Tejeda-Guzmán Carlos, Rosas-Arellano Abraham, Kroll Thomas, Webb Samuel M, Barajas-Aceves Martha, Osorio Beatriz, Missirlis Fanis
Departamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México, C.P. 07360, México.
Stanford Synchrotron Radiation Lightsource, SLAC National Accelerator Laboratory, Stanford University, Menlo Park, CA 94025, USA.
J Exp Biol. 2018 Mar 19;221(Pt 6):jeb168419. doi: 10.1242/jeb.168419.
Membrane transporters and sequestration mechanisms concentrate metal ions differentially into discrete subcellular microenvironments for use in protein cofactors, signalling, storage or excretion. Here we identify zinc storage granules as the insect's major zinc reservoir in principal Malpighian tubule epithelial cells of The concerted action of Adaptor Protein-3, Rab32, HOPS and BLOC complexes as well as of the white-scarlet (ABCG2-like) and ZnT35C (ZnT2/ZnT3/ZnT8-like) transporters is required for zinc storage granule biogenesis. Due to lysosome-related organelle defects caused by mutations in the homologous human genes, patients with Hermansky-Pudlak syndrome may lack zinc granules in beta pancreatic cells, intestinal paneth cells and presynaptic vesicles of hippocampal mossy fibers.
膜转运蛋白和隔离机制将金属离子以不同方式浓缩到离散的亚细胞微环境中，用于蛋白质辅因子、信号传导、储存或排泄。在这里，我们确定锌储存颗粒是昆虫主要马氏管上皮细胞中的主要锌储存库。衔接蛋白3、Rab32、HOPS和BLOC复合物以及白色-猩红色（ABCG2样）和ZnT35C（ZnT2/ZnT3/ZnT8样）转运蛋白的协同作用是锌储存颗粒生物发生所必需的。由于同源人类基因突变导致溶酶体相关细胞器缺陷，赫尔曼斯基-普德拉克综合征患者的β胰腺细胞、肠道潘氏细胞和海马苔藓纤维的突触前囊泡中可能缺乏锌颗粒。
