About

Professor Anna La Torre is a faculty member in the Department of Cell Biology and Human Anatomy at the School of Medicine, University of California, Davis. She grew up in Campdevànol, a small town in the Catalan Pyrenees north of Barcelona, and is the daughter of a long line of bakers. Anna earned her PhD in Neuroscience from the University of Barcelona, where she studied central nervous system development and tyrosine kinase signaling pathways under the mentorship of Dr. Eduardo Soriano and Dr. Jesús Ureña. Her doctoral training emphasized critical thinking and the joy of scientific discovery. She then moved to Seattle for postdoctoral work with Dr. Tom Reh, focusing on eye development and applying stem cell technologies to study neurogenesis and cell fate specification. This experience reinforced her commitment to following data with curiosity and optimism. Since joining UC Davis in 2014, Professor La Torre has led a research program dedicated to understanding retinal development and degeneration. Her work integrates developmental biology and neurobiology to uncover mechanisms underlying retinal formation and the processes that lead to retinal diseases. A significant and rewarding aspect of her career is mentoring trainees, fostering their development of independent ideas and scientific growth. Outside of her professional work, she enjoys traveling, spending time in the mountains, and photography, often capturing moments with her son Marc.

Research topics

• Neuroscience
• Biology
• Genetics
• Cell biology
• Medicine
• Pathology
• Psychology
• Surgery

Selected publications

• Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy

  Figshare · 2026-02-06

  otherOpen accessSenior author

  Abstract Mitochondrial dysfunction is a central hallmark of many optic neuropathies, yet the mechanisms linking intrinsic metabolic stress to retinal ganglion cell (RGC) degeneration remain unclear. To bridge this gap, we developed conditional transgenic models targeting the mitochondrial complex I subunit Ndufs4 in the retina. Broad deletion of Ndufs4 in the retina resulted in vision loss, progressive RGC degeneration, and pronounced immune activation before overt RGC death. Strikingly, depletion of myeloid cells significantly preserved RGCs, demonstrating that inflammation is not simply a downstream consequence but a participant in the degeneration process. To further distinguish between intrinsic and extrinsic mechanisms, we generated a mosaic model in which only subsets of retinal cells lacked Ndufs4. In this paradigm, the degeneration first appeared selectively in mutant regions, suggesting that mitochondrial impairment within RGCs is necessary to initiate vulnerability. At later stages, however, the degeneration extended beyond mutant territories, highly suggestive of a propagation through non-cell autonomous processes. Together, these findings support a model in which mitochondrial dysfunction creates the conditions for neuronal vulnerability, while immune responses govern the timing and extent of cell loss. This framework explains the consistent co-occurrence of metabolic deficits and neuroinflammation in optic neuropathies and highlights the importance of their interactions in disease progression. By clarifying the intersection of intrinsic and extrinsic mechanisms, this work advances our understanding of RGC degeneration and provides a conceptual basis for deciphering pathogenic processes across diverse optic neuropathies.

  PublisherDOI

• Additional file 1 of Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy

  Figshare · 2026-02-06

  otherOpen accessSenior author

  Supplementary Material 1. Supplementary Fig S1. Ndufs4 loss results in defects of the myelin sheath. Electron microscopy images of retrobulbar optic nerves show disrupted myelin sheaths (arrows) in both P30 and P45 Rax-Cre; Ndufs4fl/fl animals.

  PublisherDOI

• Additional file 6 of Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy

  Figshare · 2026-02-06

  otherOpen accessSenior author

  Supplementary Material 6. Supplementary Fig S6. T-cells are present in α-Cre; Ndufs4fl/fl retinas. CD3 immunostaining (magenta) on flat-mounted retinas at P45 and P120 identified T-cells in both central and peripheral regions of α-Cre; Ndufs4fl/fl (arrows). Note the unspecific labeling of erythrocytes within blood vessels in all conditions. All samples were counterstained with RBPMS to identify RGCs.

  PublisherDOI

• Additional file 5 of Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy

  Figshare · 2026-02-06

  otherOpen accessSenior author

  Supplementary Material 5. Supplementary Fig S5. Myeloid cell depletion improves survival of peripheral RGCs in α-Cre; Ndufs4fl/fl retinas. A) Retinal flat-mounts stained with RBPMS (teal) show a partial rescue of RGCs in the periphery of α-Cre; Ndufs4fl/fl mice upon myeloid cell depletion with PLX5622 when compared to AIN76A control chow. B and C) Quantification of RBPMS+ RGCs per mm2 in animals fed with regular chow, AIN76A, or AIN76A supplemented with PLX5622. The central and peripheral retina were quantified separately (two-way ANOVA, n.s. not significant, **P < 0.01, ***P < 0.001, and ****P < 0.0001).

  PublisherDOI

• Additional file 4 of Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy

  Figshare · 2026-02-06

  otherOpen accessSenior author

  Supplementary Material 4. Supplementary Fig S4. CCR2+ myeloid cells populate the retina of α-Cre; Ndufs4fl/fl mice at P45.Immunostaining of retinal flat-mounts from P45 α-Cre; Ndufs4fl/fl mice suggests the presence of infiltrating monocytes in both central and peripheral retina, indicated by co-localization of Iba1 (magenta) and CCR2 (teal) (arrows).

  PublisherDOI

• Additional file 4 of Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy

  Figshare · 2026-02-06

  otherOpen accessSenior author

  Supplementary Material 4. Supplementary Fig S4. CCR2+ myeloid cells populate the retina of α-Cre; Ndufs4fl/fl mice at P45.Immunostaining of retinal flat-mounts from P45 α-Cre; Ndufs4fl/fl mice suggests the presence of infiltrating monocytes in both central and peripheral retina, indicated by co-localization of Iba1 (magenta) and CCR2 (teal) (arrows).

  PublisherDOI

• Additional file 6 of Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy

  Figshare · 2026-02-06

  otherOpen accessSenior author

  Supplementary Material 6. Supplementary Fig S6. T-cells are present in α-Cre; Ndufs4fl/fl retinas. CD3 immunostaining (magenta) on flat-mounted retinas at P45 and P120 identified T-cells in both central and peripheral regions of α-Cre; Ndufs4fl/fl (arrows). Note the unspecific labeling of erythrocytes within blood vessels in all conditions. All samples were counterstained with RBPMS to identify RGCs.

  PublisherDOI

• Retinal development

  Handbook of clinical neurology · 2026-01-01

  book-chapterSenior author
  PublisherDOI

• Afadin sorts different retinal neuron types into accurate cellular layers

  eLife · 2026-01-05

  articleOpen access

  Neurons use cell-adhesion molecules (CAMs) to interact with other neurons and the extracellular environment: the combination of CAMs specifies migration patterns, neuronal morphologies, and synaptic connections across diverse neuron types. Yet little is known regarding the intracellular signaling cascade mediating the CAM recognitions at the cell surface across different neuron types. Using mouse genetics and viral labeling, we investigated the neural developmental role of Afadin (Mandai et al., 1997; Takai and Nakanishi, 2003; Takahashi et al., 1999), a cytosolic adapter protein that connects multiple CAM families to intracellular F-actin. We introduced the conditional Afadin mouse mutant (Beaudoin et al., 2012) to an embryonic retinal Cre, Six3 Cre (Oliver et al., 1995; Liu and Cvekl, 2017; Diacou et al., 2018). We reported that the mouse mutants lead to the scrambled retinal neuron distribution, including bipolar cells (BCs), amacrine cells (ACs), and retinal ganglion cells (RGCs), across three cellular layers of the retina. This scrambled pattern was first reported here at neuron-type resolution. Importantly, the mutants do not display deficits for BCs, ACs, or RGCs in terms of neural fate specifications or survival. Additionally, the displayed RGC types still maintain synaptic partners with putative AC types, indicating that other molecular determinants instruct synaptic choices independent of Afadin. Lastly, there is a significant decline in visual function and mis-targeting of RGC axons to incorrect zones of the superior colliculus, one of the major retinorecipient areas. Collectively, our study uncovers a unique cellular role of Afadin in sorting retinal neuron types into proper cellular layers as the structural basis for orderly visual processing.

  PublisherDOI

• Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy

  Figshare · 2026-02-06

  otherOpen accessSenior author

  Abstract Mitochondrial dysfunction is a central hallmark of many optic neuropathies, yet the mechanisms linking intrinsic metabolic stress to retinal ganglion cell (RGC) degeneration remain unclear. To bridge this gap, we developed conditional transgenic models targeting the mitochondrial complex I subunit Ndufs4 in the retina. Broad deletion of Ndufs4 in the retina resulted in vision loss, progressive RGC degeneration, and pronounced immune activation before overt RGC death. Strikingly, depletion of myeloid cells significantly preserved RGCs, demonstrating that inflammation is not simply a downstream consequence but a participant in the degeneration process. To further distinguish between intrinsic and extrinsic mechanisms, we generated a mosaic model in which only subsets of retinal cells lacked Ndufs4. In this paradigm, the degeneration first appeared selectively in mutant regions, suggesting that mitochondrial impairment within RGCs is necessary to initiate vulnerability. At later stages, however, the degeneration extended beyond mutant territories, highly suggestive of a propagation through non-cell autonomous processes. Together, these findings support a model in which mitochondrial dysfunction creates the conditions for neuronal vulnerability, while immune responses govern the timing and extent of cell loss. This framework explains the consistent co-occurrence of metabolic deficits and neuroinflammation in optic neuropathies and highlights the importance of their interactions in disease progression. By clarifying the intersection of intrinsic and extrinsic mechanisms, this work advances our understanding of RGC degeneration and provides a conceptual basis for deciphering pathogenic processes across diverse optic neuropathies.

  PublisherDOI

Recent grants

• Embryonic Stem Cell Approach to Retinal Ganglion Cell Replacement: an In Vivo Study

  NIH · $2.0M · 2016–2022

• MicroRNAs as Regulators of Neural Progenitor Competence in the Neocortex

  NIH · $416k · 2018–2020

Frequent coauthors

• Cecilia Sironi

  53 shared

• Giancarlo Celeri Bellotti

  Azienda Socio Sanitaria Territoriale Santi Paolo e Carlo

  52 shared

• Winifred C. Connerton

  Health and Human Development (2HD) Research Network

  49 shared

• Susan Armstrong-Reid

  University of Wisconsin–Madison

  49 shared

• Liesbeth Hesselink

  49 shared

• Sue Hawkins

  49 shared

• Helen Sweet

  University of Wisconsin–Madison

  49 shared

• Eduardo Soriano

  Universitat de Barcelona

  26 shared

Labs

• La Torre LabPI

Education

• Postdoc, Biological Structure

  University of Washington

  2014

• Ph.D., Cell Biology

  University of Barcelona

  2008