All Seminars are held in the Gavin De Beer Lecture Theatre, Anatomy Building, Thursday 1-2pm
Tom Wyatt (Charras lab) "Oriented division in stretched epithelial monolayers"
Ravi Desai (Oates lab) “Micropatterning to interrogate cell biology”
23 Oct: Prof William Wisden, Imperial College
30 Oct: Harold
Burgess , NIH
31 Oct: SPECIAL SEMINAR - Sophie Jarriault (IGBMC) – Title TBC (Host: Dr Richard Poole)
6 Nov: Aude Marzo (Salinas lab)/ Maite Ogueta (Stanewsky lab)
13 Nov: (Paluch lab)/ Robert Bentham (Szabadkai lab)
27 Nov: Irene (Stern lab)/Cristina Benito(Jessen lab)
11 Dec: Marcus Ghosh (Rihel lab)/ (Chubbs lab)
Welcome to the lab of David Becker and Jeremy Cook
The diverse interests of our lab in skin, connective tissue, muscle and nervous system repair, regeneration and development are held together by the intellectual gravity of a very small 'black hole', the non-selective transmembrane molecular channel known as a connexon, which is made from six similar (usually identical) protein subunits.
A connexon on one cell docks with a connexon on an adjacent cell to form a gap junction channel, which is permeable to charged and uncharged molecules of up to a kilodalton. A cluster of these channels forms a microscopically visible molecular sieve connecting the two cells, a gap junction, through which the cells can communicate directly, bypassing the extracellular space.
Single connexons, often called hemichannels, exist transiently during gap junction assembly and are increasingly being found to have important signalling functions in their own right. They are normally kept closed to prevent the catastrophic leakage of intracellular contents, but they can be gated to release pulses of small messenger molecules. One such is adenosine triphosphate (ATP), which can function as a purinergic transmitter in the extracellular space.
The varied ways in which
gap junctions and connexon hemichannels (connexin-based channels) control cell
survival, proliferation and motility in the different environments of wound
healing, retinal development, spinal cord injury and muscle cell regeneration
are outlined on the pages that are linked below.
Research programme pages
- Wound healing in normal and diabetic skin — David Becker, Ava Aihua Ma and Jeremy Cook in collaboration with Dr Jill Lincoln (UCL) and Prof. Colin Green (Auckland, New Zealand). Outlines the complex regulation of different members of the connexin family in the dermis and epidermis of wounded skin, and the ability of antisense oligonucleotides to promote healing in normal and diabetic animals.
- Proliferation, migration and differentiation of neuronal stem cells — David Becker, Jeremy Cook and Regina Nickel. Outlines the behaviour of neuronal precursor cells in an embryonic neuroepithelium and the evidence that connexin-based channels regulate proliferation, cycle exit and the postmitotic migration of young neurons.
- Does intercellular communication through gap junctions influence the zebrafish circadian clock? — David Becker in collaboration with David Whitmore and Lucy Young (CCMD, UCL) Investigates the contribution of gap-junctional intercellular coupling to the coordination of circadian clock signals among populations of zebrafish cells.
- Bystander responses in central nervous system injury — David Becker and Jeremy Cook in collaboration with Prof. Patrick Anderson (UCL). Outlines the role of connexin-based channels in the responses of CNS tissue to traumatic injury, and the potential for antisense oligonucleotides to Cx43 to reduce 'bystander' injury and cell death.
- Proliferation and differentiation of regenerating skeletal muscle — David Becker and Jeremy Cook in collaboration with Dr Anikó Görbe and Prof. Tibor Krenács (Szeged, Hungary). Outlines the events that lead to myofibre formation in regenerating muscle and the potential roles of connexin-based communication in the control of myoblast proliferation and fusion.
Page last modified on 03 jun 10 14:37 by Glenda Young