Robert Hindges

Robert Hindges heldur öndvegiserindi á líffræðiráðstefnunni 2015. Erindi hans fjallar um, eins og hann orðar það, “hvernig við sjáum heiminn”.(How do we see the world: Mechanisms to establish specific circuits in the vertebrate retina).

Hann starfar við King’s College í Lundúnum og stundar rannsóknir á þroskun taugakerfisns við rannsóknasetur skólans í taugaþroskunarfræði (MRC Centre for Developmental Neurobiology).

Robert Hindges mun fjalla ferli taugaþroskunar í augum hryggdýra. Hann rannsakar hvernig tengingar myndast milli lithimnu og úrvinnslustöðva heilans, með því að rannsaka þroskun augna og tauga í zebrafiskum. Sameindaerfðafræði-, frumulíffræði- og lífeðlisfræðilegar aðferðir eru notaðar til að rannsaka RGG frumur í lithimnunni sem senda boð til heilans og mæla virkni gena í þessum ferlum.

Doktorsverkefni Roberts Hindges við háskólann í Zürich fjallaði um DNA fjölliðunarensím heilkjörnunga (leiðbeinendur hans voru Ulrich Hübscher og Walter Schaffner). Hann snéri sér að rannsóknum á þroskun taugakerfisins í samstarfi við Dennis O’Leary við Salk stofnunina í La Jolla, BNA og lagði megináherslu á rannsóknir á þroskun sjóntaugakerfisins. Stærsta afrek hans var að finna sameindir sem tryggja réttar tengingar milli augna og heilans. Árið 2006 fékk hann stöðu við King’s College og hefur síðan rannsakað þroskun taugamóta í sjóntaugakerfinu, í músum, hænum og nýverið zebrafiskum. Uppgötvanir hans eru tíundaðar í kennslubókum í taugalíffræði.

 

Robert Hindges gives a plenary talk at the Biology in Iceland conference, titled How do we see the world: Mechanisms to establish specific circuits in the vertebrate retina.

Robert is a Reader in Developmental Neurobiology at the MRC Centre for Developmental Neurobiology at King’s College London.

His talk will describe some of the molecular and physiological mechanisms that are crucial to ensure that information captured by the eyes is correctly preprocessed in the retina, before being transmitted to the brain proper. His study focuses on cell surface molecules, which specify the recognition and connection between neurons that are part of the same functional circuit. In the presentation, Robert Hindges will show that the lack of these molecules or the retinal cell types that express them, will lead to a loss of specific visual function. The work therefore represents a step towards our general understanding of the strategies employed by the brain to process visual information.  

Robert Hindges studied molecular biology and worked on eukaryotic DNA polymerases during his PhD at the University of Zürich, Switzerland (with Ueli Hübscher and Walter Schaffner). He then moved for his postdoctoral training to the Salk Institute in La Jolla, USA (with Dennis O’Leary), where he changed his focus to developmental neurobiology. In particular, he worked on the development of the visual system in vertebrates and identified the fundamental molecular mechanisms that guarantee the correct connectivity from the eye to the brain.  These findings are now described in general neurobiology textbooks. In 2006, he moved to King’s College London to establish his own research group. In addition to his continued work in mouse and chick, he has since then used also zebrafish as a model to investigate synaptic connectivity and functionality of visual circuits, using in vivo optical imaging.

Selected publications:

Missaire, M. & Hindges, R. (2015). The role of cell adhesion molecules in visual circuit formation: From neurite outgrowth to maps and synaptic specificity. Dev Neurobiol. 75: 569-583.

Antinucci, P., Nikolaou, N., Meyer, M.P. & Hindges, R. (2013). Teneurin-3 specifies morphological and functional connectivity of retinal ganglion cells in the vertebrate visual system. Cell Reports 5: 582-592.

Maiorano N.A. & Hindges, R. (2013) Restricted perinatal retinal degeneration induces retina reshaping and correlated structural rearrangement of the retinotopic map, Nature Commun. 4:1938 doi: 10.1038/ncomms2926 (2013).

Pinter, R. & Hindges, R. (2010). Perturbations of MicroRNA Function in Mouse Dicer Mutants Produce Retinal Defects and Lead to Aberrant Axon Pathfinding at the Optic Chiasm, PLoS ONE 5(4): e10021.

Hindges, R., McLaughlin, T., Genoud, N., Henkemeyer, M. & O’Leary, D.D.M. (2002). EphB forward signaling controls directional branch extension and arborization required for dorsal-ventral retinotopic mapping. Neuron 35: 475-487.