The PDF file includes:

• Supplementary Materials and Methods
• Fig. S1. The complex analysis of the hits from the mitochondrial morphology screening.
• Fig. S2. The mitochondrial morphology in the fat body tissues with indicated gene RNAi is shown.
• Fig. S3. Sixteen genes encoding proteasome components were identified in this mitochondrial morphology screening.
• Fig. S4. Twenty-seven genes encoding spliceosome components were identified in this mitochondrial morphology screening.
• Fig. S5. The reduction of the enzymes involved in tyrosine and lysine metabolism led to abnormal mitochondrial morphology.
• Fig. S6. Loss of Dhpr leads to the reduction of life span and increase of the ROS production.
• Fig. S7. The overexpression of Pink1 or park partially rescues muscle defects caused by Dhpr RNAi.
• Fig. S8. The genetic interaction between Dhpr and genes whose products consume or produce BH4.
• Fig. S9. The genetic interaction between Dhpr and other core machinery of mitochondrial fusion and fission.
• Fig. S10. The model of how Dhpr regulates mitochondrial morphology.

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Other Supplementary Material for this manuscript includes the following:

• Table S1 (Microsoft Excel format). The list of the RNAi lines used in this screening and their corresponding genes.
• Table S2 (Microsoft Excel format). The annotation of the phenotypes and the quantification data.
• Table S3 (Microsoft Excel format). The list of genes that had two or three independent RNAi lines and genes that had been reported to be involved in regulating mitochondria.
• Table S4 (Microsoft Excel format). The list of protein complexes required for mitochondrial morphology maintenance.
• Table S5 (Microsoft Excel format). The lists of genes encoding spliceosome, proteasome, and electron transfer chain components that have been identified in this screen.