A study identified new lysosomal proteins in brain cells, including SLC45A1, linked to a neurological disease. Loss of SLC45A1 disrupts lysosomal function, impacting V-ATPase stability and causing mitochondrial dysfunction.
Cryo-ET showed protein aggregates, altered cristae, and reduced ribosome complexes in stressed mitochondria. Mitochondrial Hsp60 undergoes conformational changes to aid in protein folding, shedding light on mitochondrial proteostasis mechanisms.
G51D α-synuclein mice mimic disease symptoms, showing cilia loss in specific neurons and impaired neurotrophic signaling, contributing to disease progression. This highlights the role of ciliary dysfunction in Parkinson’s.
