About the Project
A project is available in the lab to better understand how the golgins and related proteins function in membrane trafficking within the secretory pathway. The project will employ a combination of methods to reveal how these proteins function in healthy cells, but also how their function is altered in disease. Amongst these methods is CRISPR-mediated genome editing, to generate modified versions of the proteins at endogenous levels, and proteomics, which allows the identification of associated protein complexes and post-translational modifications in an unbiased and systematic manner. These approaches will be combined with cell biology experiments to determine the functional roles of the golgins and related proteins in specific protein trafficking events within cells.
Training will be provided in mammalian cell culture, molecular cloning, genome editing using CRISPR, various microscopy techniques including fluorescence microscopy, and proteomics.
For further details about our work please see https://www.research.manchester.ac.uk/portal/martin.p.lowe.html, or feel free to contact Prof Martin Lowe for further details on the various available topics at [email protected]
This project has a Band 3 fee. Details of our different fee bands can be found on our website (View Website). For information on how to apply for this project, please visit the Faculty of Biology, Medicine and Health Doctoral Academy website (View Website).
Hennies et al (2008). Gerodermia osteodysplastica is caused by mutations in SCYL1BP1, a Rab-6 interacting golgin. Nat. Gen. 40, 1410-1412.
Liu et al (2017). Loss of the golgin GM130 causes Golgi disruption, Purkinje neuron loss, and ataxia in mice. Proc. Natl. Acad. Sci. 114, 346-351
Witkos and Lowe (2016). The golgin family of coiled-coil tethering proteins. Front. Cell Dev. Biol. 3: 86.
Witkos and Lowe (2017). Recognition and tethering of transport vesicles at the Golgi apparatus. Curr. Op. Cell Biol. 47, 16-23.
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