Project description:The laminated structure of the retina is fundamental for the organization of the synaptic circuitry that translates light input into patterns of action potentials. However, the molecular mechanisms underlying cell migration and layering of the retina are poorly understood. Here, we show that RBX2, a core component of the E3 ubiquitin ligase CRL5, is essential for retinal layering and function. RBX2 regulates the final cell position of rod bipolar cells, cone photoreceptors and Muller glia. Our data indicate that sustained RELN/DAB1 signaling, triggered by depletion of RBX2 or SOCS7 - a CRL5 substrate adaptor known to recruit DAB1 - causes rod bipolar cell misposition. Moreover, whereas SOCS7 also controls Muller glia cell lamination, it is not responsible for cone photoreceptor positioning, suggesting that RBX2, most likely through CRL5 activity, controls other signaling pathways required for proper cone localization. Furthermore, RBX2 depletion reduces the number of ribbon synapses and disrupts cone photoreceptor function. Together, these results uncover RBX2 as a crucial molecular regulator of retina morphogenesis and cone photoreceptor function.
Project description:Retinal microvascularization can provide important informations to systemic vascular phenomena. The non-invasive quantitative description of the retinal vascularization is now possible by performing OCT-angiography and their image analysis software (vascular density and retinal perfusion). Systemic microvacular changes during the establishment of oncological treatment by targeted antiangiogenic therapy are little described in the literature. The objective of this pilot study is to describe the evolution of the retinal vascular density of patients with antiangiogenic drugs. In addition, the evolution of the retinal vascular density of patients on antiangiogenic drugs will study as a function of the response to the treatment and the toxicity of these treatments.
Project description:Retinal ganglion cells (RGCs) are the projection neurons in the retina that connect the visual sensing tissue to the brain. We found that Ascl1/Brn3b/Isl1 transcription factor combination can quickly and efficiently reprogramming mouse embryonic fibroblasts (MEFs) into retinal ganglion cell-like neurons (iRGCs). Using RNA-seq, we analyzed the transcriptomes of MEFs infected with Ascl1/Brn3b/Isl1-overexpressing viruses on day 2 or day 7 of reprogramming, or the final iRGCs on day 13 of reprogramming.
Project description:retinal ganglion cells die after optic nerve injury, either crush or transection. The molecular causesunderlying this degeneration are largely unkwon the purpose of this job is to find which (if any) gene regulation triggers RGC death with the final goal of design neuroprotective protocols Keywords: time course
Project description:Targeted analysis of retinal-cysteine adduct in Opsin 5 like-1 (Opn5L1) protein
Chicken Opn5L1 E177K/Q192K mutant was expressed in HEK293T, regenerated by all-trans-retinal, solubilized by dodecyl maltoside, and purified using Rho1D4 antibody-conjugated Sephalose. Semi-quantitative targeted analyses of trypsinized Opn5L1 with or without light irradiation were carried out using reverse phase LC-ESI-MSn to detect light-dependent formation of retinal-cysteine adduct. The results were analyzed by Mass++, mMass and Igor Pro softwares.