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BWJoneslab Moving To The University of Pittsburgh

I can now officially reveal that we are moving the BWJoneslab from the University of Utah, Moran Eye Center to the University of Pittsburgh, Department of Ophthalmology, effective August 1st, 2025.

I’ve been at the University of Utah since 1989 as an undergraduate, so 36 years at this institution and 26 years at the Moran Eye Center where I started as a graduate student. I have earned my bachelors degree here, a PhD, two postdoctoral fellowships in cell cycle biology, and neuroscience, and then my roles as faculty in multiple departments, and leadership on the University of Utah Senate. I have taught undergraduates, graduate students, medical students, and postdoctoral fellows over the years.

I have worked with development to help raise millions of dollars in donations to my department and others. I worked with Greg Jones (no relation) when he was the Governors science advisor to help advocate for the University of Utah. I have appeared in television ads for research here at the University of Utah and the Moran Eye Center.

As an undergraduate, I worked with the Biology Department to create some of the world’s first online teaching tools for anatomy and embryology using Hypercard. As an undergrad and then graduate student, I ran some of the first websites and blogs on the Internet from servers here at the University of Utah with the encouragement and blessing of the University of Utah, and have worked with IT over the years to allow this information to be disseminated around the world. I have managed the world’s first online textbook, Webvision for over 25 years that has been hosted on servers in my office or lab, and paid for out of my own pocket. We have modeled Moran CORE on Webvision that is garnering millions of visits per year. We have partnered with the Scientific Computing Institute to create the tools that allowed us to construct the world’s first retinal connectomes. My lab has also created the world’s first pathoconnectomes in any system with software that we have continued to develop, and for many years, we were the only NIH funded laboratory that performed connectomics related work. We have absolutely been global pioneers in this space. This was all possible because the computational environment at the University of Utah allowed and encouraged experimentation and exploration with novel new computational tools.

I will forever be grateful to the people here who helped me along from my chairman, Randy Olson on down. I will absolutely miss folks here, and it will be bittersweet leaving, but the University of Pittsburgh Ophthalmology program is such an amazing opportunity filled with phenomenal people and goals that I could not resist the offer. Every year has brought at least one offer to move the lab to another institution, and it’s been easy to turn down many of those offers, but this move to Pitt was the most compelling yet, filled with amazing colleagues who also happen to be good human beings who are engaged in exciting science. Leadership at Pitt understands that to continue pushing science forward means a commitment to a computational IT environment that is supportive of that work and the role of computational science in it. They are supportive and eager to grow initiatives there that take advantage of those aspects of biomedicine. Housing is far more affordable around Pittsburgh than it is here in Salt Lake City, and the vibe in Pittsburgh is one of excitement, equity, and investment in the diverse people that make up the communities around Pittsburgh. This level of support and commitment to people makes moving the whole lab and all the personnel there much more attractive.

And my vote will count in Pennsylvania.

We will be anchoring histology, ultrastructure and connectomics at Pitt, as well as helping them to hire out the next phase of expansion with sensory neurosciences as a focus. I’m grateful to José-Alain Sahel, and John Ash for their commitment and efforts to bring us on, and to the entire faculty of the Ophthalmology department, the neurosciences and engineering communities at Pitt who will be our colleagues and collaborators on a variety of science projects moving forward to help understand vision and vision rescues. As part of this, Becca will be leaving the BWJoneslab team, and taking a completely independent faculty line job with her own startup package at Pitt, so we’ll still be working collaboratively at the same institution which is verrrrry cool.

On a personal note, 2025 has been chaotic and tumultuous for so many reasons. It has been the most difficult, stressful year of my life with changes desired and very much undesired. This move is a decision that Hilari and I were very much looking forward to as a new adventure for Team Jones, and I am absolutely heartbroken to be making this move without the love of my life and my best friend. She was looking forward to living in a new city, and all of the excitement of starting fresh and discovering new things, new arts, new opportunities for philanthropy and exploration. I don’t know how to even process this as it feels like I’ve lost the part of me that helps understand, plan and contextualize everything. Every move like this has its downsides, but those aspects are the ones that scare me most, and feel the most destabilizing. I miss you, my love. And I will continue to work to make you proud of me.

Injury and Repair: Retinal Remodeling for the Encyclopedia of the Eye, 2nd Edition

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We’ve got a new chapter out from Bryan Jones and Robert Marc, Injury and Repair: Retinal Remodeling for the 2nd Edition of Encyclopedia of the Eye. (PDF here)

Abstract: Retinal remodeling is a collection of molecular and cellular revisions triggered by retinitis pigmentosa (RP), Usher syndrome, age-related macular degeneration (AMD), and likely glaucoma. These revisions include neuronal rewiring and neurotransmitter receptor reprogramming; neuritogenesis and synaptogenesis (chemical and electrical); self-signaling; neuronal migration; neuronal death; glial hypertrophy; altered glial gene expression; vascular remodeling; retinal pigmented epithelium (RPE) invasion and hyperpigmentation, and in the terminal stages, extensive proteinopathies. Metabolic and circuit revisions begin as soon as photoreceptor stress is initiated, and accelerate upon complete local photoreceptor loss. Retinal remodeling impacts the timing and potential outcomes of gene therapy, survival factor treatments, stem or progenitor cell implantation, retinal transplantation, and bionic implants.

Metabolic, Excitation and Functional Mapping of Diabetic Retinopathy

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This abstract was presented today, Monday, April 30th at the 2018 Association for Research in Vision and Opthalmology (ARVO) meetings in Honolulu, Hawaii by Felix R. Vazquez-Chona, Tam T.T. Phuong, Oleg Yarishkin, Bryan W. Jones, and David Krizaj

Purpose:
Loss of vision in diabetic retinopathy is associated with extensive shifts in retinal metabolic and synaptic function yet the general principles that govern the metabolic remodeling remain unknown. To define the metabolic signature in hyperglycemic retina we took advantage of in situ metabolomics, excitation mapping and gene knockdown. Specifically, we investigated whether manipulation of the swelling-activated calcium-permeable TRPV4 (transient receptor potential isoform 4) channel contributes to the metabolic program of the degenerating neurogliovascular subunit in diabetic mice.

Methods:
Type I diabetes in wild type (WT) and TRPV4-/- mice was induced with streptozotocin (STZ). We visualized glutamate (NMDA)-gated excitation and glucose transport using the organic cation agmatine (AGB2+) and the glucose analog glucosamine (GCN). Retinas were fixed in glutaraldehyde, sectioned, and incubated with antibodies targeting GCN and AGB. Cell classification and metabolic status were interrogated using Computational Metabolic Profiling (CMP) and probes against ADP, alanine, arginine, aspartate, citrulline, GABA, glutamate, glycine, glutathione, glutamine, isoleucine, taurine, glutamine synthetase, CRALBP, GFAP, and tomato lectin.

Results:
Amacrine and ganglion cells in control retinas responded to NMDA activation with a large elevations in AGB and GCN signals. Diabetic amacrine cells maintained a robust dynamic range of AGB and GCN signals which however were markedly diminished in RGCs. Metabolomic maps of diabetic WT retinas showed that the outer retina remains metabolically quiescent whereas the ganglion cell layer displayed cells with lower glutamate and GABA signals. Diabetic TRPV4-deficient retinas displayed metabolomic, excitation, and glucose transport maps that were comparable to control retinas. ERG analysis showed modest STZ-induced changes in scotopic a- and b-waves of WT and KO eyes.

Conclusions:
Our preliminary electrophysiological and metabolomic findings suggest that STZ-induced diabetes spares the inner retina but alters amacrine-ganglion cell signaling, the neurogliovascular unit organization together with RGC metabolism. TRPV4 inactivation partially rescues the metabolic, excitation, physiologic phenotypes imposed by hyperglycemia. These results suggest that ambient sensing through polymodal TRP channels links retinal neuronal, glial and endothelial signaling to cellular metabolism and visual function.

Ultrastructural Connectomics Reveals The Entire Chemical And Electrical Synaptic Cohort Of An ON Cone Bipolar Cell In The Inner Plexiform Layer Of The Rabbit Retina

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This abstract was presented at the 2014 Society for Neuroscience meeting in Washington D.C. by J. Scott Lauritzen, Crystal L. Sigulinsky, Danny P. Emrich, Joshua M. Dudleston, Noah T. Nelson, Rebecca L. Pfeiffer, Nathan R. Sherbotie, John V. Hoang, Jefferson R. Brown, Carl B. Watt, James R. Anderson, Bryan W. Jones and Robert E. Marc.

Purpose: Despite large-scale efforts aimed at mapping the mammalian nervous system, the entire synaptic cohort of a single mammalian neuron of any class has never been mapped. To this end we reconstructed all chemical and electrical synaptic partners of a single ON cone bipolar cell (ON CBC) in the inner plexiform layer (IPL) of the rabbit retina. We then searched all members of the same cell class for repeating network motifs and explored postsynaptic cell sampling topologies from this bipolar cell (BC).

Methods: Cells in retinal connectome 1 (RC1) were annotated with Viking viewer, and explored via graph visualization of connectivity and 3D rendering (Anderson et al., 2011 J Microscopy). Small molecule signals in RC1, e.g. GABA, glycine, and L-glutamate, combined with morphological reconstruction and connectivity analysis allow robust cell classification. The default resolution of RC1 is 2.18nm/pixel, however goniometric recapture at 0.273 nm/pixel was performed as needed for synapse verification.

Results: ON CBC 593 is one of 20 BCs of this class in RC1, the axonal arbors of which tile with gap junctions between nearest neighbors at their distal axonal tips. ON CBC 593 contains 194 ribbons, 274 postsynaptic densities, 20 gap junctions, and 66 conventional synapses, for a total of 554 synaptic connections. Twenty ganglion cells sample the glutamatergic output. ON CBC 593 is presynaptic to 262 amacrine cell (AC) processes, and is postsynaptic to 228 AC processes. Of these, 33% form reciprocal connections. We approximate that ON CBC 593 forms synapses with 50 distinct ACs. ON CBC 593 is routinely pre- and postsynaptic to within-class, cross-class, feedback, and feedforward inhibition motifs, including 1 instance of OFF-ON crossover inhibition. ON CBC 593 forms 12 gap junctions with at least 2 AII ACs, 7 with 5 ON CBCs, and 1 with itself. We searched for repeating network motifs across all ON CBCs of this class in RC1. Thus far, 80% of these form in-class inhibitory motifs, and 75% form cross-class inhibitory motifs. All ACs and GCs discovered to contact multiple branches of ON CBC 593 form synapses on every branch.

Conclusions: An individual bipolar cell is inherently multi-kinetic, receiving inhibition driven by all ON CBC classes, sharing these signals via gap junctions with ON CBCs of the same class, and driving inhibition of all ON CBC classes. This constitutes a substrate for multi-channel coordination throughout the IPL, and predicts multi-kinetic BC responses. The results establish a normative framework against which members of the same and different classes may be compared, and foster interpretation of BC physiological behavior under different stimulus regimes.

Robust Segmentation based Tracking using an Adaptive Wrapper for Inducing Priors

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We have published another manuscript, Robust Segmentation based Tracking using an Adaptive Wrapper for Inducing Priors. This manuscript describes the work on adaptive tracing and proposes an algorithm that adapts a generic tracing algorithm to an application of interest. In our specific case, it is boundaries of cells in high frequency space in transmission electron microscopy images. But the approach in this paper is applicable to biological, medical, remote sensing and surveillance data as well utilizing priors specific to the application. The co-authors on the paper are: Vignesh Jagadeesh, James Anderson, Bryan W. Jones, Robert E. Marc, Steven K Fisher and B.S Manjunath.