Department of Genetics, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.
Ubiquitin Project, Tokyo Metropolitan Institute of Medical Science, Setagaya, Tokyo 156-8506, Japan.
Proc Natl Acad Sci U S A. 2024 Jan 9;121(2):e2306454120. doi: 10.1073/pnas.2306454120. Epub 2024 Jan 3.
Mitochondrial and lysosomal functions are intimately linked and are critical for cellular homeostasis, as evidenced by the fact that cellular senescence, aging, and multiple prominent diseases are associated with concomitant dysfunction of both organelles. However, it is not well understood how the two important organelles are regulated. Transcription factor EB (TFEB) is the master regulator of lysosomal function and is also implicated in regulating mitochondrial function; however, the mechanism underlying the maintenance of both organelles remains to be fully elucidated. Here, by comprehensive transcriptome analysis and subsequent chromatin immunoprecipitation-qPCR, we identified hexokinase domain containing 1 (HKDC1), which is known to function in the glycolysis pathway as a direct TFEB target. Moreover, HKDC1 was upregulated in both mitochondrial and lysosomal stress in a TFEB-dependent manner, and its function was critical for the maintenance of both organelles under stress conditions. Mechanistically, the TFEB-HKDC1 axis was essential for PINK1 (PTEN-induced kinase 1)/Parkin-dependent mitophagy via its initial step, PINK1 stabilization. In addition, the functions of HKDC1 and voltage-dependent anion channels, with which HKDC1 interacts, were essential for the clearance of damaged lysosomes and maintaining mitochondria-lysosome contact. Interestingly, HKDC1 regulated mitophagy and lysosomal repair independently of its prospective function in glycolysis. Furthermore, loss function of HKDC1 accelerated DNA damage-induced cellular senescence with the accumulation of hyperfused mitochondria and damaged lysosomes. Our results show that HKDC1, a factor downstream of TFEB, maintains both mitochondrial and lysosomal homeostasis, which is critical to prevent cellular senescence.
线粒体和溶酶体的功能密切相关,对于细胞内稳态至关重要,事实上,细胞衰老、老化和多种突出的疾病都与这两个细胞器的同时功能障碍有关。然而,人们对这两个重要细胞器是如何被调节的还了解甚少。转录因子 EB(TFEB)是溶酶体功能的主要调节因子,也与调节线粒体功能有关;然而,维持这两个细胞器的机制仍有待充分阐明。在这里,通过全面的转录组分析和随后的染色质免疫沉淀-qPCR,我们鉴定了己糖激酶结构域包含 1(HKDC1),它作为糖酵解途径中的一个直接 TFEB 靶标而被熟知。此外,HKDC1 在依赖 TFEB 的方式下在线粒体和溶酶体应激中均上调,其功能对于应激条件下这两个细胞器的维持至关重要。从机制上讲,TFEB-HKDC1 轴对于 PINK1(PTEN 诱导的激酶 1)/Parkin 依赖性线粒体自噬至关重要,因为它是 PINK1 稳定的初始步骤。此外,HKDC1 与电压依赖性阴离子通道的相互作用对于清除受损的溶酶体和维持线粒体-溶酶体接触至关重要,HKDC1 和电压依赖性阴离子通道的功能都是必需的。有趣的是,HKDC1 调节线粒体自噬和溶酶体修复,而不依赖其在糖酵解中的预期功能。此外,HKDC1 的功能丧失加速了 DNA 损伤诱导的细胞衰老,伴随着过度融合的线粒体和受损的溶酶体的积累。我们的结果表明,作为 TFEB 下游的因子,HKDC1 维持了线粒体和溶酶体的内稳态,这对于防止细胞衰老至关重要。