ArticleThe Journal of biological chemistry2026
Arylsulfatase L is a Golgi chondroitin sulfatase regulating skeletal development.
Article in The Journal of biological chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Sulfatases are a family of enzymes that hydrolyze sulfate esters from various substrates. Defects, in sulfatase activity, are associated with various human diseases due to the accumulation of sulfated substrates. Deficiency in ARSL, a Golgi sulfatase, is associated with X-linked recessive chondrodysplasia punctata (CDPX), a disorder characterized by defects in cartilage and bone development. However, until now, ARSL function has remained unknown. In this study, we demonstrate that ARSL promotes 4-O-desulfation of chondroitin sulfate (CS) during proteoglycan biosynthesis. Chondrocytes lacking ARSL exhibit hypersulfated CS and altered responses to TGF-β stimulation. Loss of function of ARSL orthologous in medaka fish (Ol-Arsd) results in hyper-4-O-sulfated CS, skeletal malformations, and craniofacial defects that partly resemble the human CDPX phenotype. Our findings uncover a previously unrecognized step in glycosaminoglycan (GAG) maturation-Golgi-based desulfation-and reveal a new layer of regulatory control in skeletal development.
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