Conferences and Workshops

Intracellular vesicles like lysosomes move bidirectionally and in a stop-and-go fashion along microtubules. This involves the activities of two motor types; the dynein-dynactin motor complex for inward and the kinesin motors for outward transport. We considered this transport in the context of living cells using endogenously tagged fluorescent proteins. We show how the perinuclear cloud of lysosomes is positioned and how the mobile pool of lysosomes surf on the surface of the ER while moving along microtubules. The motor proteins utilize anchors on the lysosomal membrane for binding. By quantifying the different components in this system, motor binding appears to be the limiting factor. In fact, movement is not controlled by the number of motors on a vesicle but by their activation, a process controlled by microtubule-associated proteins. The activated dynein-dynactin motor is assembled at the growing microtubule plus end and then moves inward to be intercepted by Rab7-RILP on lysosomes for lysosomal inward movement. The kinesin motor is activated at various sites along microtubules. We present a new model explaining bidirectional transport of lysosomes by considering these in the context of living cells.

Glaucoma, a progressive age-related optic neuropathy characterized by retinal ganglion cell degeneration and alteration of the optic nerve head is a worldwide leading cause of irreversible blindness. Elevated intraocular pressure (IOP), is one of the main, and the only modifiable, risk factor. However, despite the efficient control of IOP values (either pharmacologically or surgically), the loss of retinal ganglion cells progresses in a significant percentage of patients suggesting that IOP-independent, and still unidentified factors, are relevant for the onset and evolution of the disease.
Dysregulation of the autophagy-lysosome system, which is responsible responsible for the selective e non-selectivedegradation of proteins and organelles, has been associated with several central and peripheral neurodegenerative pathologies although its role in glaucoma-related neurodegeneration is still debated.
Here we show that neurodegeneration observed in experimental models of glaucoma is associated with autophagy and mitophagy dysregulation, and explore the pharmacological modulation of the process as potential neuroprotective strategy.

Please feel free to forward this email and poster to friends and colleagues, who may be interested in joining.
If you are interested in an in-person discussion with Rossella Russo, please approach me until the 4th of October 2024.
 
We are looking forward to welcoming you to the lecture.