Fig. 9: Working model. | Nature Communications

Fig. 9: Working model.

From: Impaired mitochondria-initiated crosstalk with lysosomes reciprocally aggravates mitochondrial defect through LManVI

Fig. 9

Knockdown of dMterf4 results in mitochondrial dysfunction, leading to the upregulation of transcription-related genes Med8 and Tfb4. Med8 and Tfb4 form a complex to upregulate the E(z) and pho, which inhibit LManVI transcription, thus affecting the structure and function of lysosomes. Interestingly, inhibited LManVI decreases the transcription level of PGC-1, which further downregulates the expression of nuclear-encoded mitochondrial genes Tim13, ttm3, mtTFB2 and mitochondria-encoded genes ND1, ND3, ND4, ND5, CoI, CoIII, ATPase6, and Cytb through mitochondrial transcription factors mtTFB2. Ultimately, the downregulation of PGC-1 aggravates the mitochondrial defect phenotypes of dMterf4 RNAi. Therefore, the communication between mitochondria and lysosomes after knockdown of dMterf4 can modulate the phenotypes of impaired mitochondria.

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