About

Cagla Eroglu is a Duke University faculty member holding the positions of Duke Health Distinguished Professor of Cell Biology, Professor of Cell Biology, and Vice Chair of Research. She is also a Professor in Neurobiology and a Faculty Network Member of the Duke Institute for Brain Sciences. Additionally, she is an Associate of the Duke Initiative for Science & Society and an Affiliate of the Duke Regeneration Center. Her research focuses on cell and molecular biology, with involvement in programs such as Developmental & Stem Cell Biology and the University Program in Genetics and Genomics. She is based at the 333A Nanaline Duke Building in Durham, North Carolina.

Research topics

• Biology
• Neuroscience
• Genetics
• Internal medicine
• Medicine
• Cell biology
• Physiology
• Psychology
• Biochemistry

Selected publications

• Phosphatidylserine exposure by developing astrocytes initiates microglia-mediated developmental cell death

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-21

  articleOpen access

  Developmental cell death is classically attributed to apoptosis, yet in mammalian retina, large numbers of developing astrocytes die non-apoptotically during a defined developmental window. Astrocyte death is important for patterning a cellular template that guides angiogenesis, but the underlying mechanism remains unknown. Here we show that healthy developing astrocytes initiate their own elimination by recruiting microglia via regulated exposure of the membrane lipid phosphatidylserine. Experimentally increasing phosphatidylserine exposure in astrocytes, but not neurons, accelerates their removal by microglia without changing how many astrocytes ultimately survive. This acceleration causes profound vascular defects resembling pathological features of retinopathy of prematurity. Genetic disruption of MFGE8, a phosphatidylserine-binding protein, suppresses microglia-mediated astrocyte killing and prevents vascular pathology despite continued phosphatidylserine exposure. This mechanism extends beyond the retina, because phosphatidylserine also initiates astrocyte death in developing cerebral cortex. Together, these findings identify phosphatidylserine exposure as a developmental signal that times microglia-mediated astrocyte elimination, with essential consequences for neurovascular development.

  PublisherDOI

• Mitochondrial transfer from glia to neurons protects against peripheral neuropathy

  Nature · 2026-01-07 · 12 citations

  articleOpen access

  Primary sensory neurons in dorsal root ganglia (DRG) have long axons and a high demand for mitochondria, and mitochondrial dysfunction has been implicated in peripheral neuropathy after diabetes and chemotherapy1,2. However, the mechanisms by which primary sensory neurons maintain their mitochondrial supply remain unclear. Satellite glial cells (SGCs) in DRG encircle sensory neurons and regulate neuronal activity and pain3. Here we show that SGCs are capable of transferring mitochondria to DRG sensory neurons in vitro, ex vivo and in vivo by the formation of tunnelling nanotubes with SGC-derived myosin 10 (MYO10). Scanning and transmission electron microscopy revealed tunnelling nanotube-like ultrastructures between SGCs and sensory neurons in mouse and human DRG. Blockade of mitochondrial transfer in naive mice leads to nerve degeneration and neuropathic pain. Single-nucleus RNA sequencing and in situ hybridization revealed that MYO10 is highly expressed in human SGCs. Furthermore, SGCs from DRG of people with diabetes exhibit reduced MYO10 expression and mitochondrial transfer to neurons. Adoptive transfer of human SGCs into the mouse DRG provides MYO10-dependent protection against peripheral neuropathy. This study uncovers a previously unrecognized role of peripheral glia and provides insights into small fibre neuropathy in diabetes, offering new therapeutic strategies for the management of neuropathic pain. Mitochondria that are transported from satellite glial cells in dorsal root ganglia to peripheral sensory neurons through tunneling nanotube-like structures provide protection against peripheral neuropathy.

  PublisherDOI

• Astrocyte-microglia crosstalk through Hevin and Toll-like receptor signaling controls developmental thalamocortical synapse refinement

  Neuron · 2026-02-19 · 1 citations

  articleOpen accessSenior author

  Synapse formation and elimination are two crucial processes that occur concurrently in the developing brain. Astrocytes and microglia control both processes, yet how these two major glial cell types of the central nervous system (CNS) communicate to balance synapse formation and elimination is unknown. Astrocytes secrete the synaptogenic protein Hevin/SPARCL1, which induces the formation and plasticity of thalamocortical synapses in the mouse visual cortex. Here, we found that, in addition to this synaptogenic function, Hevin directly signals to microglia by interacting with Toll-like receptor 4 (TLR4). This signaling occurs when Hevin is proteolytically cleaved, producing a C-terminal fragment that is no longer synaptogenic. We found that Hevin, through TLR4, induces a distinct microglial state defined by increased TLR2 expression and phago-lysosomal content in vitro and in vivo. Microglial TLR4 signaling is required for the proper elimination of thalamocortical synapses during early postnatal development.

  PublisherDOI

• Reprogramming of neuronal genome function and phenotype by astrocytes

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-07

  articleOpen access

  Abstract Heterotypic cell-cell interactions are critical to governing cellular physiology, disease progression, and responses to the environment and pharmacologic interventions. For example, neurons and astrocytes engage in intricate interactions that are essential for brain development and function 1–3 . However, the transformation of these extracellular signals into epigenomic regulation that governs cell function is poorly understood. Here, we report that weeks of co-culture between human induced pluripotent stem cell (hiPSC)-derived neurons and mouse cortical astrocytes extensively reprograms gene expression and the chromatin accessibility landscape in neurons, affecting thousands of genes and putative gene regulatory elements (REs), including many transcription factors (TFs). These genes are enriched for functions implicated in neuronal differentiation and maturation, and tend to be impacted in schizophrenia, and autosomal dominant Alzheimer’s disease. Through complementary CRISPR interference and activation screens, we recapitulated hundreds of astrocyte-induced transcriptional and chromatin remodeling events in mono-cultured neurons at both promoters and distal regulatory elements (REs) of TF genes. We discovered functional REs for ∼50 astrocyte-responsive TF genes, providing a map of gene regulatory network control. Astrocyte-responsive TF genes fall into groups that exert independent or counter-balancing transcriptional effects, highlighting the complex coordination of the neuronal response to astrocytes. Functional effects of specific TFs, including POU3F2 and TFAP2E, on neurite morphology and neuronal electrophysiology are consistent with transcriptional effects, demonstrating the capacity of direct epigenetic control to mimic heterotypic cellular signals. This work illuminates the regulation of neurodevelopment-and disease-relevant gene modules by neuron-astrocyte interactions, and provides a blueprint for applying modern functional genomics to uncover the links between cell microenvironment and epigenomic programming. Highlights Neuronal gene expression and chromatin accessibility landscape are profoundly remodeled by astrocytes over weeks of co-culture Astrocyte-responsive neuronal gene modules and neuron-responsive astrocytic gene modules are enriched for genes associated with schizophrenia and familial Alzheimer’s Disease Single-cell CRISPR interference and activation screens of astrocyte-responsive gene regulatory elements identified dozens of functional regulatory elements of TF genes in neurons Single-cell CRISPR interference and activation screens of >200 astrocyte-responsive TF genes uncovered discrete functional clusters that promote neuronal maturity or stemness Astrocyte-responsive TF genes reprogram neuronal electrophysiology and neurite morphology

  PublisherDOI

• CBCT-Based Differentiation of Odontogenic and Non-Odontogenic Maxillary Sinus Pathology: A Retrospective Imaging Study

  Research Square · 2026-01-16

  preprintOpen access
  PublisherOA PDFDOI

• Astrocytes, hidden puppet masters of the brain

  Science · 2025-05-15 · 9 citations

  article1st authorCorresponding

  Astrocyte signaling pathways influence neuronal networks and behavioral responses to neuromodulators.

  PublisherDOI

• Microglia-astrocyte crosstalk regulates synapse remodeling via Wnt signaling

  Cell · 2025-09-01 · 31 citations

  articleOpen access
  PublisherOA PDFDOI

• Mitochondrial fission controls astrocyte morphogenesis and organization in the cortex

  The Journal of Cell Biology · 2025-09-03 · 6 citations

  articleOpen accessSenior author

  Dysfunctional mitochondrial dynamics are a hallmark of devastating neurodevelopmental disorders such as childhood refractory epilepsy. However, the role of glial mitochondria in proper brain development is not well understood. We show that astrocyte mitochondria undergo extensive fission while populating astrocyte distal branches during postnatal cortical development. Loss of mitochondrial fission regulator, dynamin-related protein 1 (Drp1), decreases mitochondrial localization to distal astrocyte processes, and this mitochondrial mislocalization reduces astrocyte morphological complexity. Functionally, astrocyte-specific conditional deletion of Drp1 induces astrocyte reactivity and disrupts astrocyte organization in the cortex. These morphological and organizational deficits are accompanied by loss of perisynaptic astrocyte process (PAP) proteins such as gap junction protein connexin 43. These findings uncover a crucial role for mitochondrial fission in coordinating astrocytic morphogenesis and organization, revealing the regulation of astrocytic mitochondrial dynamics as a critical step in neurodevelopment.

  PublisherOA PDFDOI

• PD-linked LRRK2 G2019S mutation impairs astrocyte morphology and synapse maintenance via ERM hyperphosphorylation

  eLife · 2025-07-14

  preprintOpen accessSenior author

  Abstract Astrocytes are highly complex cells that mediate critical roles in synapse formation and maintenance by establishing thousands of direct contacts with synapses through their perisynaptic processes. Here, we found that the most common Parkinsonism gene mutation, LRRK2 G2019S, enhances the phosphorylation of the ERM proteins (Ezrin, Radixin, and Moesin), components of the perisynaptic astrocyte processes in a subset of cortical astrocytes. The ERM hyperphosphorylation was accompanied by decreased astrocyte morphological complexity and reduced excitatory synapse density and function. Dampening ERM phosphorylation levels in LRRK2 G2019S mouse astrocytes restored both their morphology and the excitatory synapse density in the anterior cingulate cortex. To determine how LRRK2 mutation impacts Ezrin interactome, we used an in vivo BioID proteomic approach, and we found that astrocytic Ezrin interacts with Atg7, a master regulator of autophagy. The Ezrin/Atg7 interaction is inhibited by Ezrin phosphorylation, thus diminished in LRRK2 G2019S astrocytes. Importantly, the Atg7 function is required to maintain proper astrocyte morphology. Our data provide a molecular pathway through which the LRRK2 G2019S mutation alters astrocyte morphology and synaptic density in a brain-region-specific manner.

  PublisherDOI

• PD-linked LRRK2 G2019S mutation impairs astrocyte morphology and synapse maintenance via ERM hyperphosphorylation

  eLife · 2025-07-14 · 2 citations

  preprintOpen accessSenior author

  Abstract Astrocytes are highly complex cells that mediate critical roles in synapse formation and maintenance by establishing thousands of direct contacts with synapses through their perisynaptic processes. Here, we found that the most common Parkinsonism gene mutation, LRRK2 G2019S, enhances the phosphorylation of the ERM proteins (Ezrin, Radixin, and Moesin), components of the perisynaptic astrocyte processes in a subset of cortical astrocytes. The ERM hyperphosphorylation was accompanied by decreased astrocyte morphological complexity and reduced excitatory synapse density and function. Dampening ERM phosphorylation levels in LRRK2 G2019S mouse astrocytes restored both their morphology and the excitatory synapse density in the anterior cingulate cortex. To determine how LRRK2 mutation impacts Ezrin interactome, we used an in vivo BioID proteomic approach, and we found that astrocytic Ezrin interacts with Atg7, a master regulator of autophagy. The Ezrin/Atg7 interaction is inhibited by Ezrin phosphorylation, thus diminished in LRRK2 G2019S astrocytes. Importantly, the Atg7 function is required to maintain proper astrocyte morphology. Our data provide a molecular pathway through which the LRRK2 G2019S mutation alters astrocyte morphology and synaptic density in a brain-region-specific manner.

  PublisherDOI

Recent grants

• Control of synapse formation and maturation by astrocytes

  NIH · $1.7M · 2012–2018

• Control of Astrocyte Development and Astrocyte-Synapse Interactions

  NIH · $1.9M · 2018–2023

• Environmental Toxins and Microglia-Synapse Interactions in Autism

  NIH · $2.1M · 2016–2021

• New Proteomic and Genome Engineering Approaches to Decipher Astrocyte Function at Synapses

  NIH · $2.1M · 2018–2021

• The Regulation of Synaptic Connectivity and Homeostasis by Huntingtin

  NIH · $1.7M · 2016–2020

Frequent coauthors

• Dhanesh Sivadasan Bindu

  Duke University Hospital

  104 shared

• Justin T Savage

  Duke University Hospital

  92 shared

• Francesco Paolo Ulloa Severino

  Duke University

  90 shared

• Kristina Sakers

  Duke University

  76 shared

• Scott H. Soderling

  Duke University

  73 shared

• J.J. Ramirez

  Duke University

  70 shared

• Christabel Xin Tan

  Duke University Hospital

  67 shared

• W. Christopher Risher

  Marshall University

  66 shared

Education

• Postdoctoral Research, Neurobiology

  Stanford University

  2008

• Ph.D., Biology

  Ruprecht Karls Universitat Heidelberg

  2002

• Predoctoral Student, Structural Biology

  European Molecular Biology Laboratory

  2002

• M.Sc., Molecular Biology and Genetics

  Bilkent Universitesi

  1998

• B.Sc., Chemical Engineering

  Orta Dogu Teknik Universitesi

  1996