Expression of OA1 limits the fusion of a subset of MVBs with lysosomes – a mechanism potentially involved in the initial biogenesis of melanosomes

Abstract

There was an error published in J. Cell Sci. 126, 5143-5152.The affiliations for Rosanna Piccirillo and Maria Vittoria Schiaffino were given incorrectly.

Evidence for Protein–Protein Interaction between Dopamine Receptors and the G Protein-Coupled Receptor 143

“…Rather than small distinct organelles, macromelanosomes form, thus GPR143 appears to function as a “sensor” of melanosomal maturation to prevent formation of macro-organelles [ 30 ]. GPR143 function has also been shown to modulate the number of early-stage melanosomes [ 59 ] and form the trafficking fork separating lysosome and early melanosome bound proteins [ 60 ]. GPR143 may also control intracellular melanosome transport by regulating microtubule-mediated motility through interaction with tubulin [ 37 ].…”

The Convergence of Extracellular Vesicle and GPCR Biology

“…In addition, GPCR signaling can influence MVB fusion with lysosomes (Figure 1, step b), as has been shown for GPR143 (ocular albinism 1). This receptor resides in the limiting membrane of pigment cell MVBs and limits their fusion with lysosomes to promote melanosome (see Glossary) biogenesis [27]. Further, the orphan receptor GPR137 localizes to late endosomal/lysosomal compartments, where it regulates lysosome morphology and autophagy via the recruitment and activation of mTORC1 (Figure 1) [28].…”

Lysosomal storage disease in the brain: mutations of the β-mannosidase gene identified in autosomal dominant nystagmus

“…33,34 Yet, the G-protein-coupled receptor 143 encoded by GPR143, which is responsible for X-linked congenital nystagmus 6, also targets the lysosome 35 and delays delivery of multivesicular bodies, not the GPR143 gene product itself, to the lysosome. 36 Many G-protein-coupled receptors regulate myelin-associated glycoprotein in neuronal cells. Moreover, it is worth noting that nystagmus has been proposed as a key clinical symptom for the diagnosis of CNS hypomyelination.…”