Professor Jon Lane
My lab work studies autophagy and other cellular responses to stress. We use transformed human cells and human iPSC-derived neurons and glia to understand how autophagy shapes neuronal responses to stress Parkinson's.
- membrane trafficking
- cell death
Professor of Cell BiologySchool of Biochemistry
I graduated with a BSc in Biology from Southampton University, and then studies for a PhD in Exeter on the cell cycle regulation of microtubule dynamics. This led to PostDoctoral work in Manchester on developmental microtubule motor control, and organelle disruption and altered protein trafficking in apoptosis. A Wellcome Trust Career Development Fellowship brought me to Bristol, where I have continued researching cellular responses to stress, with a focus on membrane trafficking and dynamics.
Over recent years, my group has concentrated on the process of autophagy - a crucial cellular stress response pathway that plays important roles in a variety of human diseases. We study how autophagy influences neuronal resilience in Parkinson's, using human induced pluripotent stem cells (hiPSCs) from which we grow human neurons and glia in the lab.
My lab is interested in autophagy - the regulated recycling of cytoplasmic material through delivery and degradation in the lysosome.
Please visit the Lab website https://thelanelab.blogs.bristol.ac.uk/
Follow Jon on Twitter @Jon_D_Lane
Autophagy (macroautophagy) is characterised by the formation of double membrane-bound organelles that sequester regions of cytoplasm including misfolded protein aggregates and organelles.The autophagosome membrane is decorated with a protein known as Atg8 (commonly known as LC3), which plays roles in autophagosome assembly and cargo selection.
We use live-cell imaging as well as fixed cell microscopy (including electron microscopy) to explore how and where autophagosomes are assembled. Through the application of cell-lines expressing GFP-tagged autophagy proteins (such as Atg5; Atg14; Atg16L; DFCP1), we can determine how the sequential recruitment of autophagy factors influences autophagosome assembly.
In our studies we used various human and mouse cell culture lines, primary human erythroid precursors and induced pluripotent stem cells from human patients. The latter we differentiate into specific neural lineages to understand how autophagy is regulated in neurons for research into the causes of neurodegenerative diseases (Parkinson’s disease; Alzheimer’s disease).
01/03/2022 to 28/02/2023
13/10/2020 to 12/10/2023
Managing organisational unitBristol Medical School (THS)
01/10/2020 to 30/09/2023
01/01/2012 to 01/01/2015
Reciprocal Autophagy Control by the LIM Homeodomain Transcription Factors LMX1A and LMX1B Safeguards Human Midbrain Dopaminergic Neurons
Investigation into the Effect of Protein Disulphide Isomerase A3 on the Prom-Metastatic Phenotype of Breast Cancer Cells
Proteomics-Based Analysis of The Coordination of Membrane Trafficking Events by The ATG12-ATG5 Autophagy Complex
Genome-wide analysis of mitochondrial DNA copy number reveals loci implicated in nucleotide metabolism, platelet activation, and megakaryocyte proliferation
The ATG5 interactome links clathrin-mediated vesicular trafficking with the autophagosome assembly machinery
Efficient and Scalable Generation of Human Ventral Midbrain Astrocytes from Human-Induced Pluripotent Stem Cells
Journal of Visualized Experiments
I teach on all years of the Biochemistry BSc/MSci programmes, covering mitosis and the cell cycle, apoptosis, and autophagy in health and disease. I also contribute to teachng on MSc and PhD programmes, including through lectures, Journal clubs, tutorials, and workshops.