Author

Ashlyn M. Spring

University of North Carolina at Chapel Hill

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Genetics· 2 Neuroscience· 2

Signature Assays, Organisms & Methods

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Organism:Drosophila· 4 Approach:experimental assay· 4 Research Focus:cell type annotation· 2 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Assay:electronic health records· 1 Research Focus:gene regulatory network inference· 1 Assay:proteomics· 1

Frequent Co-Authors

A. Gregory MateraiD· 3 shared Amanda C. Raimer· 3 shared C. Andrew FrankiD· 1 shared Catherine J. YeatesiD· 1 shared Christine D. Hamilton· 1 shared Douglas J BrusichiD· 1 shared Eric L. GarciaiD· 1 shared Laura E. HerringiD· 1 shared

Activity by Year

2018-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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3 shared papersGenetics

A. Gregory MateraORCID

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4 papers

Recent·Most cited

Dysregulation of innate immune signaling in animal models of Spinal Muscular Atrophy

Eric L. Garcia, Rebecca E. Steiner, Amanda C. Raimer, Laura E. Herring, A. Gregory Matera, Ashlyn M. Spring

This study identifies hyperactivation of innate immune signaling as a consequence of SMN depletion in Drosophila SMA models, revealing a conserved regulatory role of the SMN complex.

BMC Biology · Apr 25, 2024Peer-reviewedGenetics

Temperature sensitive SMA-causing point mutations lead to SMN instability, locomotor defects, and premature lethality in Drosophila

Amanda C. Raimer, Suhana S. Singh, Maina R. Edula, Tamara Paris‐Davila, Vasudha Vandadi, Ashlyn M. Spring, A. Gregory Matera

This paper shows that temperature-sensitive SMA-causing mutations in Drosophila SMN lead to SMN instability, locomotor defects, and premature death, highlighting SMN's role in development.

Disease Models & Mechanisms · Jan 1, 2020Peer-reviewedGenetics

Comprehensive modeling of Spinal Muscular Atrophy in Drosophila melanogaster

Ashlyn M. Spring, Amanda C. Raimer, Christine D. Hamilton, Michela J. Schillinger, A. Gregory Matera

This study models spinal muscular atrophy in Drosophila using patient-derived missense mutations, showing similar phenotypes to human SMA across multiple adult neuromuscular metrics.

Frontiers in Molecular Neuroscience · May 16, 2019Peer-reviewedNeuroscience

Drosophila CaV2 Channels Harboring Human Migraine Mutations Cause Synapse Hyperexcitability That Can Be Suppressed By Inhibition Of A Ca2+ Store Release Pathway

Douglas J Brusich, Ashlyn M. Spring, Thomas D. James, Catherine J. Yeates, Timothy H. Helms, C. Andrew Frank

This study introduces Drosophila models with human migraine mutations in CaV2 channels, showing hyperexcitability that can be suppressed by inhibiting intracellular Ca2+ release.

PLoS Genetics · Aug 6, 2018Peer-reviewedNeuroscience