A cell-permeable phenylhydrazone that restores mitochondrial tubular network formation in MEF lacking either of the two outer mitochondrial membrane (OMM) mitofusins (EC50=5.3 and 4.42 mM, respectively, in Mfn1 or Mfn2 knockout MEF cells) or in MPP+-treated SH-SY5Y cells (5uM 24h), but not in MEF lacking both Mfn1/2 or the inner mitochondrial membrane (IMM) fusion mediator Opa1 (optic atrophy1). M1 (5uM 24h) is reported to boost the downregulated ATP5A & ATP5B protein level in Mfn1 or Mfn2 knockout MEF to the wild-type MEF level and ATPase inhibitor oligomycin at 5uM is shown to completely offset the mitochondrial fusion effect by 5uM M1 in Mfn1 knockout MEF. Comparing to mdivi-1, M1 exerts its effect via promoting fusion rather than inhibiting fission or division.
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