Neisch Amanda L, Pengo Thomas, Avery Adam W, Li Min-Gang, Hays Thomas S
Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455, USA.
University of Minnesota Informatics Institute, University of Minnesota, Minneapolis, MN 55455, USA.
J Cell Sci. 2025 Mar 1;138(5). doi: 10.1242/jcs.263844. Epub 2025 Mar 12.
Cytoplasmic dynein is essential in motor neurons for retrograde cargo transport that sustains neuronal connectivity. Little, however, is known about dynein function on the postsynaptic side of the circuit. Here, we report distinct postsynaptic roles for dynein at neuromuscular junctions in Drosophila. Intriguingly, we show that dynein puncta accumulate postsynaptically at glutamatergic synaptic terminals. Moreover, Skittles (Sktl), a phosphatidylinositol 4-phosphate 5-kinase that produces phosphatidylinositol 4,5-bisphosphate (PIP2) to organize the spectrin cytoskeleton, also localizes specifically to glutamatergic synaptic terminals. Depletion of postsynaptic dynein disrupted the accumulation of Skittles and the PIP2 phospholipid, and organization of the spectrin cytoskeleton at the postsynaptic membrane. Coincidental with dynein depletion, we observed an increase in the size of ionotropic glutamate receptor (iGluR) fields and an increase in the amplitude and frequency of miniature excitatory junctional potentials. PIP2 levels did not affect iGluR clustering, nor did dynein affect the levels of iGluR subunits at the neuromuscular junction. Our observations suggest a separate, transport-independent function for dynein in iGluR cluster organization. Based on the close apposition of dynein puncta to the iGluR fields, we speculate that dynein at the postsynaptic membrane contributes to the organization of the receptor fields, hence ensuring proper synaptic transmission.
胞质动力蛋白对于运动神经元中维持神经元连接性的逆行货物运输至关重要。然而,对于动力蛋白在神经回路突触后一侧的功能却知之甚少。在此,我们报告了果蝇神经肌肉接头处动力蛋白在突触后具有不同的作用。有趣的是,我们发现动力蛋白斑点在谷氨酸能突触终末的突触后积累。此外,Skittles(Sktl),一种产生磷脂酰肌醇4,5-二磷酸(PIP2)以组织血影蛋白细胞骨架的磷脂酰肌醇4-磷酸5-激酶,也特异性地定位于谷氨酸能突触终末。突触后动力蛋白的缺失破坏了Skittles和PIP2磷脂的积累,以及突触后膜血影蛋白细胞骨架的组织。与动力蛋白缺失同时发生的是,我们观察到离子型谷氨酸受体(iGluR)场的大小增加,以及微小兴奋性突触后电位的幅度和频率增加。PIP2水平不影响iGluR的聚集,动力蛋白也不影响神经肌肉接头处iGluR亚基的水平。我们的观察结果表明动力蛋白在iGluR簇组织中具有独立于运输的功能。基于动力蛋白斑点与iGluR场的紧密相邻,我们推测突触后膜上的动力蛋白有助于受体场的组织,从而确保适当的突触传递。