Galectins are β-galactoside-binding animal lectins primarily found in the cytosol, while their carbohydrate ligands are mainly distributed in the extracellular space. Cytosolic galectins are anticipated to accumulate on damaged endocytic vesicles through binding to glycans initially displayed on the cell surface and subsequently located in the lumen of the vesicles, and this can be followed by cellular responses. To facilitate elucidation of the mechanism underlying this process, we adopted a model system involving induction of endocytic vesicle damage with light that targets the endocytosed amphiphilic photosensitizer disulfonated aluminum phthalocyanine. We demonstrate that the levels of galectins around damaged endosomes are dependent on the composition of carbohydrates recognized by the proteins. By super resolution imaging, galectin-3 and galectin-8 aggregates were found to be distributed in distinct microcompartments. Importantly, galectin accumulation is significantly affected when cell surface glycans are altered. Furthermore, accumulated galectins can direct autophagy adaptor proteins toward damaged endocytic vesicles, which are also significantly affected following alteration of cell surface glycans. We conclude that cytosolic galectins control cellular responses reflect dynamic modifications of cell surface glycans.

中文翻译：

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细胞内半乳糖凝集素控制与细胞表面碳水化合物组成相对应的细胞反应。

半乳凝素是主要存在于细胞质中的β-半乳糖苷结合动物凝集素，而它们的碳水化合物配体则主要分布在细胞外空间。预计通过与最初显示在细胞表面并随后位于囊泡内腔中的聚糖结合，胞质半乳糖凝集素会积聚在受损的内吞囊泡上。为便于阐明该过程的潜在机制，我们采用了一种模型系统，该系统涉及以内吞的两亲光敏剂二磺化铝酞菁为目标的光诱导内吞小泡损伤。我们证明受损的内体周围的半乳糖凝集素水平取决于蛋白质识别的碳水化合物的组成。通过超分辨率成像，发现galectin-3和galectin-8聚集体分布在不同的微区室中。重要的是，当细胞表面聚糖被改变时，半乳糖凝集素的积累会受到显着影响。此外，积累的半乳糖凝集素可以将自噬衔接蛋白引导至受损的内吞小泡，这些内吞小泡在细胞表面聚糖改变后也会受到明显影响。我们得出结论，胞质半乳糖凝集素控制细胞反应反映了细胞表面聚糖的动态修饰。细胞表面聚糖的改变也明显地影响了它们。我们得出结论，胞质半乳糖凝集素控制细胞反应反映了细胞表面聚糖的动态修饰。细胞表面聚糖的改变也明显地影响了它们。我们得出结论，胞质半乳糖凝集素控制细胞反应反映了细胞表面聚糖的动态修饰。