Dr. Julia Abitbol received her B.Sc with Honour's specialization in Biology and Medical Cell Biology at the University of Western Ontario, London, Ontario, Canada. She then received her PhD in Anatomy and Cell Biology at the University of Western Ontario. During her PhD she studied the role of large-pore channel proteins, connexins and pannexins, in the auditory system.
Honors & Awards
Suzanne M. Bernier publication Award 2019, The University of Western Ontario (06/2019)
Marine Biology Laboratory Travel Award to attend "The Biology of the Inner Ear” workshop, Marine Biology Laboratory (05/2019)
Selected Cover Image for Journal of Molecular Medicine, May cover, Journal of Molecular Medicine (05/2019)
Feature Platform Presentation Winner, London Health Research Day 2019, London Health Research Day Committee (04/2019)
Selected Cover Image Journal of Cell Science, Volume 131, Issue 9, Journal of Cell Science (05/2018)
First Author Interview Feature in the Journal of Cell Science, Journal of Cell Science (04/2018)
Best Poster Presentation Award, Anatomy and Cell Biology Research Day, Anatomy and Cell Biology Research Day Committee (10/2017)
Best Poster Presentation Award, International Gap Junction Meeting, International Gap Junction Meeting Committee (07/2017)
Travel Scholarship, International Gap Junction Meeting, International Gap Junction Meeting Organizing Committee (07/2017)
Natural Sciences and Engineering Research Council (NSERC) CGS Doctoral Scholarship, Natural Sciences and Engineering Research Council (09/2017-11/2019)
Ontario Graduate Scholarship (Declined), The University of Western Ontario (09/2017-08/2018)
Ontario Graduate Scholarship, The University of Western Ontario (09/2016-04/2017)
JAX Lab Mouse Research Travel Scholarship, JAX Lab, Bar Harbour, Maine (09/2016)
Anatomy and Cell Biology Travel Award, The Department of Anatomy and Cell Biology, The University of Western Ontario (04/2016)
Western Graduate Research Scholarship, The University of Western Ontario (09/2014-08/2019)
Bachelor of Science, The University of Western Ontario, Honors Specialization in Biology and Medical Cell Biology (2014)
Doctor of Philosophy, The University of Western Ontario, Anatomy and Cell Biology (2019)
Alan Cheng, Postdoctoral Faculty Sponsor
Current Research and Scholarly Interests
Hearing loss is one of the most common sensory deficits and is permanent. We have known for quite some time that avian species retain the ability to spontaneously regenerate hair cells when they are damaged, however, this does not occur in the adult mammalian cochlea. My research interests are to enhance the proliferative regeneration capacity of the mammalian cochlea by findings genes that may up-regulate this process. Further, my goal is to track the dynamics of proliferating cochlear cells after damage in the cochlear. The ultimate goal is to identify genes that may enhance spontaneous regeneration of cochlear cells upon damage to treat patients with hearing loss.
Selection of viral capsids and promoters affects the efficacy of rescue of Tmprss3-deficient cochlea.
Molecular therapy. Methods & clinical development
2023; 30: 413-428
Adeno-associated virus (AAV)-mediated gene transfer has shown promise in rescuing mouse models of genetic hearing loss, but how viral capsid and promoter selection affects efficacy is poorly characterized. Here, we tested combinations of AAVs and promoters to deliver Tmprss3, mutations in which are associated with hearing loss in humans. Tmprss3tm1/tm1 mice display severe cochlear hair cell degeneration, loss of auditory brainstem responses, and delayed loss of spiral ganglion neurons. Under the ubiquitous CAG promoter and AAV-KP1 capsid, Tmprss3 overexpression caused striking cytotoxicity in vitro and in vivo and failed to rescue degeneration or dysfunction of the Tmprss3tm1/tm1 cochlea. Reducing the dosage or using AAV-DJ-CAG-Tmprss3 diminished cytotoxicity without rescue of the Tmprss3tm1/tm1 cochlea. Finally, the combination of AAV-KP1 capsid and the EF1α promoter prevented cytotoxicity and reduced hair cell degeneration, loss of spiral ganglion neurons, and improved hearing thresholds in Tmprss3tm1/tm1 mice. Together, our study illustrates toxicity of exogenous genes and factors governing rescue efficiency, and suggests that cochlear gene therapy likely requires precisely targeted transgene expression.
View details for DOI 10.1016/j.omtm.2023.08.004
View details for PubMedID 37663645
View details for PubMedCentralID PMC10471831
Lineage-tracing and translatomic analysis of damage-inducible mitotic cochlear progenitors identifies candidate genes regulating regeneration.
2021; 19 (11): e3001445
Cochlear supporting cells (SCs) are glia-like cells critical for hearing function. In the neonatal cochlea, the greater epithelial ridge (GER) is a mitotically quiescent and transient organ, which has been shown to nonmitotically regenerate SCs. Here, we ablated Lgr5+ SCs using Lgr5-DTR mice and found mitotic regeneration of SCs by GER cells in vivo. With lineage tracing, we show that the GER houses progenitor cells that robustly divide and migrate into the organ of Corti to replenish ablated SCs. Regenerated SCs display coordinated calcium transients, markers of the SC subtype inner phalangeal cells, and survive in the mature cochlea. Via RiboTag, RNA-sequencing, and gene clustering algorithms, we reveal 11 distinct gene clusters comprising markers of the quiescent and damaged GER, and damage-responsive genes driving cell migration and mitotic regeneration. Together, our study characterizes GER cells as mitotic progenitors with regenerative potential and unveils their quiescent and damaged translatomes.
View details for DOI 10.1371/journal.pbio.3001445
View details for PubMedID 34758021
GJB2 mutations linked to hearing loss exhibit differential trafficking and functional defects as revealed in cochlear-relevant cells
Frontiers in Cell and Development Biology
2020; 8 (215)
View details for DOI 10.3389/fcell.2020.00215
- Cisplatin-induced ototoxicity occurs independent of gap junctional intercellular communication, in press Cell Death and Differentiation 2020
The connexin 30 A88V mutant reduces cochlear gap junction expression and confers long-term protection against hearing loss
The Journal of Cell Science
2019; 132 (2)
View details for DOI 10.1242/jcs.224097
Double deletion of Panx1 and Panx3 affects skin and bone but not hearing
Journal of Molecular Medicine
2019; 97 (5): 723-736
View details for DOI 10.1007/s00109-019-01779-9
Mice harbouring an oculodentodigital dysplasia-linked Cx43 G60S mutation have severe hearing loss.
The Journal of Cell Science
View details for DOI 10.1242/jcs.214635
Differential effects of pannexins on noise-induced hearing loss
2016; 473 (24): 4665-4680
View details for DOI 10.1042/BCJ20160668