Justyna Zmorzyńska, PhD
Laboratory of Developmental Neurobiology
ORCID ID: 0000-0001-8489-8732
- RESEARCH
- MEMBERS OF THE GROUP
- PUBLICATIONS
- GROUP LEADER
- FIRST TEAM PROJECT
- MORE
Research interests
The lab investigates how early brain development shapes vulnerability to neuropsychiatric disorders, with a focus on the molecular and environmental factors that influence the formation and function of neural circuits. We frequently use zebrafish to visualize developing brain networks and to model genetic conditions.
Using zebrafish, we visualize developing brain networks and model genetic conditions such as tuberous sclerosis complex (TSC), where mutations in the TSC1 or TSC2 genes lead to chronic overactivation of the mTORC1 signaling pathway. This pathway acts as a central hub that helps the developing brain interpret and respond to internal and external cues, and when it becomes hyperactive – as is often seen in autism spectrum disorder (ASD) – sensory information can be processed in atypical ways. In our TSC zebrafish model, we discovered that the loss of normal light preference stems from disrupted processing of light signals in a brain region called the left dorsal habenula. Neurons in this region in Tsc2-deficient fish were overly active and failed to adapt to repeated light exposure, indicating a breakdown in normal sensory filtering. Importantly, these abnormalities were reversed with rapamycin, a drug that inhibits mTORC1. This work reveals how excessive mTORC1 activity can directly impair sensory processing, providing a mechanistic link between early developmental signaling defects and the atypical sensory responses often observed in ASD.
Yet, only around 50% of people with TSC actually develop ASD. A central question driving our work is why individuals carrying the same mutation can exhibit strikingly different neuropsychiatric symptoms (variable expressivity). To address this, we examine how prenatal environments, maternal immune activation, and other early-life influences interact with genetic variation to produce diverse developmental outcomes. Patients with genetic disorders often present highly variable neuropsychiatric phenotypes that do not correlate with mutation burden. The lab focuses on autism spectrum disorders and anxiety disorders. We investigate the molecular and cellular mechanisms underlying this variability using high‑throughput approaches. Our goal is to uncover the mechanistic basis of variable expressivity in neuropsychiatric disease. To achieve this, our research integrates genetics, molecular neuroscience, and large‑scale screening, with a strong emphasis on zebrafish models to reveal how disrupted developmental processes shape behavior and pathology.
Members of the group
| Name | Surname | Degree | |||||
| Shivani | Dogra | s.dogra@imol.institute | |||||
| Tomasz | Dulski | PhD | t.dulski@imol.institute | ||||
| Rabia | Hayat | PhD | r.hayat@imol.institute | ||||
| Ruchi | Jain | r.jain@imol.institute | |||||
| Satya Ranjan | Pattnaik | s.pattnaik@imol.institute | |||||
| Vishrutha | Prakash | v.prakash@imol.institute | |||||
| Sanata | Tolak | s.tolak@imol.institute | |||||
| Agnieszka | Wardak | PhD | a.wardak@imol.institute | ||||
| Klaudia | Wojtal | k.wojtal@imol.institute | |||||
| Justyna | Zmorzyńska | PhD | j.zmorzynska@imol.institute | ||||
| Former members | |||||||
| Olga | Doszyń | o.doszyn@imol.institute |
Publications
- Z. Sas, M. Zakrzewski, W. Czestkowski, P. Wanat, A. Wardak, J. Zmorzynska, A. Marusiak and R. Serwa, Minimal-tag polyamines for in situ probing of their intracellular distribution. Chem. Commun., 2026, Advance online publication. DOI: 10.1039/D5CC06304C.
- T. Dulski*, S. Tolak*, J. Zmorzyńska, Challenges and hopes for treatment of anxiety disorder in the autistic population, Brain Research (2025), https://doi.org/10.1016/j.brainres.2025.149675. *equal contribution
- Maciag, M., Doszyn, O., Wnorowski, A., Zmorzynska, J., & Budzynska, B. (2025). Exploring the impact of MDMA and oxytocin ligands on anxiety and social responses: A comprehensive behavioural and molecular study in the zebrafish model. Journal of psychopharmacology (Oxford, England), 2698811251324596.
- Doszyn, O., Dulski, T., & Zmorzynska, J. (2025). Protocol for microinjection of rapamycin into the zebrafish habenula. STAR protocols, 6(1), 103566. Advance online publication. https://doi.org/10.1016/j.xpro.2024.103566
- Doszyn, O., Dulski, T., & Zmorzynska, J. (2025). Protocol for the visualization of pRps6-positive cells in larval zebrafish brains using whole-mount immunofluorescence and light-sheet microscopy. STAR protocols, 6(1), 103587. Advance online publication. https://doi.org/10.1016/j.xpro.2024.103587
- Doszyn, O., Kedra, M., & Zmorzynska, J. (2024). Hyperactive mTORC1 disrupts habenula function and light preference in zebrafish model of Tuberous sclerosis complex. iScience, 27(6), 110149. https://doi.org/10.1016/j.isci.2024.110149
- Doszyn, O.*, Dulski, T.*, & Zmorzynska, J. (2024). Diving into the zebrafish brain: exploring neuroscience frontiers with genetic tools, imaging techniques, and behavioral insights. Frontiers in Molecular Neuroscience, 17. 10.3389/fnmol.2024.1358844 (*equal contribution)
- O Doszyn, T Dulski, J Zmorzynska. The zebrafish model of Tuberous Sclerosis Complex to study epilepsy in the Handbook of Animal Models in Neurological Disease edited by Colin Martin, Vinood B Patel and Victor R Preedy, Elsevier, 2023.
- Olga Doszyn, Magdalena Kedra, Justyna Zmorzynska. mTORC1 hyperactivation causes sensory integration deficits due to habenula impairment. doi.org/10.1101/2022.07.20.500762, biorxiv, 2022.
- MT Prentzell*, U Rehbein*, MC Sandoval*, A De Meulemeester*, R Baumeister, L Brohée, B Berdel, M Bockwoldt, B Carroll, SR Chowdhury, A von Deimling, C Demetriades, G Figlia, Genomics England Research Consortium, M Eca, G de Araujo, AM Heberle, I Heiland, B Holzwarth, LA Huber, J Jaworski, M Kedra, K Kern, A Kopach, VI Korolchuk, I van ‘t Land-Kuper, M Macias, M Nellist, W Palm, S Pusch, JM Ramos Pitto, M Reil, A Reintjes, F Reuter, JR Sampson, C Scheldeman, A Siekierska, E Stefan, A Teleman, LE Thomas, O Torres-Quesada, S Trump, HD West, P de Witte, S Woltering, T Yordanov, J Zmorzynska, CA Opitz, K Thedieck. The G3BP proteins tether the TSC complex to lysosomes and suppress mTORC1 signaling. Cell, 2021, Feb 4; 184(3):655-674. (*equal contribution).
- M Kedra, K Kisielewska, K Banasiak, L Wolinska-Niziol, J Jaworski, J Zmorzynska. TrkB hyperactivity contributes to brain dysconnectivity, epileptogenesis, and anxiety in a zebrafish model of Tuberous Sclerosis Complex. Proc Natl Acad Sci (PNAS). 2020 Jan 28;117(4):2170-2179.
- Koscielny A, Malik AR, Liszewska E, Zmorzynska J, Tempes A, Tarkowski B, Jaworski J. Adaptor Complex 2 Controls Dendrite Morphology via mTOR-Dependent Expression of GluA2. Molecular Neurobiology, 2018, Feb; 55(2):1590-1606.
- K Switon, K Kotulska, A Janusz-Kaminska, J Zmorzynska, J Jaworski. Molecular neurobiology of mTOR. Neuroscience, 2017, Jan 26; 341:112-153.
- K Switon, K Kotulska, A Janusz-Kaminska, J Zmorzynska, J Jaworski. Tuberous Sclerosis Complex: From Molecular Biology to Novel Therapeutic Approaches. IUBMB Life, 2016 Dec; 68(12):955-962.
- Smeets CJ, Zmorzyńska J, Melo MN, Stargardt A, Dooley C, Bakalkin G, McLaughlin J, Sinke RJ, Marrink SJ, Reits E, Verbeek DS. Altered secondary structure of Dynorphin A associates with loss of opioid signalling and NMDA-mediated excitotoxicity in SCA23. Human Molecular Genetics, 2016 Jul 1;25(13):2728-2737.
- C Smeets*, J Jezierska*, H Watanabe, A Duarri, MR Fokkens, M Meijer, Q Zhou, T Yakovleva, E Boddeke, W den Dunnen, J van Deursen, G Bakalkin, HH Kampinga, B van de Sluis, DS Verbeek. Elevated mutant dynorphin A causes Purkinje cell loss and motor dysfunction in spinocerebellar ataxia type 23. Brain. 2015 Sep; 138(Pt 9):2537-52. (*equal contribution)
- J Jezierska, J Goedhart, HH Kampinga, EA Reits, DS Verbeek. SCA14 mutation V138E leads to partly unfolded PKCγ associated with an exposed C-terminus, altered kinetics, phosphorylation and enhanced insolubilization. Journal of Neurochemistry, 2014 Mar;128(5):741-51.
- J Jezierska, G Stevanin, H Watanabe, MR Fokkens, F Zagnoli, J Kok, J Goas, P Bertrand, C Robin, A Brice, G Bakalkin, A Durr, DS Verbeek. Identification and characterization of novel PDYN mutations in dominant cerebellar ataxia cases. Journal of Neurology, 2013; Vol. 260, Issue 7:1807-1812.
- A Duarri, J Jezierska, MR Fokkens, M Meijer, HJ Schelhaas, WFA den Dunnen, F van Dijk, C Verschuuren-Bemelmans, G Hageman, P van de Vlies, B Küsters, BP van de Warrenburg, B Kremer, C Wijmenga, RJ Sinke, MA Swertz, HH Kampinga, E Boddeke, DS Verbeek. Mutations in potassium channel kcnd3 cause spinocerebellar ataxia type 19. Annals of Neurololy, 2012 Dec; 72(6):870-80.
- G Bakalkin, H Watanabe*, J Jezierska*, C Depoorter, C Verschuuren-Bemelmans, I Bazov, KA Artemenko, T Yakovleva, D Dooijes, BPC Van de Warrenburg, RA Zubarev, B Kremer, PE Knapp, KF Hauser, C Wijmenga, F Nyberg, RJ Sinke, DS Verbeek. Prodynorphin mutations cause the neurodegenerative disorder spinocerebellar ataxia type 23. American Journal of Human Genetics, 87(5), 593-603, Nov 12, 2010. (*equal contribution)
About Group Leader
Justyna Zmorzynska is a head of The Laboratory of Developmental Neurobiology. She graduated from University of Warsaw with a MSc degree in Molecular Biology performing her Master project in the Department of Medical Genetics in the Institute of Mother and Child (Warsaw, PL). She did her PhD projects in the Department of Genetics, University Medical Center Groningen in Netherlands. She was awarded the Jan Kornelius de Cock stichting, grants for PhD students, three years in a row (2011-2013). She was a post-doctoral fellow and then senior researcher in the Laboratory of Molecular and Cellular Neurobiology, International Institute of Molecular and Cell Biology in Warsaw (PL). She did internships in in prof. Didier Stainier lab (Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany) and in Prof. William Harris lab (Department of Physiology, Development and Neuroscience, Cambridge, UK). She is also a founder and a scientific consultant of PIXEL-ANALYSIS, an SME that deals with automated solutions for image analysis. She was a project leader of a SONATA grant and then an OPUS grant. In December 2023, she became a group leader at the IMol PAS.
Memberships and awards
- Member of Polish Zebrafish Society
- Member of Polish Neuroscience Society
- Member of Federation of European Neuroscience Societies (FENS)
- Member of European Zebrafish Society
- Award of the 2nd Department of Biological and Agricultural Sciences of the Polish Academy of Sciences in 2020 for the scientific team of the IIMCB composed of: prof. J. Jaworski, M. Kedra, B. Tarkowski, M. Urbanska, and J. Zmorzynska for the series of publications on „New molecular mechanisms of mTORopathy and epilepsy”
- Distinction in Konorski award for the best publication for 2020 year. The Jerzy Konorski award is given every year for the best work in the field of neurobiology done in Poland and is awarded by the Polish Neuroscience Society and the Committee of Neurobiology of the Polish Academy of Sciences.
- Scholarship of the Minister of Science and Higher Education for Outstanding Young Scientists, Poland. In 2016, a 4-year-long scholarship from the Minister of Science and Higher Education for outstanding young scientists. It is an award for scientific and research achievements. There were only 200 such scholarships granted each year for the whole country.
- START II (edition 2016) from Foundation for Polish Science (FNP), Poland, for the outstanding achievements in their field. The prize is awarded a maximum of two times and getting it two times in a row is a great distiction. The START fellowship serves as recognition of the scientific attainments by the young researchers and as an incentive for further growth by enabling them to devote themselves fully to their research.
- START (edition 2015) from Foundation for Polish Science (FNP), Poland, for the outstanding achievements in their field. The START fellowship is a personal award and serves as recognition of the scientific attainments by the young scholars and as an incentive for further growth by enabling them to devote themselves fully to their research.
Funding
- First Team grant from Foundation for Polish Science. New strategies for treating anxiety disorders in autism (FENG.02.02-IP.05-0064/24; 3 955 050 PLN).
- SONATA BIS grant from National Science Centre. Influence of environmental factors related to maternal infection during pregnancy on the development of neuropsychiatric disorders in offspring with Tuberous Sclerosis Complex in the zebrafish model (2023/50/E/NZ3/00252; 4 812 704 PLN).
- HORIZON-MSCA-2023-DN-01 from ERC. Metabolic control of cell growth by mTOR in health and disease: a multi-disciplinary training (MENTOR) (No. 101168624; 226 512 EUR).
- OPUS19 grant from National Science Centre. Rac1 contribution to brain connectivity impairments and neuropsychiatric disorders in Tuberous Sclerosis Complex (2020/37/B/NZ3/02345; 2,251,260 PLN).
- SONATA9 grant from National Science Centre. The role of Zebrafish mTOR in neuronal development in vivo as a key regulator of neuronal circuit formation (2015/17/D/NZ3/03735; 689,000 PLN).
- JK de Cock Stichting 2013, a one-year-long research grant for PhD students, for NMDAR interaction with DynA in Spinocerebellar ataxia type 23 (27 000 EUR), NL. It is a great distinction to get it three times in a row.
- Travel Grant for Ataxia Research Conference 2012 (Simonsfonds), NL.
- JK de Cock Stichting 2012 for Expression study of mouse model of Spinocerebellar ataxia type 23 (60 000 EUR), NL.
- Travel Grant for 5th Molecular mechanisms of Neurodegeneration meeting 2011 (Simonsfonds), NL.
- JK de Cock Stichting 2011 for Development of a fruit fly model of Spinocerebellar ataxia type 23 (36 000 EUR), NL.
Międzynarodowy Instytut Mechanizmów i Maszyn Molekularnych PAN uzyskał dotację z Unii Europejskiej na projekt FENG.02.02-IP.05-0064/24 “Nowe strategie leczenia zaburzeń lękowych w autyzmie”.
Celem projektu jest znalezienie bezpiecznych i skutecznych substancji bioaktywnych, które mogą zostać włączone do terapii zaburzeń lękowych w autyzmie związanym ze stwardnieniem guzowatym. Wyniki projektu mogą przyczynić się także do terapii zaburzeń lękowych w innych formach autyzmu lub nawet zaburzeń lękowych niewspółwystępujących z innymi chorobami.
W ramach tego projektu zostanie przesiana biblioteka substancji bioaktywnych pod kątem toksyczności, właściwości przeciwlękowych, wpływu na zachowania społeczne oraz na rozwój mózgu.
Projekt skierowany jest do szerokiego grona odbiorców, którzy w różny sposób są związani z tematyką spektrum autyzmu: osoby z zaburzeniami ze spektrum autyzmu; ich rodziny i opiekunowie; specjaliści: lekarze, psycholodzy, terapeuci, pedagodzy; organizacje wspierające i instytucje publiczne.
Efektem projektu będzie znalezienie bezpiecznych i skutecznych substancji bioaktywnych, które mogą zostać włączone do terapii zaburzeń lękowych w autyzmie związanym ze stwardnieniem guzowatym. Wyniki projektu mogą przyczynić się także do terapii zaburzeń lękowych w innych formach autyzmu lub nawet zaburzeń lękowych niewspółwystępujących z innymi chorobami.
Wartość projektu: 3.955.050 zł
Wysokość wkładu z Funduszy Europejskich: 3.955.050 zł
—
The International Institute of Molecular Mechanisms and Machines of the Polish Academy of Sciences has received European Union funding for the project FENG.02.02-IP.05-0064/24 “New treatment strategies for anxiety disorders in autism”.
The aim of the proposed project is to identify safe and effective bioactive substances that can be incorporated into the treatment of anxiety disorders in autism associated with tuberous sclerosis. The project’s results may also contribute to the treatment of anxiety disorders in other forms of autism, or even anxiety disorders not comorbid with other conditions.
In this project, we will screen a library of bioactive substances for toxicity, anxiolytic properties, effects on social behavior, and brain development.
The project is aimed at a wide audience who are involved in various ways with the topic of autism spectrum disorders: people with autism spectrum disorders; their families and caregivers; specialists: doctors, psychologists, therapists, educators; support organizations and public institutions.
The outcome will be to find safe and effective bioactive substances that can be incorporated into the treatment of anxiety disorders in autism associated with tuberous sclerosis. The project’s results may also contribute to the treatment of anxiety disorders in other forms of autism, or even anxiety disorders not comorbid with other conditions.
Total project value: 3.955.050 zł
Amount of the contribution from European Funds: 3.955.050 zł