细胞铁稳态受到严密调控，而线粒体在细胞代谢及铁稳态调控中居于核心地位，通过囊泡向线粒体输送铁是一种高效安全的方式。SNARE家族参与不同膜性细胞器囊泡识别与融合，而专一性负责线粒体囊泡融合的SNARE蛋白及其复合体仍然未知。我们前期工作表明SNARE家族蛋白Syntaxin12与线粒体存在共定位，Syntaxin12敲除小鼠心肌线粒体形态异常及心脏功能异常。同时，Syntaxin12敲除小鼠心脏铁缺乏。因此提出假说，Syntaxin12参与线粒体囊泡融合及铁转运，进一步影响心脏发育。我们拟利用超高分辨实时监测Syntaxin12囊泡，明确其是否参与线粒体囊泡融合；通过免疫共沉淀与质谱结合的方式筛出与Syntaxin12互作且调控线粒体囊泡融合的蛋白，阐明其作用机制。我们将进一步明确Syntaxin12调控线粒体铁转运及心脏发育的方式，为研究铁紊乱导致的发育异常及人类疾病提供理论基础。

Iron homeostasis of cells is tightly regulated, and mitochondria play a central role in cell metabolism and iron homeostasis regulation. SNARE family proteins are involved in vesicle recognition and fusion of different membranous organelles, however, the specific SNARE proteins and complexes responsible for mitochondrial vesicle fusion are still unclear. Our previous work indicated that Syntaxin 12, a SNARE family member, co-located with mitochondria, and Syntaxin 12 knockout mice had abnormal mitochondrial morphology and cardiac function. Meanwhile, Syntaxin 12 knocked out mice showed iron deficiency in the heart. Therefore, it was hypothesized that Syntaxin 12 was involved in mitochondrial vesicular fusion and iron transport, which further affected heart development. We intend to use ultra-high resolution real-time monitoring of Syntaxin 12 vesicles to determine whether it is involved in mitochondrial vesicle fusion. Proteins that interact with Syntaxin 12 and regulate mitochondrial vesicular fusion were screened out by means of immunoprecipitation and mass spectrometry, and the regulatory mechanism was elucided. We will further clarify how Syntaxin 12 regulates mitochondrial iron transport and heart development, providing a theoretical basis for the study of development defects and human diseases caused by iron disorders.