Project ID CM-HD2026_23

ThemeCM-HD

Co Supervisor 1A Dr Robert Seaborne Faculty of Life Sciences & Medicine, School of Basic & Medical Biosciences, Randall Centre for Cell & Molecular BiophysicsEmail

Co Supervisor 1B Dr Sarah Marzi Faculty of Dentistry, Oral & Craniofacial Sciences, Centre for Craniofacial & Regenerative BiologyEmail

Third Supervisor Dr. Jacqueline Mitchell

The brain-muscle epigenetic interplay in neuromuscular disease

Background:
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease marked by progressive motor neuron loss. Emerging evidence suggests a critical, previously underappreciated role for skeletal muscle in ALS onset and progression, highlighting pathological and molecular interplay between brain and muscle. However, systematic, high-resolution molecular analyses across these tissues remain scarce. This project will use advanced wet-lab and computational techniques—including single-cell and bulk sequencing—to investigate conserved and tissue-specific molecular signatures in ALS-affected brain and muscle. Findings may uncover systemic drivers of ALS and identify novel therapeutic targets.

Aim:
To define conserved and tissue-specific molecular perturbations in brain and muscle in ALS using multi-omic approaches at single-cell and bulk resolution.
Student Development:

The student will undertake a truly cross-disciplinary, multi-laboratory PhD that integrates the fields of muscle biology, neurobiology, and neurology. This program will provide training in both advanced wet-lab techniques and computational methodologies, fostering expertise in molecular and systems-level analyses. The student will acquire hands-on experience in isolating, purifying, and preparing key biomolecules for high-throughput sequencing in both whole tissue and single-cell samples. This will be complemented by training in computational biology. Development in non-technical skills, for example scientific communication, manuscript preparation, will also be targeted.

Milestones:
• Year 1: Establish mouse colonies; collect brain and muscle tissues at defined disease stages; isolate single-cell/nuclei; pilot single-cell/bulk sequencing; develop computational skills for handling and pre-processing of data.
• Year 2: Generate full-scale datasets; conduct cell-type-specific analyses and data integration.
• Year 3: Identify conserved and specific ALS perturbations; validate key targets; begin human sample analyses.
• Year 4: Finalise integrative analyses; prepare thesis/publications; present findings.

Rotation Project:
The student will analyse single-cell co-assayed RNA+methylome data from ALS muscle to identify epigenomic and transcriptomic defects across muscle subtypes. Analyses will include clustering, subtyping, differential expression, and pathway enrichment, informing the broader PhD project.

Representative Publications

1. Integrated single cell functional proteomic profiling reveals a shift in myofibre specificity in human nemaline myopathy: A proof of principle study. Seaborne R.A.E., Moreno Justicia R., Laitila J., Lewis C.T.A., Savoure L., Zanoteli E., Lawlor M.W., Jungbluth H., Deshmukh A.S., Ochala J. (2025). The Journal of Physiology. doi:10.1113/JP288363
2. Myosin ATPase inhibition fails to rescue the metabolically dysregulated proteome of nebulin-deficient muscle. Laitila J., Seaborne R.A.E., Ranu N., Kolb J.S., Wallgren Pettersson C., Witting N., Vissing J., Vilchez J.J., Zanoteli E., Palmio J., Huovinen S., Granzier H., Ochala J. (2024). The Journal of Physiology. doi:10.1113/JP286870
3. Human skeletal muscle fiber heterogeneity beyond myosin heavy chains. Moreno Justicia R., Van der Stede T., Stocks B., Laitila J., Seaborne R.A., Van de Loock A., Lievens E., Samodova D., Marín Arraiza L., Dmytriyeva O., Browaeys R., Van Vossel K., Moesgaard L., Yigit N., Anckaert J., Weyns A., Van Thienen R., Sahl R.E., Zanoteli E., Lawlor M.W., Wierer M., Mestdagh P., Vandesompele J., Ochala J., Hostrup M., Derave W., Deshmukh A.S. (2025). Nature Communications. doi:10.1038/s41467-025-56896-6

1. CUT&Tag recovers up to half of ENCODE ChIP-seq histone acetylation peaks. Abbasova, L., Urbanaviciute, P., Hu, D., Ismail, J. N., Schilder, B. M., Nott, A., Skene, N. G., & Marzi, S. J. (2025). Nature Communications. doi:10.1038/s41467-025-58137-2
2. CHAS infers cell type-specific signatures in bulk brain histone acetylation studies of neurological and psychiatric disorders. Murphy, K. B., Ye, Y., Nott, A., & Marzi, S. J. (2024). European Neuropsychopharmacology. doi:10.1016/j.euroneuro.2024.10.003
3. Genetic risk for neurodegenerative conditions is linked to disease-specific microglial pathways. Aydan Askarova, Reuben M. Yaa, Sarah J. Marzi & Alexi Nott (2025). PLoS Genetics. doi:10.1371/journal.pgen.1011407