Projects
Our central hypothesis that the need for visual information to be captured with the required resolution and sensitivity must be counterbalanced by the metabolic capacity of the visual system.
To address this, limits2vision aims (i) to generate an integrated view on how the retina and the early visual system overcome the many challenges they face, and (ii) to extract general rules that help neural systems to adapt to rapidly changing conditions. The key questions are:
- To what extent do genetics define health or pathology of the (aging) retina and, especially, how do genetics impact metabolism in the different cell types (i.e. in the outer retina)?
- What characterises healthy retinal metabolism and how do its limits shape visual function and information processing?
- What are the general principles that enable effective and dynamic information processing in the (early) visual system in view of those metabolic limitations and challenges?
To address these goals, limits2vision will combine the broad spectrum of approaches (from cell and tissue cultures to the whole organism) and techniques (from single-cell genetics to in vivo imaging and computational modelling).
The outcomes of limits2vision are expected to greatly improve our understanding of how the retina can fulfil its unique functions. Knowing the mechanisms that allow the tissue to “live on the edge” may also guide the rational design of future therapeutic interventions for retinal diseases and visual disorders.
The following projects from the French (FR) and German (DE) partners cover a range of topics that can be grouped into three main scientific sectors, namely genetics, metabolism, and information processing.
DE-9 The role of HCN1 channels in shaping of retinal signal output.
DE-9 – The role of HCN1 channels in shaping of retinal signal output.
Mathias Seeliger – Institute for Ophthalmic Research, Tübingen
Why?
This project aims to provide novel insights in HCN1 ion channel activity for the comprehensive understanding of outer retinal signalling and ultimately disclose new targets for therapy. Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels modulate the timing of electrical signals in many cell types including neurons. In the retina, type 1 HCN channels (HCN1) enable short-term adaptation (via their voltage sensing capability with delayed channel action) and increase temporal resolution (Seeliger 2011). The aim of this project is to elucidate the differential roles of Hyperpolarization-activated Cyclic Nucleotide-gated-1 (HCN1) channels in retinal signalling of photoreceptors in health and disease.
How?
We will establish an informative set of functional in vivo data in respective mouse lines using Electroretinography (ERG) supported by a histological workup in normal and mutant retina.
What can you expect?
The successful candidate will gain state-of-the-art expertise in neuroscience, ophthalmic genetics, tests of retinal function (ERG) and structure (imaging), and insight into retinal degenerative disorders. Within the consortium, the project offers extensive international collaboration opportunities through secondments to the labs of the French partners. Further, the candidate will benefit from the interdisciplinary training activities of the iRTG program and develop skills in neurodegenerative diseases and mechanisms, positioning them for a career in neuroscience both in academia and industry.
Where?
The project will be performed in the Division of Neurodegeneration (Seeliger lab) at the Institute for Ophthalmic Research, Department of Ophthalmology in Tübingen. Additional collaborations include partnerships with French researchers (FR-1/8/11/12) and groups in Tübingen (DE-4/5/6).
Who are we?
For more information about our team, see Division of Neurodegeneration or Web of Science.
FR-1 Deciphering the role of DUSP4 in the retina and its putative implication in the development of myopia.
FR-1 – Deciphering the role of DUSP4 in the retina and its putative implication in the development of myopia
Christina Zeitz – Institut de la Vision; Sorbonne Université, Paris
Not starting in January 2026.
FR-2 Metabolic dysregulation in disease models for novel IRD gene defects.
FR-2 – Metabolic dysregulation in disease models for novel IRD gene defects.
Isabelle Audo – Institut de la Vision; Sorbonne Université, Paris
Not starting in January 2026
DE-1 Krebs cycle aconitase deficiency in inherited retinal ganglion cell dysfunction: Functional validation of ACO2 variants in patients with optic atrophy and their metabolic impact.
DE-1 – Krebs cycle aconitase deficiency in inherited retinal ganglion cell dysfunction: Functional validation of ACO2 variants in patients with optic atrophy and their metabolic impact
Bernd Wissinger – Institute for Ophthalmic Research, Tübingen
Susanne Kohl – Institute for Ophthalmic Research, Tübingen
Why?
Mutations in the ACO2 gene, encoding aconitase-2, a key enzyme of the mitochondrial tricarboxylic acid cycle (Krebs cycle), cause a spectrum of rare inherited neurometabolic diseases including syndromic but also isolated optic atrophy, a progressive blinding disease due to the degeneration of retinal ganglion cells and their axons which form the optic nerve. Interpreting ACO2 gene variants detected in patient by genetic testing as either pathogenic mutations or benign polymorphisms is particularly challenging for missense variants (which lead to single amino acid substitutions) and for intronic variants that may affect transcript splicing. These issues hamper reliable genetic diagnostics and proper counselling of patients and families. The project aims to assess the pathogenic impact of such putative disease-associated variants in ACO2 by i. applying functional in vitro bioassays, ii. investigating disease-related metabolic dysfunction by means of mitochondrial function assays and iii. exploring the presence of ACO2-deficiency specific metabolic biomarkers or biomarker profiles in biofluids.
How?
First, a comprehensive ACO2 variant dataset from in-house and public genetic databases will be compiled, and the evidence for the pathogenicity of each putative disease-associated variants scored from available functional or genetic data or from the application of a bioinformatic prediction toolset. For the analysis of potential splicing variants, ACO2 transcript analysis will be done on patient blood samples (where available) or applying minigene assays based on the expression of mutant versus wildtype ACO2 constructs in HEK293 cells. For the evaluation of missense variants, a high-throughput complementation assay in aco2-deficient yeast will be established and applied. In addition, mtDNA content (compared to nuclear DNA) will be determined in patient blood samples by dPCR and metabolomic profiles explored in patient biofluids as potential disease-associated biomarkers.
What can you expect?
The successful candidate will gain expertise in neuroscience, molecular genetics and biology, as well as metabolomic techniques. The project offers insight in international collaborations through a secondment to the French partner labs. Additionally, the candidate will benefit from the interdisciplinary training activities of the iRTG program and develop skills in research in neurodegenerative diseases and genetics, positioning them for a career in neuroscience and genetics.
Where?
The project is based in the Wissinger lab (Institute for Ophthalmic Research), and a secondment is anticipated in the Zeitz/Audo lab in Paris.
Who are we?
For more information about our team, see Wissinger lab.
DE-2 Impact of Complement Factor H risk variant Y402H on metabolic damage asso-ciated to age-related macular degeneration (AMD).
DE-2 – Impact of Complement Factor H risk variant Y402H on metabolic damage associated to age-related macular degeneration (AMD)
Angela Armento – Institute for Ophthalmic Research, Tübingen
Marius Ueffing – Institute for Ophthalmic Research, Tübingen
Why?
Age-related macular degeneration (AMD) is a progressive degenerative disease of the macula, which leads to blindness in the elderly population and for which therapeutic options are limited. The retinal pigment epithelium (RPE) cells and the adjacent neuroretina, mainly photoreceptors, coexist in a well-regulated metabolic balance with each other. During disease progression, this balance is altered by several risk factors contributing to AMD, such as ageing, genetic risks, unhealthy life-style habits, such as smoking or poor diet. Our group and others have shown that the AMD-associated genetic variants alter the metabolism of RPE cells, causing mitochondria damage, autophagy dysfunction, and oxidative stress. In this project, we aim to identify genetic risk-dependent metabolic changes and the different metabolic response of the RPE cells and photoreceptors. These findings may help to identify novel therapeutic targets to treat AMD.
How?
We will investigate the impact of AMD-genetic risk and life-style factors on the metabolism of RPE cells differentiated from induced pluripotent stem cells (iPSCs). Moreover, we will employ organotypic retinal explants derived from porcine eyes and co-culture them with iPSC-RPE cells to study the metabolic changes in the photoreceptors. RPE and retina metabolism will be studied by a combination of multiplexed in vitro assays, immunofluorescence, CO-Detection by indEXing (CODEX), high-resolution microscopy (2-photons) and functional tests. This will create a technical platform for pharmacological testing.
What can you expect?
The successful candidate will gain expertise in neuroscience, cellular and molecular biology, biochemistry, and advanced stem cell cultures and organotypic cultures techniques. The project offers extensive international collaboration opportunities through secondments to the labs of the French partners. Additionally, the candidate will benefit from the interdisciplinary training activities of the iRTG program and develop skills in neurodegenerative diseases and mechanisms, as well as stem cell technology, positioning them for a career in neuroscience and pathobiology.
Where?
The project will be performed with Prof. Ueffing and Dr. Armento (Ueffing Lab, Institute for Ophthalmic Research) in Tübingen. Additional collaborations include partnerships with French researchers (FR-2/3/4/7) and groups in Tübingen (DE-1/3/4/5/7).
Who are we?
For more information about our team, see Ueffing Lab.
FR-3 Inflammation-metabolism crosstalk as a driver of retinal degeneration.
FR-3 – Inflammation-metabolism crosstalk as a driver of retinal degeneration
Kaitryn Ronning – Institut de la Vision; Sorbonne Université, Paris
Florian Sennlaub – Institut de la Vision; Sorbonne Université, Paris
Why?
Age-related macular degeneration (AMD) is a leading cause of vision loss, and growing evidence links it to the interplay between chronic inflammation and metabolic dysfunction in the retina. Understanding how these processes influence disease progression is essential for developing better treatments. This project will help uncover fundamental mechanisms at the intersection of inflammation, metabolism, and neurodegeneration.
How?
We will explore how modulating inflammation — genetically and pharmacologically — affects disease severity in outer retinal metabolic dysfunction relevant to AMD. The project uses a multidisciplinary approach, including in vivo retinal imaging, electron and fluorescence microscopy, transcriptomics, and biochemical assays.
The work will be carried out in a collaborative environment within the Sennlaub team at the Institut de la Vision in Paris, in partnership with the Institute for Ophthalmic Research in Tübingen, Germany, through the Limits2Vision training network.
What can you expect?
Cutting-edge research facilities in one of Europe’s top vision science institutes and a vibrant, international research community (English is widely spoken – no French required). Mentorship from leading scientists in inflammation, metabolism, and neurodegeneration, training in advanced experimental techniques and data analysis, and international networking opportunities and joint training workshops in Paris and Tübingen.
Where?
The work will be carried out in a collaborative environment within the Sennlaub team at the Institut de la Vision (IOR) in Paris, France, in partnership with the Institute for Ophthalmic Research in Tübingen, Germany, through the Limits2Vision training network. The IOR is located in the heart of the city, with state-of-the-art labs dedicated to understanding and treating vision disorders.
Who are we?
For more information about our team, see Inflammation & Immunology of Retinal Diseases – Institut de la Vision.
FR-4 The retinal pigment epithelium as a developmental regulator of the neural retina: Insights from albinism and FHONDA syndrome.
FR-4 – The retinal pigment epithelium as a developmental regulator of the neural retina: Insights from albinism and FHONDA syndrome
Alexandra Rebsam – Institut de la Vision; Sorbonne Université, Paris
Why?
Proper development of the neural retina is critically dependent on signals from the adjacent retinal pigment epithelium (RPE), a monolayer of pigmented epithelial cells essential for retinal homeostasis and function. During embryogenesis, the RPE not only contributes to the structural organization of the retina but also plays a pivotal role in modulating the proliferation and differentiation of retinal progenitor cells. Mutations in genes expressed in the RPE in congenital diseases such as albinism and FHONDA syndrome cause altered retinal development leading to visual impairment, but the precise mechanisms remain incompletely understood. Albinism is characterized by hypopigmentation and visual defects such as misrouting of optic nerve fibres, causing an abnormal stereovision and foveal hypoplasia, causing a reduced visual acuity. Interestingly, FHONDA syndrome (Foveal Hypoplasia, Optic Nerve Decussation defects, and Anterior segment Dysgenesis) involves analogous abnormalities of the retina and optic pathways, but without pigmentation deficits. We have identified candidate pathways playing a key role in albinism and FHONDA syndrome. The PhD project aims at studying signalling pathways in the RPE that control retinogenesis in normal and pathological development.
How?
This PhD project will use a combination of biological systems (in vitro: RPE cells and retinal organoids differentiated from human induced pluripotent stem cells (hiPSCs), in vivo: mouse models), Omics approaches (metabolomics, transcriptomics) as well as genetic modification of hiPSCs (CRISPR/Cas9). Altogether, this PhD project will decipher the cellular and molecular mechanisms underlying these two rare diseases and shed new light on the processes of visual system development.
What can you expect?
The successful candidate will gain expertise in molecular and cellular neurodevelopmental biology. They will be trained for in vitro genetic approaches in hiPSCs (CRISPR/Cas9), hiPSC culture, their differentiation in RPE and retinal organoids and biochemistry. In addition, they will benefit from the training activities scheduled by the French-German international Research Training Group (iRTG) Limits2Vision between the Institut de la Vision (IDV) in Paris, France and the Institute for Ophthalmic Research (IOR) in Tübingen, Germany (workshops, bi-annual meetings, hands-on training and more).
Where?
This project is a collaboration between the Institut de la Vision (Sorbonne University, Paris), The Saints Pères Paris Institute for the Neurosciences (SPPIN, Paris), and the Institute for Ophthalmic Research (IOR) in Tübingen, Germany. The PhD student will be hosted mainly at the IDV where they will join the Chédotal Team, under the supervision of Alexandra Rebsam. Furthermore, they will conduct a secondment for a few months at the IOR in Tübingen (Germany) first to achieve quantitative NMR metabolomics on mutant hiRPE under the supervision of Christoph Trautwein and François Paquet-Durand (DE-5). Second, they will also explore in parallel different signalling pathways such as mTOR in collaboration with Angela Armento and Marius Ueffing (DE-2).
Who are we?
For more information about our team, see Rebsam lab.
FR-12 Defining metabolic interventions to protect cone photoreceptors.
FR-12 – Defining metabolic interventions to protect cone photoreceptors
Serge Picaud – Institut de la Vision; Sorbonne Université, Paris
Why?
The loss of cone photoreceptors is the major cause of blindness in highly developed countries. Blinding diseases include hereditary retinal dystrophies and other diseases such as age-related macular degeneration or retinal detachment. In humans, cone photoreceptors are essential for colour vision and high visual acuity. Unfortunately, no treatment can prevent the loss of cone photoreceptors in any of these diseases and the mechanisms of cone degeneration are very poorly understood. However, given the very high energy demand of cones (Ingram et al., 2020), it seems likely that many cone diseases have a bearing on energy metabolism and that vice versa a strengthening of cone metabolism can produce cone neuro¬protection (Aït-Ali et al., 2015).
How?
We will evaluate neuroprotection on different in vitro and in vivo models of cone degeneration. The goal will be to define how universal the neuroprotective effect of our lead compounds is for different types of cone neurodegenerative diseases. We will therefore assess whether the selected neuroprotective molecules can prevent the loss of cone photoreceptors in a model of retinal detachment and in mouse models of primary (e.g., cpfl1) and secondary (e.g., rd1) cone degeneration. Overall, we will assess to what extent cone photoreceptor survival depends on energy metabolism and whether treatments intended to improve cone metabolism can prevent cone degeneration in a gene- and mutation-independent fashion.
What can you expect?
The PhD student will master a variety of in vitro and in vivo techniques, forwarding the pre-clinical testing and development of new therapeutic approaches for retinal diseases which are currently still untreatable. The combination of in vitro and in vivo studies will provide important data on molecule mechanism of action, efficacy, bioavailability, and pharmacokinetics. The transcriptomic and proteomic analyses will validate mechanistic pathway hypotheses and provide key data for later pre-clinical and clinical development, ideally positioning the PhD student for a later career, for instance in pharmaceutical industry or at regulatory authorities.
Where?
This project will be conducted mainly at the Institut de la Vision (Sorbonne University, Paris), under the supervision of Serge Picaud. This will include secondments 6 months or longer to the IOR in Tübingen (Germany) where the student will be supervised among others by Christoph Trautwein and François Paquet-Durand (DE-5).
Who are we?
For information on the host institution and the people involved please the website of the Picaud lab.
DE-3 Impact of damaged Bruch´s membrane on RPE metabolism: metabolic analyses of in vitro iPS-RPE models.
DE-3 – Impact of damaged Bruch´s membrane on RPE metabolism: metabolic analyses of in vitro iPS-RPE models.
Simon J. Clark – Institute for Ophthalmic Research, Tübingen
Sylvie Julien-Schraermeyer – Institute for Ophthalmic Research, Tübingen
What?
This PhD project investigates how changes in Bruch’s membrane (BrM), the extracellular matrix beneath the retinal pigment epithelium (RPE), impact RPE cell metabolism and, by extension, the health of the retina. You’ll develop and refine in vitro models using highly characterised induced pluripotent stem cell (iPSC)-derived RPE cells cultured on BrM isolated from porcine eyes. These models will be subjected to defined extracellular matrix (ECM) alterations, mimicking early changes seen in retinal diseases such as age-related macular degeneration (AMD). Using state-of-the-art imaging (electron microscopy, RAMAN, fluorescent lifetime microscopy) and transcriptomic profiling (RNAseq), you’ll map the resulting metabolic and morphological responses. The ultimate aim is to produce a comprehensive “REMIX-MAP” (Retinal Epithelium and Matrix Interaction Morphological and Metabolic Activity Profile) to identify early indicators of retinal dysfunction.
Why?
BrM plays a vital role in maintaining RPE health, and its early deterioration is a hallmark of AMD. While previous research has shown that ECM stiffness and composition can drastically alter cellular metabolism in other systems, this project addresses a major knowledge gap in how such changes affect RPE cells specifically. This is crucial because the RPE’s metabolic state directly influences its ability to support photoreceptors and maintain visual function. By exploring these interactions, you’ll help lay the foundation for future diagnostic and therapeutic approaches for retinal diseases. The project builds on robust preliminary data and leverages collaborations with leading researchers in the Limits2Vision network.
What to expect
As a PhD student, you’ll gain hands-on experience with advanced cell culture systems, multi-modal imaging, and next-generation sequencing. You’ll also work collaboratively with other Limits2Vision teams, including opportunities for secondments to develop skills in iPSC generation and metabolic intervention. Your work will contribute directly to a shared metabolomic dataset, helping to define therapeutic targets and shape experimental strategies across the network. Expect a highly interdisciplinary environment, extensive technical training, and the chance to make a tangible impact in the field of retinal disease research.
Where?
This project is based in the Institute for Ophthalmic Research at the University of Tübingen between the Molecular mechanisms driving AMD group, and the Experimental Vitreoretinal Surgery group. Additional collaborations include partnerships with French researchers (FR-2,3,4) and groups in Tübingen (DE-2,4,5)
Who are we?
For more information about our team, please visit our website.
DE-4 Single-cell multiplexed and targeted metabolic imaging of the retina to decipher energy flow and dependencies in cellular niches.
DE-4 – Single-cell multiplexed and targeted metabolic imaging of the retina to decipher energy flow and dependencies in cellular niches.
Christina Schwarz – Institute for Ophthalmic Research, Tübingen
Christian Schürch – Institute of Pathology, Tübingen
Why?
The retina is one of the most metabolically active tissues in the body, and its ability to sustain vision depends on precisely coordinated energy flow between diverse cell types. Disruption of these metabolic interactions underlies vision-threatening diseases such as retinal detachment and diabetic retinopathy. Recent discoveries reveal that retinal cells have distinct metabolic pathways that can adapt—or fail—under stress. By mapping these pathways at single-cell resolution, we can uncover how cells support each other’s metabolism and how these relationships break down in disease. This knowledge has the potential to identify novel, targeted interventions for preserving or restoring vision.
How?
You will work at the intersection of functional imaging and high-dimensional spatial biology. Using two-photon autofluorescence microscopy, you will capture the dynamic metabolic activity of retinal cells in real time by tracking NADH/FAD redox states under normal and challenged conditions. In parallel, you will apply CODEX high-multiplex microscopy to profile dozens of metabolic enzymes and cell-type markers simultaneously, generating a spatial atlas of retinal metabolism at subcellular resolution. These complementary approaches will be applied to healthy and diseased mouse retina models—including retinal detachment, acute and chronic diabetic retinopathy—using both sexes to assess possible sex-dependent effects. You will collaborate with multiple labs in the iRTG, integrate with metabolomics and intervention studies, and potentially extend the work to in vivo imaging in a second funding phase.
What can you expect?
As a PhD candidate, you will gain hands-on expertise in state-of-the-art live tissue imaging, spatial omics, and advanced image analysis. You will develop skills in experimental design for disease models, quantitative image analysis, and integration of functional and molecular datasets. The project’s interdisciplinary nature will give you access to an extensive collaborative network and opportunities for secondments, cross-training in complementary techniques, and participation in international conferences. Your work will culminate in a single-cell metabolic atlas of the retina, identification of cell-cell metabolic interactions, and discovery of potential therapeutic targets—contributing to both basic science and translational ophthalmology.
Where?
The project represents a collaboration between the Schwarz lab (Institute for Ophthalmic Research) and the Schürch lab (Institute of Pathology) in Tübingen. Additional collaborations include partnerships with French researchers (FR-1/3/4/6/7) and groups in Tübingen (DE-5/6/7).
Who are we?
For more information about our teams, see Schwarz lab and Schürch lab.
DE-5 The metabolism of rod and cone photoreceptors in health and disease.
DE-5 – The metabolism of rod and cone photoreceptors in health and disease.
François Paquet-Durand – Institute for Ophthalmic Research, Tübingen
Christoph Trautwein – M3 Center / Werner Siemens Imaging Center, Tübingen
Why?
The photoreceptors of the retina are characterized by what is likely the highest energy demand of any cell type in the human body. What fuels photoreceptors use, how these are supplied, and how they are metabolized, are largely still open questions. However, preliminary data suggests that photoreceptor energy metabolism may deviate significantly from what textbooks suggest (Chen et al., 2023, 2024). Moreover, we have reason to believe that the metabolism of rod and cone photoreceptors differs significantly between these two cell types, potentially explaining the selective vulnerability of these cells in certain neurodegenerative diseases.
How?
We will investigate the impact of targeted pharmacological and genetic manipulations on photoreceptor energy metabolism, under entirely controlled conditions, using organotypic retinal explants derived from wild-type and retinal degeneration mutant mice. A single-cell resolution expression atlas for retinal enzymes and metabolites related to energy metabolism will be established, using immunofluorescence, CO-Detection by indEXing (CODEX), high-resolution microscopy and ion mobility mass spectrometry MALDI-2 imaging with 5-µm resolution (microGRID). This will be supported by RNA sequencing and metabolomics/lipidomics, as well as NMR spectroscopy approaches, in situ biochemistry, and µERG functional testing to comprehensively assess the consequences of metabolic interventions in individual retinal cells (Trautwein et al., 2022; Singh et al., 2023).
What can you expect?
The successful candidate will gain expertise in neuroscience, biochemistry, and metabolomic techniques including organotypic neuronal tissue culture and state-of-the-art analytical chemistry techniques, such as NMR and Mass Spectrometry Imaging (MALDI). The project offers extensive international collaboration opportunities through secondments to the labs of the French partners. Additionally, the candidate will benefit from the interdisciplinary training activities of the iRTG program and develop skills in neurodegenerative diseases and mechanisms, as well as imaging technology, positioning them for a career in neuroscience and advanced bioanalytical chemistry.
Where?
The project represents a collaboration between the Paquet-Durand lab (Institute for Ophthalmic Research) and the Trautwein lab (Core Facility Metabolomics/M3 Center & Werner Siemens Imaging Center) in Tübingen. Additional collaborations include partnerships with French researchers (FR-4/6/7/12) and groups in Tübingen (DE-1/4/6).
Who are we?
For more information about our teams, see Paquet-Durand lab and Trautwein lab.
FR-6 Glial activation and metabolic changes induced by vascular leakages in diabetic retinopathy (DR).
FR-6 – Glial activation and metabolic changes induced by vascular leakages in diabetic retinopathy (DR)
Tual Monfort – Institut de la Vision; Sorbonne Université, Paris
Xavier Guillonneau – Institut de la Vision; Sorbonne Université, Paris
Why?
Diabetic retinopathy (DR) is a leading cause of vision loss worldwide, particularly among working-age adults. Despite advances in diagnosis and treatment, understanding the underlying mechanisms remains challenging. We recently showed that lipid droplets (LDs) accumulate in regions with vascular leakage and aneurysms, which are pathological hallmarks of DR and are associated with the activation of retinal glial and immune cells. These dynamic organelles play essential roles beyond energy storage—alleviating lipotoxic stress, endoplasmic reticulum stress, and oxidative stress. While lipid-lowering drugs can reduce DR progression, our knowledge of cell-specific lipid dynamics in the retina is limited by current imaging techniques, which are invasive and fail to capture the three-dimensional interactions in physiological conditions. This knowledge gap hinders the development of targeted therapies for this increasingly prevalent condition.
How?
We will pioneer an innovative approach by integrating two cutting-edge imaging techniques—Dynamic Full-Field Optical Coherence Tomography (D-FFOCT) and Coherent Anti-Stokes Raman Scattering (CARS)—into a novel microscope called No-D-EYE. This unique system will enable simultaneous, label-free, non-invasive 3D visualization of retinal cells and specific tracking of lipid droplets in living tissue over extended periods. Using mouse retinal explants treated or not with lipids or retinal explants from mouse models of vascular leakage, we will monitor lipid dynamics and cellular responses longitudinally. Advanced AI-based algorithms will automatically extract cell positions, types, and lipid droplet characteristics to provide a comprehensive physiological readout of lipid-induced modification of the glial and neuronal compartment of the retina. We will test promising compounds, including PPAR modulators and anti-inflammatory agents, to identify potential therapeutic interventions that normalize lipid handling and restore metabolism in diabetic retinopathy. Additionally, we will leverage the advanced facilities in Tübingen, including mass spectrometry and Raman spectroscopy, to precisely identify and characterize lipid types within the retinal tissue, complementing the spatial and temporal information provided by our No-D-EYE system.
What can you expect?
The successful candidate will gain expertise in cutting-edge optical imaging technologies, including nonlinear microscopy techniques (CARS) and interferometric imaging (D-FFOCT). They will develop advanced skills in AI-based image analysis, cell-type recognition, and quantitative assessment of dynamic biological processes. The project offers hands-on experience with retinal explant preparation and culture, disease modeling, and drug testing in complex 3D tissues. Additionally, the candidate will benefit from working at the intersection of physics, engineering, biology, and clinical medicine, positioning them for a career in advanced bioimaging, ophthalmology research, or pharmaceutical development.
Where?
The project will be carried out at the Vision Institute in Paris, a world-leading center for eye research. It represents a collaboration between Tual Monfort’s team, specializing in advanced imaging technologies, and Xavier Guillonneau’s team, with extensive expertise in diabetic retinopathy and retinal biology. Through collaborations with our German partners in Tübingen, we will access state-of-the-art es for detailed lipid characterization and metabolomic analysis.
Who are we?
Tual Monfort is an INSERM Researcher at the Vision Institute with extensive expertise in label-free imaging techniques, particularly D-FFOCT and CARS.
Xavier Guillonneau is an INSERM Researcher at the Vision Institute with 24 years of experience in diabetic retinopathy research. He has developed mouse models of inflammation and lipid metabolism in diabetic retinopathy and provides crucial biological expertise to the project.
FR-7 Impact of deregulated RPE metabolism on RPE and photoreceptor function and global retinal homeostasis.
FR-7 – Impact of deregulated RPE metabolism on RPE and photoreceptor function and global retinal homeostasis.
Emeline Nandrot – Institut de la Vision; Sorbonne Université, Paris
Not starting in January 2026
DE-6 From photoreceptor to brain: Spatiotemporal activity and metabolic mapping of the visual system in mouse models of retinal degeneration.
DE-6 – From photoreceptor to brain: Spatiotemporal activity and metabolic mapping of the visual system in mouse models of retinal degeneration.
Kristina Herfert – Werner Siemens Imaging Center, Tübingen
Wadood Haq – Institute for Ophthalmic Research, Tübingen
Why?
Blinding diseases are typically detected only after noticeable visual impairment has developed, limiting treatment options. Current diagnostic methods like electroretinogram (ERG) provide limited insights into early degenerative changes within specific retinal cells. We aim to identify early biomarkers of retinal degeneration by systematically mapping visual responses from photoreceptors to cortical brain areas. Understanding how early-stage retinal degeneration affects downstream signalling and metabolism could reveal new targets for treatment and vision rescue strategies.
How?
We will combine cutting-edge retinal and brain imaging techniques to create a comprehensive map of visual system dysfunction in retinal degeneration mouse models (rd1, rd10, cpfl1, and wild-type controls). Using micro-ERG (µERG) with multi-electrode arrays and calcium imaging, we will measure cell-type-specific retinal responses ex vivo. In addition, we will assess whole-brain functional activity and glucose metabolism in vivo using functional MRI and PET imaging during visual stimulation. By correlating cellular retinal responses with brain-wide activity patterns, we will identify where abnormal signal deterioration emerges in the visual pathway and investigate energy-dependent mechanisms underlying cellular dysfunction.
What can you expect?
The successful candidate will master state-of-the-art techniques in both retinal physiology and neuroimaging, including µERG recordings, multi-electrode arrays, calcium imaging, simultaneous functional PET and MRI. You will gain expertise in analysing complex spatiotemporal data and correlating cellular responses with whole-brain activity patterns. The project offers extensive collaboration opportunities through four secondments to our French partner institute, exposure to multiomics analysis, and training in deep learning approaches for modelling retinal responses on cellular and whole brain level. This interdisciplinary training will position you at the forefront of vision research and biomarker discovery using highly innovative imaging technologies.
Where?
This collaborative project spans the Werner Siemens Imaging Center and Institute for Ophthalmic Research in Tübingen, with partnerships including histological investigations (DE-5), multiomics analysis (FR-7, FR-8), and deep learning modelling (DE-8, FR-10, FR-11).
Who are we?
For more information about our teams, see Herfert lab and Haq lab.
DE-7 Visual representations in young adult and aged mice.
DE-7 – Visual representations in young adult and aged mice.
Olga Garaschuk – Institute for Physiology, Tübingen
Thomas Euler – Institute for Ophthalmic Research, Tübingen
Why?
Aging significantly reduces visual performance, but it remains unclear when and where along the visual pathway initial deficits arise. In the primary visual cortex (V1), aging causes weaker neural responses, energy homeostasis changes, and inflammation. Age-related retinal changes mirror brain alterations, with synaptic density decreases and dendritic remodelling affecting visual output. Understanding these mechanisms is crucial for developing strategies to delay or reverse aging-induced visual dysfunction.
How?
We will characterize visual stimulus representations in both retina and V1 of young adult, middle-aged, and old mice using two-photon calcium imaging. Visual stimuli including gratings and natural movies will be presented to probe contrast sensitivity, orientation/direction selectivity, and feature representations. Additionally, we will test whether caloric restriction can mitigate aging-related changes by comparing old mice to age-matched calorie-restricted animals. The project combines retinal ganglion cell analysis in explants with in vivo V1 layer 2-3 cell recordings. By comparing visual representations in retina and V1, we expect to pinpoint age-related deficits in early vision and provide an unprecedented view of the aging visual system. Together with iRTG partners, we shall elucidate underlying metabolic and circuit-level mechanisms, enabling new strategies
What can you expect?
The successful candidate will gain expertise in cutting-edge neuroscience techniques including two-photon calcium imaging, retinal explant preparation, and in vivo cortical recordings. The candidate will be trained in advanced visual stimulation paradigms, computational analysis of neural responses, and behavioural testing. The project offers extensive international collaboration opportunities through secondments to French partner institutions. Additionally, the candidate will benefit from the interdisciplinary training activities of the iRTG program and develop skills in both retinal physiology and systems neuroscience, positioning them for a career in vision research or neuroscience.
Where?
The project represents a collaboration between the Euler lab (Institute for Ophthalmic Research) and Garaschuk lab (Institute for Physiology) in Tübingen. Additional collaborations include partnerships with French researchers (FR-8/10) and groups in Tübingen (DE-4/5).
Who are we?
For more information about our teams, see Garaschuk lab and Euler lab.
DE-8 How energy demands shape optimal coding in early vision.
DE-8 – How energy demands shape optimal coding in early vision.
Philipp Berens, Hertie Institute for AI in Brain Health, Tübingen
Stephanie Palmer (Mercator Fellow), University of Chicago, USA
Why?
For decades, researchers agreed that an important goal of the early visual system is image compression for efficient information transmission. However, this view overlooks how behavioural demands and energy constraints shape neural coding. Current models focus only on spiking activity in retinal ganglion cells, ignoring that photoreceptors consume the most energy. We need a comprehensive understanding of how the entire retinal circuit balances energy consumption against behavioural needs to optimize visual coding. This knowledge could reveal how diseases and aging disrupt optimal coding principles.
How?
We will develop a computational framework combining deep reinforcement learning with biophysically detailed retinal simulations. Using our differentiable simulator Jaxley, we will model entire mouse retinal circuits with realistic energy consumption estimates for each cell type. Artificial agents with these retinal models will be trained to survive in virtual environments, allowing us to study trade-offs between energy efficiency, image compression, and behavioural demands. We will integrate statistical physics principles to create new measures of coding optimality and investigate how disease and aging processes affect these optimal coding strategies.
What can you expect?
The successful candidate will gain cutting-edge expertise in computational neuroscience, deep learning, and biophysical modelling. They will master advanced techniques including deep reinforcement learning, differentiable neural simulation, statistical physics approaches, and GPU-based large-scale modelling. The project offers extensive international collaboration through multiple secondments to our French partner institute and close collaboration with experimental teams. This interdisciplinary training in computational ecology, biophysics, and vision science will position the candidate at the forefront of theoretical neuroscience and neuro-AI.
Where?
Based at the Hertie Institute for AI in Brain Health in Tübingen, with collaborations spanning experimental retina research groups and extensive partnerships with French computational and experimental teams at the IDV in Paris.
Who are we?
For more information about our teams, see Berens lab and Palmer lab.
FR-8 The function of amacrine cells and their impact on retinal computations.
FR-8 – The function of amacrine cells and their impact on retinal computations under realistic color stimulation
Matias Goldin – Institut de la Vision; Sorbonne Université, Paris
Olivier Marre – Institut de la Vision; Sorbonne Université, Paris
What?
The Phd project aim at isolating the role of specific types of amacrine cells, by measuring and modelling how they impact retinal ganglion cell responses to visual stimulation. You will perform ex vivo experiments recording retinae where specific types of amacrine cells have been made light sensitive, and you will use state of the art 2 photon holographic stimulation to stimulate these amacrine cells while recording the impact of this stimulation on ganglion cells. The purpose is to decompose the retinal circuit and identify how a key player, amacrine cells, influence retinal computations.
Why?
Retinal neurons process natural images after they have been transformed by the imperfect optics of the eye. While spatial and temporal aspects of retinal coding have been extensively studied, the role of chromatic aberrations remains poorly understood. These optical distortions shift the focus of different wavelengths and create colored edges in natural scenes, yet their impact on neural computations has rarely been explored. We propose that such chromatic signatures provide powerful cues for feature extraction. Understanding how the retina exploits these aberrations will uncover new mechanisms of early visual processing and expand our models of sensory coding.
What can you expect ?
The successful candidate will be trained in advanced visual stimulation paradigms, two-photon calcium imaging of retinal circuits, and the analysis of neuronal population responses. They will also gain expertise in optical modeling of the eye and in machine learning approaches for understanding sensory computations. This project offers the opportunity to work at the interface of optics, physiology, and computational neuroscience, in a highly interdisciplinary research environment. The candidate will acquire a unique skillset that is broadly applicable across systems neuroscience and vision research. In addition, they will benefit from the training activities scheduled by the French-German international Research Training Group (iRTG) Limits2Vision between the Institut de la Vision (IDV) in Paris, France and the Institute for Ophthalmic Research (IOR) in Tübingen, Germany (workshops, bi-annual meetings, hands-on training and more).
Where?
he project will be carried out at the Institut de la Vision (IDV) (Sorbonne University, Paris) under the supervision of Matias Goldin, within a team specializing in retinal circuits and computations. This project will include extended secondments in Tübingen (Germany). Collaborations with the photonics groups at the Institut de la Vision (IDV) will provide access to state-of-the-art imaging and stimulation technologies.
Who are we?
For more information about our team, see Goldin lab
FR-9 How does correlated variability impact retinal information transmission?
FR-9 – How does correlated variability impact retinal information transmission?
Ulisse Ferrari – Institut de la Vision; Sorbonne Université, Paris
Why
Understanding how the retina efficiently transmits visual information despite intrinsic cellular noise is a fundamental challenge in neuroscience. Neurons in the retina communicate with sparse, stochastic electrical spikes, vastly increasing energy efficiency compared to artificial networks, but introducing noise that threatens reliable information transmission. Remarkably, biological visual systems continue to outperform artificial ones in many complex tasks, suggesting evolved mechanisms that mitigate the detrimental effects of noise—possibly through correlated activity among retinal ganglion cells. This project seeks to reveal whether, and how, correlations in neuronal variability improve information encoding while conserving energy.
How
The investigation combines cutting-edge machine learning models and information-theoretic analysis of retinal activity. We leverage large datasets of retinal responses to visual stimuli acquired through electrophysiological recordings and retinal calcium imaging. Deep neural network and/or Gaussian processes models—augmented with recurrent layers—are used to capture and predict correlated spiking patterns among retinal cells. Recent information estimation techniques enable us to quantify both the encoded information and the metabolic savings achieved by noise correlations in neurons’ responses. Collaborations provide access to diverse datasets and methodological expertise, supporting rigorous and multidisciplinary research.
What Can You Expect
Expect new insights into whether correlated noise is a liability or a resource for the retina. Key outcomes will include:
- Advanced models that predict retinal cell responses to complex naturalistic stimuli.
- Clear quantification of how correlated neuronal variability impacts both stimulus encoding and energy efficiency.
- Direct, data-driven evidence supporting or refuting the hypothesis that such correlations are evolutionarily beneficial.
- Methods and algorithms ready to be applied to broader neuroscience questions concerning energy-efficient information processing in the brain.
Where
The project is based at the Institut de la Vision, Sorbonne Université, Paris, with work carried out in close collaboration with leading laboratories in France and Germany. Data collection and analysis will utilize facilities at PI Marre’s and PI Euler’s labs, encompassing both electrophysiological and imaging approaches. Targeted secondments will facilitate hands-on training in advanced data processing methods and ensure a rich, collaborative environment.
Who Are We
This research is led by Ulisse Ferrari, supported by an international team of neuroscientists, physicists, and computational researchers. Our collaborators include experts from the labs of PI Marre and PI Euler, whose contributions range from experimental design to access to unique datasets. The project is part of the iRTG program, fostering interdisciplinary and cross-institutional scientific development. We are committed to pushing the boundaries of our understanding of visual processing in both biological and artificial networks.
FR-10 Perturbative approach for studying information coding in the retina.
FR-10 – Perturbative approach for studying information coding in the retina.
Matthew Chalk – Institut de la Vision; Sorbonne Université, Paris
Why?
Each moment, the retina is flooded with visual input — yet only a tiny fraction of this information is transmitted to the brain. This selective transmission allows vision to remain highly efficient, with fewer cells and less energy than would otherwise be required. But how is this efficiency achieved? A leading hypothesis is that the visual system has evolved to transmit information about natural images efficiently, by prioritising surprising visual signals that cannot be predicted from their context. In this project, we will use modern machine learning methods to test this hypothesis in the retina. Specifically, we will investigate how, and whether, the visual system is adapted to the local statistics of natural images in order to efficiently encode visual signals.
How?
We will construct mathematical models that predict how ganglion cells — the output neurons of the retina — respond to different patterns of visual stimulation. These models will be fitted and validated on electrophysiological data. In parallel, we will build generative models of natural image statistics (diffusion models). These will be used to generate predictions about how retinal responses should depend on the local statistics of visual images, under the constraint of maximising information transmission with limited energy. We will then compare these theoretical predictions with phenomenological models trained directly on retinal data.
What can you expect?
The PhD student will acquire a broad range of skills in advanced data analysis, computational modelling, and machine learning. They will learn to:
- Construct computational models of retinal neural circuits.
- Train and apply diffusion models to capture the statistics of natural images.
- Use information theory and statistical methods to test theories of efficient coding.
The student will work and exchange ideas in a close-knit, interdisciplinary research group involving both experimentalists and theoreticians. This PhD will provide an excellent foundation for future work in computational neuroscience, biological modelling, and machine learning.
How?
This project will be conducted mainly at the Institut de la Vision (Sorbonne University, Paris), under the supervision of Matthew Chalk. This will include secondments to Tübingen (Germany) where the student will be supervised among others by Philip Berens (DE-8).
Who are we?
For information on the host institution and the people involved, please visit our website.
FR-11 Neural circuit maturation in the larval zebrafish optic tectum: From functional imaging to connectomics.
FR-11 – Neural circuit maturation in the larval zebrafish optic tectum: From functional imaging to connectomics.
Filippo Del Bene – Institut de la Vision; Sorbonne Université, Paris
Not starting in January 2026