reset Science in the Post-COVID19 World.
The COVID19 crisis has magnified the issues plaguing academic science, but it has also provided the scientific establishment with an unprecedented opportunity to reset. Shoring up the foundation of academic science will require a concerted effort between funding agencies, universities, and the public to rethink how we support scientists, with a special emphasis on early career researchers.
View details for DOI 10.1016/j.cell.2020.05.045
View details for PubMedID 32533917
- Bespoke myelin tailored to neuron type. Science (New York, N.Y.) 2020; 370 (6523): 1414–15
Monosynaptic tracing maps brain-wide afferent oligodendrocyte precursor cell connectivity.
Neurons form bona fide synapses with oligodendrocyte precursor cells (OPCs), but the circuit context of these neuron to OPC synapses remains incompletely understood. Using monosynaptically-restricted rabies virus tracing of OPC afferents, we identified extensive afferent synaptic inputs to OPCs residing in secondary motor cortex, corpus callosum, and primary somatosensory cortex of adult mice. These inputs primarily arise from functionally-interconnecting cortical areas and thalamic nuclei, illustrating that OPCs have strikingly comprehensive synaptic access to brain-wide projection networks. Quantification of these inputs revealed excitatory and inhibitory components that are consistent in number across brain regions and stable in barrel cortex despite whisker trimming-induced sensory deprivation.
View details for DOI 10.7554/eLife.49291
View details for PubMedID 31625910
Modeling of axonal endoplasmic reticulum network by spastic paraplegia proteins
Axons contain a smooth tubular endoplasmic reticulum (ER) network that is thought to be continuous with ER throughout the neuron; the mechanisms that form this axonal network are unknown. Mutations affecting reticulon or REEP proteins, with intramembrane hairpin domains that model ER membranes, cause an axon degenerative disease, hereditary spastic paraplegia (HSP). We show that Drosophila axons have a dynamic axonal ER network, which these proteins help to model. Loss of HSP hairpin proteins causes ER sheet expansion, partial loss of ER from distal motor axons, and occasional discontinuities in axonal ER. Ultrastructural analysis reveals an extensive ER network in axons, which shows larger and fewer tubules in larvae that lack reticulon and REEP proteins, consistent with loss of membrane curvature. Therefore HSP hairpin-containing proteins are required for shaping and continuity of axonal ER, thus suggesting roles for ER modeling in axon maintenance and function.
View details for DOI 10.7554/eLife.23882
View details for Web of Science ID 000408627900001
View details for PubMedID 28742022
View details for PubMedCentralID PMC5576921