线粒体Par3功能验证：为何需要区室特异性靶向实验？

The study does not isolate the mitochondrial pool of Par3 as necessary and sufficient for the metabolic and growth phenotypes because all manipulations alter total Par3 rather than using mitochondria-restricted or import-defective rescues (Figures 1, 4, 5). Given Par3's extensive non-mitochondrial functions in cortical signaling and tight junction formation [1], global knockdown/overexpression can rewire proliferation and metabolism via established cortical pathways independent of OGDH. While established methods exist for mitochondrial-specific protein targeting and rescue experiments [2], these approaches were not employed. Without compartment-specific genetics, the link from mitochondrial Par3–OGDH (Figure 3) to OCR/metabolite shifts (Figure 4) and xenograft outcomes (Figure 5) remains inferential.