Lee YouJin, Ouyang Qing, Riaz Hasib Aamir, Ma Li, Fleishman Morgan, Schmidt Michael, Dupree Jeffrey L, Lambright David G, Morrow Eric M
bioRxiv. 2024 Dec 12:2024.12.09.627558. doi: 10.1101/2024.12.09.627558.
Endosome maturation requires progressive lumen acidification. To what extent is lumen acidification sensed by cytosolic-side molecules that drive endosome maturation? We show here that "inside-out" proton signaling through the endosomal Na+/H+ Exchanger 6 (NHE6) activates the late endosome master regulator Rab7. The mechanism involves potent inactivation of the Rab7 GTPase-activating protein (GAP) TBC1D5 with decreasing pH. NHE6 interacts with TBC1D5 in a complex with Rab7. Neurons from NHE6-null mice or mice engineered with a selective defect in NHE6 proton efflux exhibit blocked endosome maturation and decreased active Rab7, consistent with an overactive Rab7 GAP. Finally, epistatic knock-down of TBC1D5, thereby reducing Rab7 GAP activity, in NHE6-null neurons rescues Rab7 GTPase cycling and endosome maturation. Importantly, NHE6 is mutated in Christianson Syndrome underscoring the significance of these mechanisms to neurodegeneration. We conclude that lumen acidification regulates pH-dependent Rab GTPase cycling to coordinate late endosome maturation by a process involving proton signaling.
内体成熟需要管腔逐步酸化。驱动内体成熟的胞质侧分子在多大程度上感知到管腔酸化?我们在此表明,通过内体钠/氢交换体6(NHE6)的“由内而外”质子信号激活晚期内体主调节因子Rab7。其机制涉及随着pH降低,Rab7 GTP酶激活蛋白(GAP)TBC1D5的有效失活。NHE6在与Rab7形成的复合物中与TBC1D5相互作用。来自NHE6基因敲除小鼠或经基因工程改造具有NHE6质子外流选择性缺陷的小鼠的神经元表现出内体成熟受阻和活性Rab7降低,这与Rab7 GAP过度活跃一致。最后,在NHE6基因敲除的神经元中对TBC1D5进行上位性敲低,从而降低Rab7 GAP活性,挽救了Rab7 GTP酶循环和内体成熟。重要的是,克里斯蒂安森综合征中NHE6发生了突变,突出了这些机制对神经退行性变的重要性。我们得出结论,管腔酸化通过涉及质子信号的过程调节pH依赖的Rab GTP酶循环,以协调晚期内体成熟。