SDPR induces membrane curvature and functions in the formation of caveolae.
Bottom Line: STB colocalizes extensively with both SDPR and caveolin 1.Loss of caveolae reduces the propensity of STB to induce membrane tubulation.We conclude that SDPR is a membrane-curvature-inducing component of caveolae, and that STB-induced membrane tubulation is facilitated by caveolae.
Affiliation: MRC-LMB, Cambridge, UK.
Caveolae are plasma membrane invaginations with a characteristic flask-shaped morphology. They function in diverse cellular processes, including endocytosis. The mechanism by which caveolae are generated is not fully understood, but both caveolin proteins and PTRF (polymerase I and transcript release factor, also known as cavin) are important. Here we show that loss of SDPR (serum deprivation protein response) causes loss of caveolae. SDPR binds directly to PTRF and recruits PTRF to caveolar membranes. Overexpression of SDPR, unlike PTRF, induces deformation of caveolae and extensive tubulation of the plasma membrane. The B-subunit of Shiga toxin (STB) also induces membrane tubulation and these membrane tubes also originate from caveolae. STB colocalizes extensively with both SDPR and caveolin 1. Loss of caveolae reduces the propensity of STB to induce membrane tubulation. We conclude that SDPR is a membrane-curvature-inducing component of caveolae, and that STB-induced membrane tubulation is facilitated by caveolae.
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Mentions: Over-expression of SDPR causes accumulation of pronounced tubes in both HeLa and cav1−/− MEF cells, suggesting that SDPR may be able to stablize or generate membrane curvature. Labeling of HeLa cells with fluorescent antibodies against the plasma membrane marker CD59 confirmed that the SDPR-positive tubes are composed of plasma membrane derived membrane, and that these tubes are induced by expression of SDPR as they were not observed in non-transfected cells (Figure 5A). Expression of un-tagged SDPR also resulted in extensive membrane tubulation (Supplementary Figure 5B).