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Partnership Highlights

MRC DTP in Interdisciplinary Biomedical Research Student Conference

We hold an annual MRC DTP in IBR student conference which was in Derbyshire in July 2017. The events have an academic focus, with students presenting their latest MSc research results and progress with PhD research, along with a number of teambuilding activities. Highlights in 2017 included rock scrambling, abseiling, hiking and a lively and competitive quiz!

We are now busy planning the June 2018 conference which will be held over three days in Shropshire.


Insights into cell cycle control


Lindsey Sheppard (previous MRC DTG student) discovered one of the evolutionary conserved binding sites for spindle checkpoint proteins on the kinetochore.

Shepperd, L.A., Meadows, J.C., Sochaj, A.M., Lancaster, T.C., Zou, J., Buttrick, G.J., Rappsilber, J., Hardwick, K.G., Millar, J.B. (2012) Phosphodependent recruitment of Bub1 and Bub3 to Spc7/KNL1 by Mph1 kinase maintains the spindle checkpoint. Current Biology 22, 891-9

Liam Messin (2nd Year) then reviewed how cell cycle specific modifications and association to other regulatory proteins may modulate the function of kinesin-8 to enable it to function as a master regulator of microtubule dynamics.

Messin, L. and Millar, J.B.A. (2014) Role and Regulation of Kinesin-8 motors during the cell cycle. Systems and Synthetic Biology, 8:205–213.

Altered CO2 sensitivity of connexin26 mutant hemichannels in vitro

Joseph van de Wiel

Connexin26 (Cx26) mutations underlie human pathologies ranging from hearing loss to keratitis ichthyosis deafness (KID) syndrome. Cx26 hemichannels are directly gated by CO2 and recently the first connection between Cx26 hemichannel CO2 sensitivity and human pathology has been suggested by the Dale lab; demonstrating that the Cx26 mutant A88V is both insensitive to CO2 and associated with disordered breathing in humans with KID syndrome.

This paper builds upon the potential role for Cx26 CO2 sensitivity in human pathologies – specifically KID syndrome. It discusses the relationship between the degree of CO2-sensitivity that is lost in various Cx26 mutant hemichannels, and the pathology presented in humans expressing these mutant connexins.

de Wolf, E., van de Wiel, J., Cook, J., & Dale, N. (2016), Physiological Reports

van de Wiel article image

Hot-wiring clathrin-mediated endocytosis in human cells

The study of endogenous endocytosis is complicated by its unpredictable nature, the aim of this work was to develop a synthetic system which would allow the initiation of endocytosis to be controlled. Laura Wood (4th Year MRC DTP student) has now achieved this through the rerouting of a clathrin-binding protein (β2 adaptin) to the plasma membrane in response to rapamycin. This is capable of rapidly producing large numbers of vesicles through the direct recruitment of clathrin, bypassing the multiple steps normally required for initiation.

Wood, L.A. Clarke, N.I., Sarkar, S. & Royle, S.J. (2016)
Hot-wiring clathrin-mediated endocytosis in human cells
bioRxiv doi: